Uric acid structural formula. Uric acid: reasons for increase, norm in blood test Biochemistry of uric acid

URIC ACID(purine-2,6,8-trione), formula I, molecular mass 168.12; colorless crystals; t.various 400 °C; DH 0 burn -1919 kJ/mol; poorly soluble in water, ethanol, diethyl ether, soluble in dilute solutions of alkalis, hot H 2 SO 4, glycerin. In solution it exists in tautomeric equilibrium with the hydroxy form (formula II), with the oxo form predominating.

Uric acid, organic acid, purine trioxide; represents white crystalline substance, very soluble in water, soluble in alcohol and glycerin; it decomposes heat, developing hydrocyanic acid. It is very sensitive to oxidizing agents and exhibits characteristic Murishide and Schiff reactions. It can be synthesized using various procedures. Along with urates, it is a component of one of the most common types of urinary calculations; their accumulation in tissues, especially in the cartilage of small joints and in para-articular joints, is the most characteristic phenomenon clinical manifestations of gout, which may culminate in the formation of so-called Gothic foals.

M. is a dibasic acid (pK a 5.75 and 10.3), forms acidic and moderate salts (urates). Under the influence of caustic alkalis and conc. acids decomposes into HCl, NH 3, CO 2 and glycine. Easily alkylates first at N-9, then at N-3 and N-1. In the hydroxy form, the nucleophile reacts. substitution; for example, with POCl 3 it forms 2,6,8-trichloropurine. Composition of oxidation products URIC ACID. depends on reaction conditions; under the influence of HNO 3, alloxanthin (III) and alloxan (IV) are formed, during oxidation with a neutral or alkaline solution of KMnO 4, as well as solutions of PbO 2 and H 2 O 2 - first allantoin (V), then hydantoin (VI) and parabanic acid ( VII). Alloxanthin with NH gives murexide, which is used to identify URIC ACID.

In humans it is about 4 mg in 100 ml of total blood. There is an increase in uricemia in addition to gout and other turbines of purine replacement, cell destruction, and kidney failure. The term “uricemia” indicates pathological manifestations associated with high uricemia. Uricuria is the removal of urea. and urates, partly from tissue purine replacement, partly from dietary supplements. For example, allopurinol is an inhibitor of uricin because it acts as a competitive inhibitor of xanthine dehydrogenase and xanthine oxidase, two enzymes responsible for the conversion of hypoxanthine and xanthine to urea, purine catabolism.

Mk is a product of nitrogen metabolism in the body of animals and humans. Contained in tissues (brain, liver, blood) and sweat of mammals. The normal content in 100 ml of human blood is 2-6 mg. Monosodium salt is a component of bladder stones. Dried bird excrement (guano) contains up to 25% URIC ACID. and serve as a source for obtaining it. Synthesis methods: 1) condensation of uramyl (aminobarbituric acid) with isocyanates, isothiocyanates or cyanoate K through the formation of pseudouric acid (VIII), for example:

Their prototype is probenecid; their main indication is gout. The term "blood sugar" refers to the amount of glucose in the blood. Glucose is the main source of energy for tissues in the body and the most common indicator of carbohydrate metabolism. Maintaining blood sugar levels within certain limits is important for the proper functioning of all organs and tissues in the human body. Blood sugar testing is a screening test looking for pathological abnormalities.

This is usually done in the morning to test your fasting blood sugar levels. In patients with diabetes, a blood sugar test is performed to evaluate treatment: either diet or diet in combination with medications - tablets or insulin. Blood sugar is tested at different times of the day as prescribed by your doctor, so some measurements are taken while fasting and others are taken after a meal.

2) condensation of urea with cyanoacetic ester, followed by isomerization of the resulting cyanoacetylurea into ura-mil, from which URIC ACID is obtained according to the first method.

M.k. is the starting material for the production of allantoin, alloxan, parabanic acid, caffeine; cosmetic component creams; corrosion inhibitor; an agent that promotes uniform dyeing of fibers and fabrics.

Creatinine is one of the most important indicators for characterizing the condition of the kidneys and their function. The formation of creatinine depends on muscle mass. For this reason, its values ​​are slightly higher in men than in women. The degree of creatinine release depends on age. Serum creatinine levels contain information about the extent and stage of chronic renal failure.

Bilirubin is the main pigment in bile juice. It is this yellow color that leads to the precipitation of bilirubin in the tissues. Jaundice is a leading, although sometimes late, symptom in most diseases of the liver, bile ducts, hemolytic anemias and many inherited and acquired disorders of bilirubin metabolism.

Chemical encyclopedia. Volume 3 >>

“Gout has spread to the rich and noble.” This line is from Krylov's fable. The poem is called "Gout and the Spider." Gout was considered a disease of the rich old times, when it was in short supply and cost a lot.

She could only afford seasoning, sometimes by leaning on it. As a result, it was deposited in the joints, causing pain when moving. The disease is a metabolic disorder.

An important contributor to blood clotting, fibrinogen levels increase in response to tissue inflammation. Fibrinogen levels are one of the most common laboratory tests that indicate acute phase inflammatory reactions. Because the development of atherosclerosis and cardiovascular disease are essentially inflammatory processes, elevated fibrinogen levels may help predict the risk of heart disease and stroke.

Urea is an important end product of protein metabolism. Most of The resulting urea is excreted from the body through the kidneys, small amounts are excreted through the gastrointestinal tract and skin. In some cases, urea may be elevated above or below normal and test limits and can provide valuable information about the condition of the body.

Not just salt is deposited, but uric acid salts. They are called urates. An excess of urinary fluid in the body is called hyperurecemia. Its symptoms can be spots that resemble mosquito bites.

Joint destruction due to high uric acid

In modern times, they appear not only on the rich. Salt is available to everyone, like many other products containing urates. There is also a low urea content. But, before analyzing the diagnoses, let’s get acquainted with the properties.

Complete whey protein includes all proteins in the blood minus blood, hemoglobin and fibrinogen. In healthy adults, total protein values ​​are within certain limits. Some diseases experience abnormalities. The end product of the metabolism of purine nucleic acids in the body. The detected uric acid is excreted by the kidneys. In a healthy body, uric acid dissolves in the blood and tissue fluids. Gout is a disease in which uric acid in the blood forms urate crystals. Ureates are deposited in soft tissues, bones and internal organs and lead to joint cramps and other injuries.

Properties of uric acid

The heroine was discovered by Karl Scheele. A Swedish chemist extracted the substance from the kidneys. Therefore, the chemist named the compound. Later, Scheele found it in the urine, but did not rename the substance.

This was done by Antoine Fourcroix. However, neither he nor Scheele could establish the elementary composition of the compound. The formula was recognized by Lutus Liebig almost a century later, in the mid-19th century. In the molecule of the heroine of the article there were 5 atoms, 4, the same and 3 oxygen.

Elevated concentrations of uric acid are an important risk factor for the development of coronary heart disease. When albumin decreases to 50% or more of reference values, edema develops. Investigations: water/electrolyte imbalances; loss of albumin from the intravascular space; assessment of protein metabolism. Biological material: serum, urine.

Low density lipoproteins

Drugs that can increase albumin include: anabolic steroids, androgens, growth hormone, insulin. There are two main types of lipoproteins that work in opposite directions. They carry cholesterol from the liver to the rest of the body.

Uric acid It is not by chance that it is deposited in the kidneys. The substance is poorly soluble in water - the basis of the human body. Ethanol and diethyl ether also do not “take” the compound. Dissociation is possible only in alkali solutions. In glycerol, urea dissolves when heated.

Uric acid in the body is. They are biogenic. True, there is no article in the heroine’s products. But they contain purines, which are necessary for the formation of the compound. Most of them are in meat and...

High density lipoproteins

Transports cholesterol from the bloodstream to the liver, where cholesterol is processed and removed from the body. Triglycerides are the major portion of lipids in the diet. The other two main classes of fat are phospholipids and sterols. Triglycerides are formed by the esterification of glycerol with three fatty acid molecules. They are also called triacylglycerols. Triglycerides are taken from food or synthesized in the body. Most triggers are present in adipose, liver, skeletal muscle and the heart. Study: assess the risk of coronary heart disease, diabetes, alcoholism, pancreatitis.

Particularly active uric acid in the blood synthesized after consumption. There are also a lot of purines in turnips, eggplants, radishes, legumes and grapes. Citrus fruits are also on the list.

This condition can lead to other health problems such as gouty arthritis, kidney stones, or even kidney failure. Recent studies have also linked high uric acid levels to hypertension and cardiovascular disease.

Normal uric acid levels. These values ​​can vary from laboratory values ​​to laboratory values. The main factors contributing to increased levels of uric acid in the blood are: Excessive alcohol consumption, kidney failure, obesity, thyroid deficiency, genetics, diabetes, acidosis and other diseases. Some types of cancer and other drugs, such as diuretics, contribute to this condition. Exercise, fasting, and crash dieting can also temporarily increase uric acid levels in the blood.

Uric acid formula

Purines from food only need to be broken down, it will work. Conclusion: the heroine of the article is a purine derivative. removes excess nitrogen from the body. This is also true for reptiles. Urea does this. It is a breakdown product of proteins. The same organism produces during the breakdown of nucleic acids.

In organism uric acid properties exhibits tautomerism. This is the ability to easily change structure. The number of atoms in a molecule and the elements do not change. Their position changes. Different structures of the same substance are called isomers.

There are several tips and natural resources that can help you control his blood levels. In addition, proper diagnosis and subsequent treatment are required under the supervision of healthcare professionals. It is a natural cleanser that can help you remove various waste products from your body, including uric acid.

Add 1 teaspoon of raw, organic, unpasteurized apple cider vinegar to a glass of water. Drink this drink two or three times a day. Gradually, you can increase the amount of cider vinegar to 1 tablespoon per 1 glass of water and continue treatment until the level of uric acid in the blood decreases.

The heroine of the article goes from lactam to lactim state and back. The latter appears only in solutions. Able uric acid level– lactam isomer. Below are their structural formulas.

The heroine of the article can be qualitatively determined by an oxidation reaction. Add to urinary compound bromine water, or hydrogen peroxide. In the first stage of the reaction, alluxane-dialluric is obtained.

Note. Do not take too much cider vinegar as it also reduces potassium levels in the body. It may also negatively affect the effect of diuretics. Although it may seem that this will lead to over-regulation of the body, on the contrary. It creates an alkaline environment and helps neutralize uric acid.

In addition, vitamin C content also helps reduce uric acid levels. Squeeze one lemon juice into a jar of warm water. Continue for at least a few weeks. Ask your doctor about the correct dosage. And dark berry fruits contain compounds that stimulate the body's processes to lower uric acid levels in the blood.

It is converted to alloxatin. All that remains is to douse it. Murexide is formed. He's dark. From them they understand that in the original mixture they were dealing with uric acid.

Symptoms an overabundance of the heroine of the article, or a deficiency is classified as a disease. However, the presence in the body carries and. First, the connection stimulates the central system.

Additionally, blue and purple fruits are rich in flavonoids called anthocyanins, which help lower uric acid levels and reduce inflammation and joint stiffness. Consume one cup of cherries per day for several weeks. You can also drink one or two cups of cherry juice for four weeks.

Known chemically as sodium bicarbonate, it is very beneficial in reducing uric acid levels and lower joint pain. Helps maintain the natural alkaline balance in the body, increases the solubility of uric acid and promotes its leaching from the kidneys.

How? Urinary acts as an intermediary between adrenaline and its twin norepinephrine. Biological properties hormones are similar. The heroine of the article extends their action. In physiology I call this prolongation.

The second role of urinary acid is its antioxidant effect. The substance captures and removes free radicals from the body. In addition, the heroine of the article prevents the malignant degeneration of cells. But why does excess compound become dangerous? Let's figure it out.

Mix half a teaspoon of baking soda in a glass of warm water. Drink four glasses a day for two weeks. You can drink it every two to four hours. Note: Do not use sodium bicarbonate regularly. Avoid it if you have high blood pressure. People over 60 years of age should not drink more than three glasses of this solution daily.

Many vegetable oils turn into dull yellow fats when heated or processed. They destroy vital vitamin E in the body, which is needed to control uric acid levels in the blood. Choose the healthier alternative of cold pressing and avoid high heat exposure to cooking oil, burnt butter or cooking or baking rub.

Level of uric acid in the body

Causes of high uric acid were indicated. It was also indicated that the substance is poorly soluble in water. In the prime of life, it is 60-70 percent in the body. In older people the level drops to 40%.

Meanwhile, there is a limit that can dissolve in such a volume of liquid, as a rule, blood. Elevated uric acid in in a supersaturated solution precipitates and crystallizes.

Olive oil contains monounsaturated fats that do not change when heated. In addition, it contains high levels of vitamin E and antioxidants. It also has a relatively strong anti-inflammatory effect. Drinking large amounts helps optimize uric acid filtration.

In addition, if you drink water in reasonable quantities and regularly, you can reduce the risk of recurrent attacks on the bottom. For this reason, we recommend drinking 8 to 10 glasses of water per day. Include more fresh fruits and vegetables in your diet with a higher water content.

Nodules that occur with elevated uric acid levels

By sticking together, compacting, they form. They settle in the kidneys and joints. The body perceives formations as uninvited guests. They are surrounded by macrophages - agents of the immune system.

Low purine foods

Purines are nitrogen-containing compounds that break down into uric acid, thereby increasing its content in the body. They are most often found in animal proteins. Therefore, exclude food, especially meat, intestines, fish and poultry. Also high in purines include legumes, shrimp, mushrooms, asparagus and beans. Beer is also rich in the presence of purines.

Foods high in fiber and polysaccharides

High fiber foods help reduce uric acid by absorbing it. Therefore, consume high polysaccharide foods. In addition to fiber, they also have the advantage of only containing small amounts of purines. Whole grains, apples, pears, oranges and strawberries are examples of high fiber foods you can include in your diet.

They seek out strangers, swallow and digest them. Swallowing and digesting tiny bacteria is one thing, but large ones are another. Macrophages begin to break down, releasing hydrolytic elements.

The latter are able to break down salts with the help of water. Destroyed macrophages are essentially purulent, decaying masses. An inflammatory reaction is taking place. She's sick. Therefore, those suffering from gout cannot walk or move with difficulty.

Increased urine output in the analysis can indicate an incipient disease. At the initial stage it is easier to cure, or “preserve”. Let's find out what indicators of the heroine of the article in the analyzes should alert us.

The level of uric acid in the body

Uric acid in men and women has the same norm. The entire body contains 1-1.5 grams. The same amount is withdrawn every day. At the same time, 40% of the substance comes with food, the rest is synthesized by the body.

The last part is unchanged, because nucleic acids will not stop breaking down. Therefore, it is important to monitor the amount of urinary salts coming from outside.

If your diet contains a lot of salty, smoked, meat and alcohol, the risk of kidney stones and gout increases significantly. The risk of stone formations also increases significantly in case of renal failure. The organ begins to be unable to cope with the removal of urine from the body.

Low uric acid– also an alarming signal. Firstly, the normal level of the heroine of the article is responsible for vitality. Secondly, a drop in urinary levels may indicate liver problems.

If the heroine of the article produces kidneys, then it is the liver that produces them. The question arises why the organ fails to cope with its functions.

Sometimes, uric acid in women and men decreases naturally, temporarily, and does not pose a serious threat. We are talking, for example, about burns. When they are extensive, not only the level, but also hemoglobin drops.

The burn will go away and body functions will be restored. The same applies to the state of toxicosis during. There is less urine in the body in the first trimester.

It is during this period of pregnancy that most women suffer from nausea and reluctance to eat. This, by the way, explains the change in blood composition. less comes from food.

Inflammation of the joints due to gout, which is a consequence of increased uric acid in the body

The substance is low in the diet and among those who refuse protein diet, or often drinks strong drinks, . These drinks have a diuretic effect. More of the compound is excreted than can be absorbed into the body.

The last factor that reduces the level of the heroine of the article is taking a number of drugs. Among them: glucose, aspirin, trimethoprim. All products are classified as salicylates, that is, they contain. For it to affect urinary levels, either large doses or long-term use are needed.

From the above it is clear that the popular request “ uric acid diet" - incorrect. For low and high levels of the substance, different diets are recommended. Let's take a look at both options.

Diets for low and high uric acid levels

Let's start with elevated urinary levels in the blood. If one of the main sources of urate is meat, should you give it up? There is no need to become a vegan.

The main thing is to switch to eating exclusively lean meat and only in boiled-steamed form. It is better to avoid eating protein foods every day. Meat dishes 3-4 times a week are the norm. But the broths will have to be put on the back burner.

Diet is the basis for treating high uric acid

You will have to remove from your diet not only broths and fried foods, but also smoked foods and marinades. On the contrary, it is recommended to drink more water so that the excess is excreted in the urine. However, the recommendation applies to patients with healthy kidneys. If they are insufficient water regime discussed with the doctor separately.

The best way to cope with the conclusion of the heroine of the article is not simple, but mineral water. Infusions of flax seeds, carrots and celery are comparable to it. It’s also worth stocking up on birch bud tinctures and cranberry juice.

Alcohol is contraindicated. If drinking is unavoidable, you need to stick to small amounts. A few drinks is the limit. This is a volume that will last at least a week.

If the content of the heroine of the article in the blood reaches 714 micromoles per liter, drug treatment is necessary, and immediate. Diet is not enough here. As for the limit after which the urinary compound necessarily begins to precipitate, it is 387 micromoles per liter.

Wanting to reduce urinary levels, some begin to fast. This gives the opposite result. It seems that you are depriving the body of 40% of what it gets from food... Only this is perceived as a stressful situation.

In a state of shock, the body's systems sharply increase the production of urinary compounds, just as they store fat after going through difficult nutritional times. So, there is no need to starve yourself. You need to eat fully and often, splitting food into small portions.

If you have high uric acid, you should not eat meat.

It’s not difficult to guess that the diet for low urinary tract is the opposite of the one already given. Of course, you shouldn't drink alcohol. But you can indulge in meat dishes, fried foods and other delicacies in the absence of other contraindications, for example, diabetes.

You shouldn’t refuse sunbathing either. When exposed to the sun, lipid peroxidation begins. Fighting it, the body releases an increased dose of urinary compound into the blood. You should also expect it during active sports activities.

Interesting facts about uric acid

Finally, here are some interesting facts. Scientists cannot explain the difference in the level of the heroine of the article depending on the blood type. Thus, in those with type 3, acid levels are higher more often than in carriers of blood groups 1, 2 and 4. The Rh factor does not affect the level of uric acid.

An increased acid content in the blood not only leads to gout and “warms up” vitality, but also stimulates mental activity. Let us remember Pushkin, Darwin, da Vinci, Newton, Peter the Great, Einstein.

It is documented that they all suffered from gout. Means, uric acid level in the organisms of geniuses went off scale. It is not known whether they were carriers of blood group 3. Be that as it may, you can console yourself with thoughts of genius. The main thing is not to forget about proper nutrition and visits to the doctor while daydreaming.

It is also interesting that uric acid is needed not only by the body. The substance is used by industrialists. They use it to synthesize caffeine. The process takes place in 2 stages.

First, uric acid is attacked with formamide, or, more simply, with the amine of formic acid. The result of the reaction is xanthine, one of the purine bases. It is methylated with demethyl sulfate.

This begins the second stage of the reaction. She gives caffeine. Although, if the interaction conditions change, theobromine can also be obtained. It makes up cocoa. To synthesize the latter, heating to 70 degrees and the presence of methanol is required. Caffeine is obtained at room temperature in a weak alkaline environment.

We will talk about the peculiarities of the metabolism of purine bases. This means nothing to most people. But if you are familiar with the words “gout”, urolithiasis disease, insulin resistance, type 2 diabetes mellitus, then it is necessary to know the essence of purine metabolism. It would seem: what does surgery have to do with it? And despite the fact that many specialists diagnose “gout” with pain in the joints and high uric acid. In reality, everything is much more complicated. For example, gouty arthritis can occur with normal uric acid levels, and vice versa: high uric acid can occur in some cases in a healthy person.

The human body is mainly composed of four chemical elements, which account for 89% of the composition: C-carbon (50%), O-oxygen (20%), H-hydrogen (10%) and N-nitrogen (8.5%). Next comes a number of macroelements: calcium, phosphorus, potassium, sulfur, sodium, chlorine, etc. Then microelements, the amount of which is very small, but they are vital: manganese, iron, iodine, etc.
We will be interested in the fourth in this quantitative list - nitrogen.

A living organism is a dynamic system. To put it simply: substances constantly enter it (becoming part of the body) and are removed from it. The main source of nitrogen for the body is proteins. Protein supplied with food in the gastrointestinal tract breaks down into amino acids, which are then included in the metabolism. Well, how are nitrogen-containing substances removed from the body?

In the process of evolution, animals have developed certain characteristics of nitrogen metabolism.
Moreover, the key in determining these features will be: living conditions and access to water.

Animals are divided into three groups that have differences in nitrogen metabolism:

Ammoniolytic. The end product of nitrogen metabolism is ammonia, NH3. This includes most aquatic invertebrates and fish.
The thing is that ammonia is a toxic substance. And to remove it you need a lot, a lot of liquid. Fortunately, it is highly soluble in water. With access to land during evolution, a need arose to change metabolism. This is how they appeared:

Ureolytic. These animals developed the so-called “urea cycle.” Ammonia combines with CO2 (carbon dioxide). The final product is formed - urea. Urea is not such a toxic substance and noticeably less liquid is required to remove it. By the way, you and I belong to this group. Uric acid is also formed during metabolism in much smaller quantities, but breaks down to low-toxic and highly soluble allantoin. But... Except for humans and apes. This is very important and we will return to this.

Uricotelic. The ancestors of amphibians with ureolytic metabolism had to adapt to arid regions. These are reptiles and the direct ancestors of dinosaurs - birds. Their end product is uric acid. It dissolves very poorly in water and does not require much water to remove it from the body. In the droppings of the same birds, the amount of uric acid is very large; it is actually excreted in a semi-solid form. Therefore, bird droppings (“guano”) are the main cause of corrosion and destruction of metal structures of bridges. The car's paintwork also deteriorates - be careful and wash it right away.
This is a classic hexagonal liver lobule. In general, this is what the liver looks like under a microscope. Similar to Moscow City, only instead of the Kremlin there is a central vein. And we will be interested in “houses” that are closely adjacent to each other. These are hepatocytes - key cells liver.
The Slavic word liver comes from the word “oven”. Indeed, the temperature of the organ is one degree higher than body temperature. The reason for this is a very active metabolism in hepatocytes. Cells are truly unique; about 2 thousand chemical reactions take place in them.
The liver is the main organ that produces uric acid. 95% of excreted nitrogen is the synthesis of uric acid as the end product of chemical reactions in the liver. And only 5% is the oxidation of purine bases coming from outside with food. Therefore, nutritional correction for hyperuricemia is not the key to treatment.

Uric acid metabolism diagram

Where do purines come from?
1. Purines that come from food . As already noted, this is a small amount - about 5%. Those purines that are contained in food (most of all, of course, in the liver and kidneys, red meat).
2. Synthesis of purine bases by the body itself . Most of it is synthesized in liver hepatocytes. A very important point, we will return to it. And what does fructose have to do with it, which is recommended by diabetics and does not require insulin for absorption.
3. Purine bases, which are formed in the body due to tissue breakdown: during cancer processes, psoriasis . Why can uric acid levels rise in athletes? This is the third way. Heavy physical activity leads to increased processes of tissue breakdown and synthesis. If you did heavy work the day before physical labor, and in the morning you get tested, your uric acid level may be higher than your average.

Let's get acquainted: adenine and guanine. These are purine bases. Together with thymine and cytosine, they form a DNA helix. Medical students don’t like cramming for a biochemistry course :). As you know, DNA consists of two chains. Opposite to adenine is always thymine, and opposite to guanine is cytosine. The two strands of DNA stick together like the two halves of a zipper. The amount of these substances increases with active tissue breakdown, as happens, for example, during cancer processes

Through a series of successive chemical reactions, purines are converted to uric acid.

Metabolism of uric acid in humans and primates

I planned to make the diagram as easy to understand as possible. Let 2nd year medical students teach :). But he left the names of the enzymes. The most important point is xanthine oxidase enzyme . It is its activity that decreases during treatment allopurinol(more precisely, effectiveness, since allopurinol competes with it for the receptor), which reduces the synthesis of uric acid.
Rarely, congenital disease accompanied by genetic disorder in the synthesis of xanthine oxidase, in which the level of uric acid is reduced. In this case, xanthine and hypoxanthine accumulate. Xanthinuria. It would seem good, less uric acid. However, it turned out that uric acid is not only harmful, but also beneficial...

The conversation about the dangers and benefits of uric acid should start from afar. Then, 17 million years ago, during the Miocene era, our ancestors experienced a mutation in the gene that produces the enzyme, uricase. And we got a “cut down” version of purine metabolism.

In other mammals, uricase converts uric acid into allantoin, which is soluble and easily excreted from the body. And these animals never have gout. There may be an assumption that this mutation does not make any sense. But evolution did not exclude this gene: the mutation turned out to be necessary.

Modern research has shown that uric acid is a byproduct of the breakdown of fructose in the liver and the accumulation of uric acid salts contributes to the efficient conversion of fructose into fat. Thus, the gene for “thrift” was fixed in the genome of our ancestors. Then the gene was needed to create reserves for the hungry period. It was proven that the final inactivation of uricase coincided with global cooling of the Earth's climate. It was necessary to “eat” as many reserves as possible subcutaneous fat on cold period, convert the fructose contained in the fruits into fat reserves. A number of experiments are now being carried out with the introduction of the enzyme uricase into liver cells. It is possible that in the future, drugs for the treatment of gout will appear based on the uricase enzyme. So our tendency to become obese is in our genes. Unfortunately for those many men and women who suffer from obesity. But the problem is not only genetics. The nature of modern man's diet has changed.

About the harms and benefits of uric acid, as well as about nutrition for hyperuricemia

It is known that constant levels of uric acid can significantly increase the risk of several diseases. However, it has been proven that periodic increase uric acid levels may have a positive effect. Historically, access to meat foods (the main source of purines) was irregular. Main food: various roots, tree fruits. Well, if a primitive hunter brings prey, then it’s a holiday. Therefore, eating meat products periodically was a common way of life. There is prey - we eat to our heart's content. There is no prey - we eat plant foods. It has now been established that short-term, periodic increases in uric acid levels have a beneficial effect on the development and function of the nervous system. Maybe that's why the brain began to develop?

How is this uric acid eliminated from the body?

Two ways: kidneys and liver
The main route is excretion through the kidneys - 75%
25 percent is excreted by the liver using bile. Uric acid that enters the intestinal lumen is destroyed (thanks to our bacteria in the intestines).
Uric acid enters the kidneys in the form of sodium salt. With acidosis (acidification of urine) in renal pelvis microliths may form. The same “sand” and “stones”. By the way, alcohol greatly reduces the excretion of urate in the urine. This is why it leads to an attack of gout.

So, what conclusion should be drawn? Methods for reducing uric acid

1. Try to make 1-2 days a week purely vegetarian
2. The largest amount of purines is found in tissues of animal origin. Moreover, in animal cells with active metabolism: liver, kidneys - most of all.
3. You should eat less fatty foods, since excess saturated fat suppresses the body's ability to process uric acid.
4. Eat less fructose. Uric acid is a product of fructose metabolism. Previously, patients with diabetes were recommended to replace glucose with fructose. Indeed, fructose does not require the participation of insulin for its absorption. But fructose is even harder to digest. Attention: in sugar, the sucrose molecule is a disaccharide - glucose + fructose. So we eat less sugar.
5. Avoid drinking alcohol, especially beer. Wine in small quantities does not affect uric acid levels.
6. Very intense exercise increases uric acid levels.
7. You need to drink a lot of water. This will allow you to effectively remove uric acid.

If you have high uric acid

Well, first of all, fortunately, this is not always a pathology: a short-term rise may be a variant of the norm
If there is still a problem, you need to figure out at what level there is a violation (that very first scheme): disturbances in the synthesis of purines (the same metabolic syndrome), nutritional factor (we eat a lot of meat, drink beer), impaired renal function (impaired excretion of uric acid) or concomitant diseases accompanied by tissue destruction.

Good luck to you and competent doctors.

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What is uric acid? This is a component of not only urine, but also blood. It is a marker of purine metabolism. Its concentration in the blood helps specialists diagnose a number of diseases, including gout. Based on the level of this element in the blood, you can monitor the body’s response to treatment.

What is this element?

In the human body there are constantly metabolic processes. The result of the exchange can be salts, acids, alkalis and many other chemical compounds. To get rid of them, they need to be delivered to the appropriate part of the body. This task is performed with the help of blood, which is filtered by the kidneys. This explains the presence of uric acid in urine.

Let's look at what this is in more detail. Uric acid is the end product of the breakdown of purine bases. These elements enter the body with food. Purines are involved in the synthesis process nucleic acids(DNA and RNA), energy molecules ATP, as well as coenzymes.

It is worth noting that purines are not the only source of uric acid formation. It can be the result of the breakdown of body cells due to disease or old age. The source for the formation of uric acid can be synthesis in any cell of the human body.

The breakdown of purines occurs in the liver and intestines. The cells of the mucous membrane secrete a special enzyme - xanthine oxidase, with which purines react. The end result of this “transformation” is acid.

It contains sodium and calcium salts. The share of the first component is 90%. In addition to salts, this includes hydrogen, oxygen, nitrogen and carbon.

If uric acid is higher than normal, this indicates a metabolic disorder. As a result of such a malfunction, people experience the deposition of salts in their tissues, and as a result, severe diseases develop.

Functions of uric acid

Despite the fact that excess uric acid can cause significant harm to the body, it is still impossible to do without it. She performs protective functions and has beneficial properties.

For example, in the process of protein metabolism, it acts as a catalyst. Its influence also extends to the hormones responsible for brain activity - adrenaline and norepinephrine. This means that its presence in the blood helps stimulate brain function. Its effect is similar to caffeine. People who have increased content uric acid in the blood from birth, are more active and proactive.

It has acidic and antioxidant properties that help heal wounds and fight inflammation.

Uric acid performs protective functions in the human body. She fights free radicals. As a result, the risk of the appearance and development of benign and cancerous tumors is reduced.

Submission of analysis

A similar test is prescribed to determine the patient’s health status, as well as to diagnose a disease that could cause an increase in the level of uric acid in the blood. To obtain true results, you must first prepare for donating blood.

You cannot eat 8 hours before visiting the laboratory; biomaterial is collected on an empty stomach. Spicy, salty and peppery foods, meat and offal, and legumes should be excluded from the menu. This diet should be followed for 24 hours before donating blood. During this same period, you should stop drinking alcoholic beverages, especially wine and beer.

Uric acid may be higher than normal due to stress, emotional stress or physical activity on the eve of the test.

Medicines with a diuretic effect, vitamin C, caffeine, beta-blockers and ibuprofen can also distort the results. If you cannot refuse such medications, you should warn your doctor before taking the test.

The laboratory will take deoxygenated blood. The results of the study are prepared within 24 hours.

Uric acid level in blood test

If the results of the biochemical analysis showed figures corresponding to the data given in the table below, then everything is normal.

As can be seen from the table, the level increases with age. The greatest importance in older men is the level of uric acid in the blood, since the need for proteins in the male body is higher. This means that they consume more foods rich in purine and, as a result, increased uric acid in the blood.

What can cause deviations from the norm?

The level of uric acid in the blood depends on the balance of 2 processes:

• Protein synthesis;
• The intensity of excretion of the final products of protein metabolism.

When a protein metabolism disorder occurs, this can provoke an increase in the content of this acid in the blood. Concentrations of uric acid in the blood plasma above the normal range are referred to as hyperuricemia, concentrations below the normal range are referred to as hypouricemia. Concentrations of uric acid in urine above and below normal are known as hyperuricosuria and hypouricosuria. Salivary uric acid levels may be related to blood uric acid levels.

Causes of hyperuricemia:

• Taking diuretics (diuretics);
• Decrease in the intensity of excretion of substances by the kidneys;
• Toxicosis;
• Alcoholism;
• Kidney failure;
• Malnutrition or prolonged fasting.

Increased levels can also occur in diseases such as AIDS, diabetes, cancer, etc.

It is worth noting that even slightly increased level This substance can cause the formation of solid deposits of uric acid salts - urates - in organs and tissues.

Increased rate

Now we’ll find out why uric acid in the blood is elevated: causes, symptoms and consequences.

In medicine, hyperuricemia is divided into two types: primary and secondary.

Primary hyperuricemia

This type is congenital or idiopathic. This pathology occurs with a frequency of 1%. Such patients have a hereditary defect in the structure of the enzyme, which affects the processing of purine. As a result, there is a high level of uric acid in the blood.

The appearance of secondary hyperuricemia may occur due to poor nutrition. Eating large quantities of foods containing purine can significantly increase the excretion of uric acid in the urine.

This type of hyperuricemia may be associated with the following conditions:

Gout is a painful condition caused by needle-like crystals of uric acid deposited in joints, capillaries, skin and other tissues. Gout can occur if the serum uric acid level reaches 360 µmol/L, but there are cases when the serum uric acid value reaches 560 µmol/L without causing gout.

IN human body purines are metabolized into uric acid, which is then excreted in the urine. Regular consumption of certain types of purine-rich foods - meat, especially beef and pork liver (liver, heart, tongue, kidneys) and some types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel and tuna. There are also foods whose consumption is less dangerous: turkey, chicken and rabbit. Moderate consumption of purine-rich vegetables is not associated with increased risk gout Gout used to be called “the disease of kings” because gourmet foods and red wine contain high levels of purines.

Lesch-Nyhan syndrome

This extremely rare inherited disorder is also associated with high serum uric acid levels. This syndrome causes spasticity, involuntary movement and cognitive retardation, as well as manifestations of gout.

Hyperuricemia may increase risk factors cardiovascular diseases

Stones in the kidneys

Saturated levels of uric acid in the blood can lead to one form of kidney stones when urates crystallize in the kidneys. Acetic acid crystals may also contribute to the formation of calcium oxalate stones by acting as "seed crystals"

Kelly-Siegmiller syndrome;

Increased activity of phosphoribosylpyrophosphate synthetase synthesis;

Patients with this disease do biochemical analysis to increase uric acid annually.

Secondary hyperuricemia

This phenomenon may be a sign of the following diseases:

• AIDS;
• Fanconi syndrome;
• Cancerous tumors;
• Diabetes mellitus (Hyperuricemia may be a consequence of insulin resistance in diabetes, and not its precursor);
• High degree burns;
• Hypereosinophilia syndrome.

There are other reasons for increased uric acid - impaired kidney function. They cannot remove excess acids from the body. As a result, kidney stones may appear.

High levels of uric acid are observed in the following diseases:

• Pneumonia;
• Methyl alcohol poisoning;
• Eczema;
• Typhoid fever;
• Psoriasis;
• Erysipelas;
• Leukemia.

Asymptomatic hyperuricemia

There are cases when the patient has no symptoms of the disease, but the indicators are elevated. This condition called asymptomatic hyperuricemia. It occurs during acute gouty arthritis. Indicators for this disease are unstable. At first, the acid content seems to be normal, but after a while the numbers can double. However, these changes do not affect the patient’s well-being. This course of the disease is possible in 10% of patients.

Symptoms of hyperuricemia

With hyperuricemia, symptoms vary among different age groups.

In very young children the disease manifests itself as skin rashes: diathesis, dermatitis, allergies or psoriasis. The peculiarity of such manifestations is resistance to standard methods therapy.

In older children, the symptoms are somewhat different. They may have stomach pain, slurred speech, and bedwetting.

The course of the disease in adults is accompanied by joint pain. The feet and joints of the fingers are the first to be affected. Then the disease spreads its effect to the knees and elbow joints. In advanced cases, the skin over the affected area turns red and becomes hot. Over time, patients begin to experience pain in the stomach and lower back during urination. If measures are not taken in a timely manner, the blood vessels and nervous system will suffer. The person will suffer from insomnia and headaches. All this can lead to heart attack, angina and hypertension.

Treatment

Some specialists prescribe medications to ensure that uric acid in the blood is normal. But a certain food diet for the rest of life is a more effective treatment method.

If the patient has hyperuricemia, treatment includes dieting. The patient's diet additionally includes:

Carrot juice;

Birch juice;

Flax seed;

Celery juice;

Oatmeal broth;

Cranberry juice;

Rosehip infusion.

These herbal infusions and juices help to quickly dissolve and flush out salt deposits from the body.

Fatty foods, meat broths, fried, salted, smoked and pickled foods are excluded. Meat can only be eaten boiled or baked. It is recommended to avoid consuming meat broths, since purines are transferred from the meat into the broth during their preparation. Meat intake limit – 3 times a week.

Alcoholic drinks are specifically prohibited. IN exceptional cases, you can only have 30 g of vodka. Beer and red wine are especially contraindicated.

Give preference to alkaline mineral water.

Salt consumption should be kept to a minimum. Ideally, it is better to abandon it altogether.

It is necessary to monitor the frequency of food intake. Fasting can only worsen the patient's condition and increase uric acid levels. Therefore, the number of meals per day should be 5-6 times. It is better to spend fasting days on fermented milk products and fruits.

Some types of products should be excluded from the menu:

• Sorrel;
• Salad;
• Tomatoes;
• Grape;
• Chocolate;
• Eggs;
• Coffee;
• Cakes;
• Turnip;
• Eggplant.

Apples, potatoes, plums, pears, and apricots help reduce uric acid levels. You should also monitor water balance– 2.5 liters of liquid per day should be drunk.

Treat high level Acid levels in the blood can also be achieved through physiotherapeutic procedures. This way, plasmapheresis will help cleanse the blood of excess salts. Don't neglect therapeutic exercises. A number of simple exercises (leg swings, “bicycle”, walking in place, etc.) will help stabilize metabolism. Massage also helps break down uric acid salts.

Medicines that are prescribed include complexes that have anti-inflammatory, diuretic and analgesic properties. There are 3 types of drugs for hyperuricemia:

1. Actions aimed at removing excess uric acid: Probenecid, aspirin, sodium bicarbonate, allopurinol.
2. Helps reduce acid production. They are prescribed to patients who have had urolithiasis and those diagnosed with renal failure;
3. Helping to transfer uric acid from the tissue into the blood, and promoting its excretion: “Zinkhoven”.

The course of treatment involves the diagnosis and elimination of concomitant diseases and the factors that caused them. Thereby eliminating the reasons that caused the increase in the level of uric acid in the blood. If uric acid in the blood is elevated, this negatively affects a person’s condition. Salt sediment settles on tissues and organs. Treatment for such a deviation is varied: diet, physiotherapy, medications and ethnoscience. All these techniques together can help normalize acid levels.

URIC ACID- 2,6,8-trioxypurine; in humans it is the end product of purine metabolism. Impaired metabolism of M. is the cause or accompanies diseases such as gout, arthritis, spondylosis, urate and uric acid nephropathies, urolithiasis, obesity, diabetes mellitus, hypertonic disease etc. Significant amounts of M. salts - urates (see) are released in diseases associated with increased breakdown of cells and tissues, for example, in leukemia. Deposits of uric acid compounds (primarily monosodium urate) in tissues can cause local inflammatory and dystrophic changes(see Gout). Disorders of M.'s metabolism are hereditary (primary) and acquired (secondary). Insufficiency of hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) and a number of other enzymes in combination with increased activity Glutathione reductase (EC 1.6.4.2) is the cause of congenital idiopathic familial hyperuricemia, caused by increased synthesis of M. to. Hereditary deficiency of the enzyme hypoxanthine: guanine phosphoribosyltransferase is the cause of severe neurol syndrome in children (Lesch-Nyhan syndrome), the development of which is also associated with hyperuricemia due to increased production of uric acid.

M. can be presented in two forms: lactam, characteristic of free acid, and lactim, which is the result of enolization that occurs during the formation of salts:

M. to. was discovered by Scheele (G. W. Scheele) in 1776 in the composition of urine. M. to. is found in large quantities in the excrement of birds, snakes and in urinary stones. It is a constant component of the urine of mammals and humans, in which it is also found in small quantities in organs, tissues and blood.

Synthetically, M. was obtained by heating urea (see) with trichlorlactic acid amide. The structural formula of M. was finally established by various syntheses, of which the condensation of isodialuric acid with urea and the reaction of 5-nitrouracil in an alkaline solution with sodium dithionite should be noted. The resulting sulfamic acid fuses at 190-200° with urea.

Pure M. K. is a light white powder that crystallizes in the form of microscopic rhombic tablets. IN cold water one part of M. to. dissolves in 39,480 parts of water, in boiling water - one part of M. to. in 1,600 parts of water; M. K. easily dissolves in caustic alkalis, forming with them medium salts as a dibasic acid; M. is insoluble in alcohol and ether. Average salts of calcium and alkali metals are highly soluble in water; acid salts are much less soluble in water. To obtain M. from urine, hydrochloric acid is added to the latter. When M. stands, it precipitates in the form of a crystalline precipitate, colored dark brown. To precipitate M. from solutions, picric acid, phosphotungsten acid, silver salts, cuprous oxide and other precipitants are used. When heated, metallic material becomes charred without melting; its decomposition products are hydrocyanic acid, cyanuric acid, urea and ammonia.

The most common qualitative test for M. is based on its oxidation with nitric acid, this is the so-called. murexide test. When wet ammonia the residue obtained by heating M. with nitric acid develops a purple color, which depends on the formation of purple ammonia salt. A characteristic reaction to M. to. is also its oxidation with copper oxide, which is then reduced to copper oxide. For the quantitative determination of M., it is isolated in the form of ammonium salt and titrated with potassium permanganate. Colorimetric methods for determining M. c. are widely used. In contrast to the products of its breakdown, M. c. is characterized by intense absorption in the UV part of the spectrum with a maximum at 293 nm. This property of M. is also used for its quantitative determination.

The sources of M. excreted from the body are both food and endogenous amino- and oxypurines. In humans, M. to. forms hl. arr. in the liver as a result of the breakdown of nucleotides, deamination of aminopurines and oxidation of the resulting oxypurines - hypoxanthine (see) and xanthine (see) with the participation of the enzyme xanthine oxidase (see). In most mammals, under the influence of the enzyme uricase (EC 1.7.Z.Z.), which is not found in human and anthropoid tissues, M. is oxidized into allantoin.

When there is a disturbance in M.'s metabolism, expressed in its increased formation in the body or in a significant intake of M. into the body from the outside, the acid itself and its salts form crystalline precipitates. Precipitation of these compounds is facilitated by their increased concentration in tissue fluids compared to the norm, as well as a decrease in pH compared to physiol, the norm, temperature changes, impaired blood supply, etc.

The amount of M. in daily human urine is normally 0.4-1 g and does not exceed 2 g; usually it is approx. 1.8% total urine nitrogen. The content of M. in the blood serum of healthy people ranges from 2 to 5 - 6 mg/100 ml.

In clinical biochemistry. In laboratories, the content of M. in blood serum and urine is usually determined by a micro-method, based on the colorimetric determination of the intensity of the blue color developed by adding the Folin reagent (see Lauri method) to the protein-free filtrate of blood serum or urine.

In newborns, the content of M. in the blood immediately after birth averages 5.4 mg/100 ml, reaching 5.8 mg/100 ml by the end of the first day of life and decreasing by the third day to 4.3 mg/100 ml. The high concentration of M. in the blood of newborns in the first day of life is explained by fiziol, hemolysis of erythrocytes, sharp decline the number of leukocytes, as well as catabolic processes that are normal for this age period. Starting from the 2nd year of life and up to 7 years, the concentration of M. in the blood of children is 2.0-2.8 mg/100 ml, which is explained by the intensity of anabolic processes occurring in the child’s body. As the systems and organs of the child’s body mature and improve, the content of M. comes to values ​​characteristic of adults: for girls - 5.5 mg/100 ml, for boys - 6 mg/100 ml.

In healthy newborns, increased catabolism of nucleoproteins (as a result of birth stress) and the limited abilities of the renal tubular apparatus create conditions for the occurrence of so-called uric acid infarction (see) of the kidneys - acute damage to kidney tissue by M. crystals and urates, Ch. arr. ammonium urate and sodium urate. Damage to kidney tissue by M. crystals and urates is sometimes observed in older children treated with drugs that have a cytostatic effect. Excretion of M. to. in the urine (see Uraturia) in children, especially infants, exceeds the amount of M. to. excreted in the urine in adults; the concentration of M. to. in children's urine reaches 1 mg per 1 ml of urine.

In older children, as well as in adults, the wedge, syndromes caused by increased formation and content of M. in the blood (hyperuricemia) and urine (hyperuraturia), are combined under common name uricopathy (see Uric acid diathesis). In military nephropathies in children early age clinically manifested by leukocyturia, then hematuria appears, and in children over 10 years of age, long time suffering from urate nephropathy, proteinuria increases, and the disease begins to resemble chronic nephritis in its course.

Hereditary idiopathic familial hyperuricemia and Lesch-Nyhan syndrome are caused by increased synthesis of M. as a result of congenital deficiency of the enzyme hypoxanthine: guanine phosphoribosyltransferase. In the blood it is found increased amount glutamine, glycine and aspartic acid not only in the sick child, but also in relatives, through whom he inherited this pathology.

Secondary hyperuricemia is most often caused by increased formation of nucleic acids in blood diseases, after radiotherapy, and with decreased renal function.

Diagnosis of metabolic disorders of M. to. includes determination in the blood and urine of the concentration of M. to., purine bases (see), amino acids, carbohydrates, lipids and xanthine oxidase activity.

Bibliography: Zbarekiy B. I., Ivanov I. I. and Mardashev S. R. Biological chemistry, With. 419 and others, L., 1972; P and h l and to E. G. Gout, M., 1970; G e g t 1 e g M. M., Garn S. M. a. Levine S. A. Serum uric acid in relation to age and physique in health and in coronary heart disease, Ann. intern. Med., v. 34, p. 1421, 1951; G r e i 1 i n g H. u. a. Bioche-mische Untersuchungen iiber die Ursache der Harnsaureablagerung im Bindegewebe der Gicht, Z. Rheumaforsch., Bd 21, p. 50, 1962; Me Murray W. C. Essentials of human metabolism, p. 248 a. o., N.Y. a.o., 1977; Rapoport S. M. Medizinische Biochemie, S. 97 u. a., B., 1977.

S. E. Severin; V. P. Lebedev (ped.).

Hydroxy derivatives of purine are widespread in the plant and animal world, the most important of which are uric acid, xanthine and hypoxanthine. These compounds are formed in the body during the metabolism of nucleic acids.

Uric acid. This crystalline, poorly water-soluble substance is found in small quantities in the tissues and urine of mammals. In birds and reptiles, uric acid acts as a substance that removes excess nitrogen from the body (similar to urea in mammals). Guano (dried excrement of seabirds) contains up to 25% uric acid and serves as a source of its production.

Uric acid is characterized by lactam-lactim tautomerism . In the crystalline state, uric acid is in the lactate (oxo-) form, and in solution, a dynamic equilibrium is established between the lactam and lactim forms, in which the lactate form predominates.

Uric acid is a dibasic acid and forms salts - urates - respectively with one or two equivalents of alkali (dihydro- and hydrourates).

Alkali metal dihydrourates and ammonium hydrourate insoluble in water . In some diseases, such as gout and urolithiasis, insoluble urate, along with uric acid, is deposited in the joints and urinary tract.

The oxidation of uric acid, as well as xanthine and its derivatives, is the basis of a qualitative method for the determination of these compounds, called murexide test (qualitative reaction) .

When exposed to oxidizing agents such as nitric acid, hydrogen peroxide or bromine water, the imidazole ring opens and pyrimidine derivatives are initially formed alloxan And dialuric acid . These compounds are further converted into a kind of hemiacetal - alloxanthin , when treated with ammonia one obtains dark red murexide crystals - ammonium salt of purple acid (in its enol form).

Condensed heterocycles: purine – structure, aromaticity; purine derivatives – adenine, guanine, their tautomerism (question 22).

Adenine and guanine. These two amino derivatives of purines, shown below as 9H tautomers, are components of nucleic acids.

Adenine is also part of a number of coenzymes and natural antibiotics. Both compounds are also found in free form in plant and animal tissues. Guanine, for example, is found in fish scales (from which it is isolated) and gives it its characteristic shine.

Adenine and guanine have weak acidic and weak basic properties. Both form salts with acids and bases; picrates are convenient for identification and gravimetric analysis.

Structural analogues of adenine and guanine, acting as antimetabolites of these nucleic bases, are known as substances that suppress the growth of tumor cells. Of the dozens of compounds that proved effective in animal experiments, some are used in domestic clinical practice, for example, mercaptopurine and thioguanine (2-amino-6-mercaptopurine). Other purine-based drugs include the immunosuppressant azathioprine and the antiherpes drug acyclovir (also known as Zovirax).

Nucleosides: structure, classification, nomenclature; relation to hydrolysis.

The most important heterocyclic bases are derivatives of pyrimidine and purine, which in the chemistry of nucleic acids are usually called nucleic bases.

Nucleic bases. For nucleic bases, abbreviated designations are adopted, composed of the first three letters of their Latin names.

The most important nucleic bases include hydroxy and amino derivatives of pyrimidine - uracil, thymine, cytosine and purina - adenine And guanine. Nucleic acids differ in the heterocyclic bases they contain. Thus, uracil is found only in RNA, and thymine is found only in DNA.

Aromaticity of heterocycles in the structure of nucleic bases underlies their relatively high thermodynamic stability. In the substituted pyrimidine ring in lactam forms of nucleic bases, the six-electron π-cloud is formed by 2 p-electrons of the C=C double bond and 4 electrons of two lone pairs of nitrogen atoms. In the cytosine molecule, the aromatic sextet occurs with the participation of 4 electrons of two π-bonds (C=C and C=N) and a lone pair of electrons of pyrrole nitrogen. Delocalization of the π-electron cloud throughout the heterocycle is carried out with the participation of the sp 2 -hybridized carbon atom of the carbonyl group (one in cytosine, guanine and two in uracil, thymine). In the carbonyl group, due to the strong polarization of the π bond, the C=Op orbital of the carbon atom becomes, as it were, vacant and, therefore, capable of taking part in the delocalization of the lone pair of electrons of the neighboring amide nitrogen atom. Below, using the resonance structures of uracil, the delocalization of p-electrons is shown (using the example of one lactam fragment):

Structure of nucleosides. Nucleic bases form cD-ribose or 2-deoxy-D-riboseN-glycosides, which in nucleic acid chemistry are called nucleosides and specifically, ribonucleosides or deoxyribonucleosides, respectively.

D-Ribose and 2-deoxy-D-ribose are found in natural nucleosides in furanose form , i.e. in the form of β-D-ribofuranose or 2-deoxy-β-D-ribofuranose residues. In nucleoside formulas, carbon atoms in furanose rings are numbered with a number with a prime. N -Glycosidic bond occurs between the anomeric C-1 atom of ribose (or deoxyribose) and the N-1 atom of a pyrimidine or N-9 purine base.

(! ) Natural nucleosides are always β-anomers .

Construction titles nucleosides are illustrated by the following examples:

However, the most common names are those derived from trivial the name of the corresponding heterocyclic base with the suffix - Idin in pyrimidines (for example, uridine) and - ozine in purine (guanosine) nucleosides. The abbreviated names of nucleosides are a single-letter code using the initial letter of the Latin name of the nucleoside (with the addition of the Latin letter d in the case of deoxynucleosides):

Adenine + Ribose → Adenosine (A)

Adenine + Deoxyribose → Deoxyadenosine (dA)

Cytosine + Ribose → Cytidine (C)

Cytosine + Deoxyribose → Deoxycytidine (dC)

The exception to this rule is the title " thymidine " (not "deoxythymidine"), which is used for the deoxyriboside thymine, which is part of DNA. If thymine is linked to ribose, the corresponding nucleoside is called ribothymidine.

Being N-glycosides, nucleosides relatively alkali resistant , But easily hydrolyze when heated in the presence of acids . Pyrimidine nucleosides are more resistant to hydrolysis than purine nucleosides.

The existing “small” difference in the structure or configuration of one carbon atom (for example, C-2") in a carbohydrate residue is sufficient for the substance to act as an inhibitor of DNA biosynthesis. This principle is used in the creation of new drugs by the method of molecular modification of natural models.

Nucleotides: structure, nomenclature, relation to hydrolysis.

Nucleotides are formed as a result of partial hydrolysis of nucleic acids, or by synthesis. They are found in significant quantities in all cells. Nucleotides are nucleoside phosphates .

Depending on the nature of the carbohydrate residue, there are deoxyribonucleotides And ribonucleotides . Phosphoric acid usually esterifies the alcohol hydroxyl at S-5" or when NW" in deoxyribose (deoxyribonucleotides) or ribose (ribonucleotides) residues. In a nucleotide molecule, three structural components are used to bind ester linkage And N -glycosidic bond .

Principle of structure mononucleotides

Nucleotides can be considered as nucleoside phosphates (ethers phosphoric acid) And How acids (due to the presence of protons in the phosphoric acid residue). Due to the phosphate residue, nucleotides exhibit properties of a dibasic acid and under physiological conditions at pH ~7 are in a completely ionized state.

There are two types of names used for nucleotides. One of them includes Name nucleoside indicating the position of the phosphate residue in it, for example adenosine-3"-phosphate, uridine-5"-phosphate. Another type of name is constructed by adding the combination - silt acid to the name of the nucleic base residue, for example 3"-adenylic acid, 5"-uridylic acid.

In nucleotide chemistry it is also common to use abbreviations . Free mononucleotides, i.e. those that are not part of the polynucleotide chain, are called monophosphates with this feature reflected in the abbreviated code with the letter “M”. For example, adenosine-5"-phosphate has the abbreviated name AMP (in Russian literature - AMP, adenosine monophosphate), etc.

To record the sequence of nucleotide residues in polynucleotide chains, another type of abbreviation is used using a one-letter code for the corresponding nucleoside fragment. In this case, 5"-phosphates are written with the addition of the Latin letter "p" before the one-letter nucleoside symbol, 3"-phosphates - after the one-letter nucleoside symbol. For example, adenosine-5"-phosphate - pA, adenosine-3"-phosphate - Ap, etc.

Nucleotides are capable hydrolyze in the presence of strong inorganic acids (HC1, HBr, H 2 SO 4) and some organic acids (CC1 3 COOH, HCOOH, CH 3 COOH) at the N-glycosidic bond, the phosphorus bond exhibits relative stability. At the same time, under the action of the enzyme 5"-nucleotidase, the ester bond is hydrolyzed, while the N-glycosidic bond is retained.

Nucleotide coenzymes: ATP structure, relation to hydrolysis.

Nucleotides are of great importance not only as monomeric units of polynucleotide chains of various types of nucleic acids. In living organisms, nucleotides are participants in the most important biochemical processes. They are especially important in the role coenzymes , i.e. substances closely related to enzymes and necessary for their manifestation enzymatic activity. All tissues of the body contain mono-, di- and triphosphates of nucleosides in a free state.

Particularly famous adenine-containing nucleotides :

Adenosine-5"-phosphate (AMP, or in Russian literature AMP);

Adenosine 5"-diphosphate (ADP, or ADP);

Adenosine 5"-triphosphate (ATP, or ATP).

Nucleotides, phosphorylated to varying degrees, are capable of interconversion by increasing or eliminating phosphate groups. The diphosphate group contains one, and the triphosphate group contains two anhydride bonds, which have a large supply of energy and therefore called macroergic . When a high-energy P-O bond is split, -32 kJ/mol is released. Related to this is the critical role of ATP as a “supplier” of energy in all living cells.

Interconversions adenosine phosphates.

In the above scheme of interconversions, the formulas AMP, ADP and ATP correspond to the non-ionized state of the molecules of these compounds. With the participation of ATP and ADP, the most important biochemical process occurs in the body - the transfer of phosphate groups.

Nucleotide coenzymes: NAD + and NADP + – structure, alkylpyridinium ion and its interaction with hydride ion as the chemical basis of the oxidative action, NAD + .

Nicotinamide adenine dinucleotides. This group of compounds includes nicotinamide adenine dinucleotide (NAD, or NAD) and its phosphate (NADP, or NADP). These connections play an important role coenzymes in reactions of biological oxidation of organic substrates by their dehydrogenation (with the participation of dehydrogenase enzymes). Since these coenzymes are participants in redox reactions, they can exist in both oxidized (NAD+, NADP+) and reduced (NADH, NADPH) forms.

The structural fragment of NAD + and NADP + is nicotinamide residue as pyridinium ion . As part of NADH and NADPH, this fragment is converted into a substituted 1,4-dihydropyridine residue.

During biological dehydrogenation, which is a special case of oxidation, the substrate loses two hydrogen atoms, i.e. two protons and two electrons (2H+, 2e) or a proton and a hydride ion (H+ and H). The coenzyme NAD+ is considered as a hydride ion acceptor . As a result of reduction due to the addition of a hydride ion, the pyridinium ring transforms into a 1,4-dihydropyridine fragment. This process is reversible.

During oxidation, the aromatic pyridinium ring is converted to a non-aromatic 1,4-dihydropyridine ring. Due to the loss of aromaticity, the energy of NADH increases compared to NAD+. The increase in energy content occurs due to part of the energy released as a result of the transformation of alcohol into aldehyde. Thus, NADH stores energy, which is then used in other biochemical processes that require energy.

Nucleic acids: RNA and DNA, primary structure.

Nucleic acids occupy an exceptional place in the life processes of living organisms. They store and transmit genetic information and are a tool by which protein biosynthesis is controlled.

Nucleic acids They are high-molecular compounds (biopolymers) built from monomeric units - nucleotides, and therefore nucleic acids are also called polynucleotides.

Structure each nucleotide includes carbohydrate, heterocyclic base and phosphoric acid residues. The carbohydrate components of nucleotides are pentoses: D-ribose and 2-deoxy-D-ribose.

Based on this feature, nucleic acids are divided into two groups:

ribonucleic acids (RNA) containing ribose;

deoxyribonucleic acids (DNA) containing deoxyribose.

Template (mRNA);

Ribosomal (rRNA);

Transport (tRNA).

Primary structure of nucleic acids. DNA and RNA have common features in structure macromolecules :

The backbone of their polynucleotide chains consists of alternating pentose and phosphate residues;

Each phosphate group forms two ester bonds: with the C-3 atom of the previous nucleotide unit and with the C-5 atom of the subsequent nucleotide unit;

Nucleic bases form N-glycosidic bonds with pentose residues.

The structure of an arbitrary section of a DNA chain, chosen as a model with the inclusion of four main nucleic bases - guanine (G), cytosine (C), adenine (A), thymine (T), is presented. The principle of constructing the polynucleotide chain of RNA is the same as that of DNA, but with two differences: the pentose residue in RNA is D-ribofuranose, and the set of nucleic bases uses not thymine (as in DNA), but uracil.

(!) One end of the polynucleotide chain, on which there is a nucleotide with a free 5"-OH group, is called 5" end . The other end of the chain, on which there is a nucleotide with a free 3"-OH group, is called Z"-end .

Nucleotide units are written from left to right, starting from the 5"-terminal nucleotide. The structure of the RNA chain is written according to the same rules, with the letter “d” omitted.

In order to establish the nucleotide composition of nucleic acids, they are hydrolyzed, followed by identification of the resulting products. DNA and RNA behave differently under conditions of alkaline and acid hydrolysis. DNA is resistant to hydrolysis in an alkaline environment , while RNA is hydrolyzed very quickly to nucleotides, which, in turn, are able to cleave off a phosphoric acid residue to form nucleosides. N -Glycosidic bonds are stable in alkaline and neutral environments . Therefore, to split them acid hydrolysis is used . Optimal results are obtained by enzymatic hydrolysis using nucleases, including snake venom phosphodiesterase, which break down ester bonds.

Along with nucleotide composition The most important characteristic of nucleic acids is nucleotide sequence , i.e., the order of alternation of nucleotide units. Both of these characteristics are included in the concept of the primary structure of nucleic acids.

Primary structure Nucleic acids are determined by the sequence of nucleotide units linked by phosphodiester bonds into a continuous polynucleotide chain.

The general approach to establishing the sequence of nucleotide units is to use the block method. First, the polynucleotide chain is specifically cleaved using enzymes and chemical reagents into smaller fragments (oligonucleotides), which are deciphered using specific methods and, based on the data obtained, the structural sequence of the entire polynucleotide chain is reproduced.

Knowledge of the primary structure of nucleic acids is necessary to identify the relationship between their structure and biological function, as well as to understand the mechanism of their biological action.

Complementarity bases underlie the laws that govern the nucleotide composition of DNA. These patterns are formulated E. Chargaff :

The number of purine bases is equal to the number of pyrimidine bases;

The amount of adenine is equal to the amount of thymine, and the amount of guanine is equal to the amount of cytosine;

The number of bases containing an amino group in positions 4 of the pyrimidine and 6 of the purine cores is equal to the number of bases containing an oxo group in the same positions. This means that the sum of adenine and cytosine is equal to the sum of guanine and thymine.

For RNA, these rules are either not fulfilled or are fulfilled with some approximation, since RNA contains many minor bases.

Complementarity of chains forms the chemical basis of the most important function of DNA - storage and transmission of hereditary characteristics. The preservation of the nucleotide sequence is the key to the error-free transmission of genetic information. A change in the sequence of bases in any DNA chain leads to stable hereditary changes, and, consequently, to changes in the structure of the encoded protein. Such changes are called mutations . Mutations can occur as a result of replacing a complementary base pair with another. The reason for this replacement may be a shift in the tautomeric equilibrium.

For example, in the case of guanine, a shift in equilibrium towards the lactim form makes it possible to form hydrogen bonds with an unusual base for guanine, thymine, and the emergence of a new guanine-thymine pair instead of the traditional guanine-cytosine pair.

The replacement of “normal” base pairs is then transmitted during the “rewriting” (transcription) of the genetic code from DNA to RNA and ultimately leads to a change in the amino acid sequence in the synthesized protein.

Alkaloids: chemical classification; basic properties, formation of salts. Representatives: quinine, nicotine, atropine.

Alkaloids represent a large group of natural nitrogen-containing compounds mainly of plant origin. Natural alkaloids serve as models for the creation of new drugs, often more effective and at the same time simpler in structure.

Currently, depending on the origin of the nitrogen atom in the structure of the molecule, Alkaloids include:

True alkaloids – compounds that are formed from amino acids and contain a nitrogen atom as part of a heterocycle (hyoscyamine, caffeine, platiphylline).

Protoalkaloids – compounds that are formed from amino acids and contain an aliphatic nitrogen atom in the side chain (ephedrine, capsaicin).

Pseudoalkaloids – nitrogen-containing compounds of terpene and steroid nature (solasodine).

IN classifications alkaloids there are two approaches. Chemical classification based on the structure of the carbon-nitrogen skeleton:

Derivatives of pyridine and piperidine (anabasine, nicotine).

With fused pyrrolidine and piperidine rings (tropane derivatives) - atropine, cocaine, hyoscyamine, scopolamine.

Quinoline derivatives (quinine).

Isoquinoline derivatives (morphine, codeine, papaverine).

Indole derivatives (strychnine, brucine, reserpine).

Purine derivatives (caffeine, theobromine, theophylline).

Imidazole derivatives (pilocarpine)

Steroid alkaloids (solasonine).

Acyclic alkaloids and alkaloids with an exocyclic nitrogen atom (ephedrine, spherophysin, colhamine).

Another type of classification of alkaloids is based on a botanical characteristic, according to which alkaloids are grouped according to plant sources.

Most alkaloids has basic properties , which is what their name is associated with. In plants, alkaloids are contained in the form of salts with organic acids (citric, malic, tartaric, oxalic).

Isolation from plant materials:

1st method (extraction in the form of salts):

2nd method (extraction in the form of bases):

Basic (alkaline) properties alkaloids are expressed to varying degrees. In nature, alkaloids that are more often found are tertiary, less often - secondary or quaternary ammonium bases.

Due to their basic nature, alkaloids form salts with acids of varying degrees of strength. Alkaloid salts easily decomposes under the influence of caustic alkalis and ammonia . In this case, free bases are released.

Due to their basic nature, alkaloids react with acids form salts . This property is used in the isolation and purification of alkaloids, their quantification and preparation of drugs.

Alkaloids-salts Fine soluble in water and ethanol (especially when diluted) when heated, poorly or not at all soluble in organic solvents (chloroform, ethyl ether, etc.). As exceptions can be called scopolamine hydrobromide, cocaine hydrochlorides and some opium alkaloids.

Base alkaloids usually do not dissolve in water , but easily dissolve in organic solvents. Exception consist of nicotine, ephedrine, anabasine, caffeine, which are highly soluble in both water and organic solvents.

Representatives.

Quinine - an alkaloid isolated from the bark of the cinchona tree ( Cinchona officinalis) - are colorless crystals with a very bitter taste. Quinine and its derivatives have antipyretic and antimalarial effects

Nicotine - the main alkaloid of tobacco and shag. Nicotine is very toxic, the lethal dose for humans is 40 mg/kg, and natural levorotatory nicotine is 2-3 times more toxic than synthetic dextrorotatory nicotine.

Atropine - racemic form of hyoscyamine , has an anticholinergic effect (spasmolytic and mydriatic).

Alkaloids: methylated xanthines (caffeine, theophylline, theobromine); acid-base properties; their qualitative reactions.

Purine alkaloids should be considered as N-methylated xanthines – based on the xanthine core (2,6-dihydroxopurine). The most famous representatives of this group are caffeine (1,3,7-trimethylxanthine), theobromine (3,7-dimethylxanthine) and theophylline (1,3-dimethylxanthine), which is found in coffee beans and tea, cocoa bean husks, and cola nuts. Caffeine, theobromine and theophylline are widely used in medicine. Caffeine is used primarily as a psychostimulant, theobromine and theophylline as cardiovascular drugs.