• Гідрологія і Гідрометрія
• Господарське право
• Економіка будівництва
• Економіка природокористування
• Економічна теорія
• Земельне право
• Історія України
• Кримінально виконавче право
• Медична радіологія
• Методи аналізу
• Міжнародне приватне право
• Міжнародний маркетинг
• Основи екології
• Предмет Політологія
• Соціальне страхування
• Технічні засоби організації дорожнього руху
• Товарознавство продовольчих товарів

Thiamin, vB1, antinevrose

It contains dimethylpyrimidine’s ring, connected with thiazole with the help of one methyl group of the pyrimidine ring.

The biological significance

Thiamin undergoes phosphorilation and forms (creates) thiamindiphosphate, which is a coferment of ketoacids decarboxylases.

It is a chemical compound of complex ferment system – pyruvate – and a-ketoglutaratedehydrogenase, catalysing oxidative decarboxilation of pyruvate and a-ketoglutarate. Thus, thiamin transfered anaerobic glycolysis in aerobic and bonds it with the tricarboxylic acid cycle, that assists full oxidation of glucose, yield energy with formation of ATP.

Thus thiamin has an influence of exchange of carbohydrates, increases the aerobic phase of decomposition of glucose and reservation of energy, the exchange of lipids, increases the quantity of acetylKoA, speeding synthesis of free fat acids, cholesterol and others sterols. Thiamin diphosphate is a compound of one of the leading ferments of pentose cycle the called transketolase. The absence of the vB1 stops the pentose cycle and lowering the contents of NADPH2, ribose-5-phosphate which are necessary for synthesis of fat acids etc.

The food requirement in thiamin. The need in thiamin grows with the rise of the quantity of used calorics. It is recommended for a grown-up to use about 1.5 mg of thyamin per a day. The minimum quantity of thyamin must not be less than 1 mg per a day even if energy entering is less than 200 kc.

Requirement in thiamin is higher for those persons, who eat food with high contents of carbohydrates, during the periods of lactation, pregnancy, sick persons suffering from hyperthyreoidism.

Avitaminose. The lack of the vB1 in the organism causes the development of the disease called beri-beri (in hindi – sheep). The sick persons suffering from the strong pains in carf muscles try to go on their toes, they can not step on their heels, they go like sheep.

In this case the aerobic process of decomposition of carbohydrates, secretion and reservation of energy is violated. Ketoacids (in the main – pyruvic acid) are accumulated in tissues and blood. Later they appear in urine and the acidosis is developing.

The process of synthesis of free fatty acids and lipids is also violated. The inhibition of the process of oxidation of carbohydrates changes the exchange processes in tissues and first of all in nervous and cerebral tissues because for them carbohydrates serve the only source of energy.

Plural ruins of nervous system happen, appear polynevritis and paralysis. The lack of vB1 breaks the heart activity, functions of the alimentary canal, developing caries and convulsions.

Nowadays the typical cases of beri-beri one can meet rather seldom though hypovitaminosis are often marked, when carbohydrates previal in nutrition, when products from coarse-ground flour are little used.

The manifestation of thiamin insufficency may have chronic alcoholics, who may suffer from of the disorder of the moving coordination, the loss of memory, consciousness, apathy – vernike-korsakov syndrome. It is urgent state and if thiamin will not be infused may be case of a coma, irreversible changes in brain and a death.

Riboflavin, the vB2, Riboflavin is the methyl derivation of flavin joined with the residues of ribitol (6,7dimethyl,9ribitilisoalloksazin).

Riboflavin has oxidizing-reducing characteristics, joining 2 atoms of hydrogen riboflavin turns into colourless compound (combination), then after oxidizing it changes and becomes yellow.

The biological significance. Riboflavin entering with food in tissues forms riboflavin-5-phosphate or flavinmononucleotide, which is the coferment of flavinferments or flavoproteins

Riboflavin + ATP--------------à riboflavin-5-phosphate + ADP

The second coferment of flavinferments is FAD (flavinadenindinucleotide) it is formed from FMN in next reaction:

FMN + ATP----------------à FAD + pyrophosphate

Flavoproteins including FMN as CoE take part in biological oxidation, transporting protons and electrons from NADH2.

Flavoproteins containing FAD as a cof catalyse oxidation of pyruvic acid, fat acid, succinate, oxidative desamination of aminoacids, biogen amines.

The vB2 provides enough intencity of tissue breath and ensures the formation of macroergic compounds, which are used for the process of the biosynthesis.

The vB2 influences the process of sight improving suction and usage of the vA and eys are sensitive to the short wave violet and blue rays of light.

The spreading of riboflavin. Milk, eggs, a liver, green plant leaves are the important sources of riboflavin. Vegetarians do not drink milk that is why their riboflavin is low.

The vB2 may be easily destroyed under the sun rays. The need in riboflavin depends on energy ensuring and make up about 1,5 mg a day for a grown-up.

Minimum recommended quantity of riboflavin is about 1,2 mg/a day.

Avitaminosis: the lack of vB2 violates oxidizing and reducing processes in the organism, lowering synthetic processes. In the case of the lack of the vB2 we may observe the following factors: young man suffering from the stop of the height, the prolapse of hair, the inflammation of the tongue – glossit, chaps in the corners of the mouth the light dread the keratitis.

Vitamin B5 (sometimes B3) – pantothenic acid, antidermathitic. It is a watersoluble, yellow colored compound, oily in existence. It is stable to heat moisture, and to the action of oxidizing and reducing agents. However, it is destroyed when heated in alkaline or acidic solution. Pantothenic acid isolated from yeast has been found.

Sources: the important sources of pantothenic acid are liver, kidney, eggs, lean and milk. Among the plant sources are molasses, peas, cabbage, cauliflower, sweet potatoes, yeast, potatoes, tomatoes.

Functions: pantothenic acid forms the part of the structure of coenzyme A (see acyltransferase) and by virtue of that it participates in carbohydrate, lipid and protein metabolism. In carbohydrate metabolism it is involved in the activation of pyruvic acid (also obtained prom proteins) to form acetylCoA (active form of acetic acid), which can easily enter the Krebs cycle reactions and get oxidized or can enter into biosynthetic pathway leading to the formation of long chain and short chain fatty acids or steroids.

In lipid metabolism, pantothenic acid in the form of CoA is involved in the activation of fatty acids forming their CoA derivatives which can enter oxidative or synthetic pathways. It is also involved in the biosynthesis of acetylcholin at the myoneural junctions. CoA is also involved in the disposal of ketone bodies. In adrenal glands cholesterol concentration is lowered in pantothenic acid deficiency. CoA has also been shown to be concerned with pigmentation of skin and hairs.

Deficiency symptoms In man pantothenic acid deficiency is rarely. The deficiency can be created by feeding w-methylpantothenic acid (antogonist of p.a.) 100mg daily together with p.a. deficient diets. Under such condition the vitamin the vitamin deficiency human subjects develop irritability, restlessnes, insomnia, fatigue, staggering gates and gastrointestinal troubles. Administration of p.a. relieves the condition. In the past, it had been believed that deficiency of p.a. was responsible for graying of hairs and this vitamin is an “antigraying factor”.

In rats, pantothenic acid deficiency causes retarded growth, lesser reproductive power, necrosis of adrenal cortex and resorption of the litters. Cholesterol content of adrenals is lowered considerably.

Requirements: usually 10-15 mg p.a. is derived from the average diets per day.

Niacin – this v is also known as nicotinic acid amid, or pellagra preventive factor (PP factor or v.B5). nicotinic acid also possesses vitamin activity. Pelle agra – rough skin. Nicotinic acid contains a pyridine nucleus, possessing a carboxylic group at position 3. In nicotinamide, the carboxy group is present in the form of amide at position 3 of the pyridine ring.

Nicotinic acid is a water-soluble, white, crystalline compound and is fairly stable when exposed to atmosphere air, or heat.

Sources: the rich sources of this vitamin are liver, meat, fish, eggs and vegetables. Whole wheat and unpolished rice do also contain this vitamin in significant quantities.

Functions: nicotinamide forms the part of the molecular structure of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) and thus forms coenzyme of a large number dehydrogenases. The important known function of this vitamin is thus oxidative. It is involved in the oxidation of carbohydrates, lipids, deamination of aminoacids and metabolism of a-ketoacids. It in the form NAD forms the normal component of electron transport chain.

NAD takes part also as a substrate of DNA-ligase, which is basis of the processes of replecation and reparation. The deficiency NAD can to prove the violation of the deletion of cells.

Deficiency diseases: usually deficiency of niacin is developed rarely, because niacin distributes in nature widely. In animal the nicotinic acid forms from tryptophan with the parting riboflavin and pyridoxin. Frequently the presence antivitamin piridinesulphate lead to the development avitaminose. Piridinsulfate is presence in the corn, because avitaminos – pellagra widely distributed in South America.

Deficiency of nicotinic acid has been shown to result in the development of pellagra in which patches develop on the skin, mouth and tongue develop soreness, inflammation, achlorhydria, diarrhoea, thickening and pigmentation of skin. Rashes appear in the body symmetrically: in the advanced stages, there might occur nervous disorder – pareses and muscular atrophy, hallucinations, loss of memory, violation of physiology, delirium and dementia.

Deficiency symptoms of this vitamin are classified under three D’s namely: dermatitis, diarhoea, dementia. Administration of nicotinamide relieves these symptoms.

Requirements: normal adults require about 13-19 mg nicotinamide per day. During pregnancy, lactation and active muscular work about 22-25mg. Even excess of this vitamin does not cause toxicity.

Pyridoxine, vitamin B6 – antidermatitic. There are three compounds which belong to the group of pyridoxine, namely, pyridoxal, pyridoxol, pyridoxamine

These are water-soluble and sensitive to ultraviolet irradiation. Pyridoxol is resistant to heat but its derivatives pyridoxal and pyridoxamine are readily destroyed on heating.

The primary alcoholic group of pyridoxol is oxidized to aldehydic group in pyridoxal; and methylaminogroup in pyridoxamine. All three forms exist in tissues as phosphate derivatives.

Sources: the rich sources of pyridoxine are egg – yolk, meat, fish, milk, whole grains, cabbage and leguminous seeds.

Function pyridoxal phosphate is required as coenzyme in the decarboxylation reactions – decarboxylases of aminoacids.

All the transaminases require pyridoxal phosphate. Pyridoxine is also considered to be essential for metabolism of unsaturated fatty acids. Vitamin B6 has been found to be associated with the active transport of aminoacids into the cells. The vitamin B6 has also been reported to promote transport of potassium across the membranes from exterior to interior. Isonicotinic acid (INH) hydrzide which is used in the treatment of tuberculosis is antagonist of vitamin B6.

Deficiency symptoms: deficiency of this vitamin produces skin lesions. Prolonged deficiency leads to fall in hemoglobin content, mental depression and confusion. It may also cause vomiting, diarrhoea, abdominal dystension and convulsions. Patients taking antitubercular drug, INH, might sometimes develop peripheral neuritis. These abnormalities can however be corrected by administering pyridoxine. Deficiency of pyridoxine present to women, what take oral contraceptive and to drinklers.

Requirements: normal adult man requires 1,5 – 2,0 mg pyridoxine per day. During second half of pregnancy and in patients receiving antitubercular treatment the requirement is increased to 6-7 mg per day. If daily dose of pyridoxine is more than 2 g per day the neurological symptoms can to develop.

Biotin

This vitamin is also known as vitamin B7, coenzyme R or vitamin H. It is a crystalline water-soluble vitamin having the following structure. A bound form of biotin known as biocytin was isolated from yeast which was also found to exist in many animal and plant tissues.

The important sources of biotin are liver, kidney, milk, molasses and some extent other vegetables.

Functions biotin is involved in the carboxylation reactions. It is involved in the activation of CO2 in the following manner.

ATP + biotin-enzyme--- Mg à ADP-biotin-enzyme + Pi;

ADP-biotin-enzyme + CO2---à CO2-biotin-enzyme (activated CO2) + ADP

Later on, this CO2 can be fixed on other compounds such as pyruvic acid, propionic acid, and acetylcoenzyme A. Active CO2 is involved in the synthesis of carbomyl phosphate. Fatty acid synthesis is significantly reduced to biotin deficiency.

Biotin has been found to form prosthetic group of the enzyme propionyl-CoA carboxylase in pig heart which contains 4 moles of biotin per mole of protein.

Deficiency symptoms deficiency of this vitamin can be created by giving low-vitamin diet containing egg-white. Egg-white protein avidin combines with biotin and renders it unavailable to the individual. In human beings deficient in this vitamin transient dermatitis is seen which is followed by anorexia, muscular pain and hyperesthesia.

In rats, biotin deficiency leads to loss of hair and muscular control.

Requirement: although, large amounts of this vitamin are synthesized by intestinal flora of microorganisms, yet 150 to 300 mkg biotin must be provided in the diet.

Folic acid, folacin, vitamin Bc, vitamin of growth, pteroilglutamic acid (PGA). This vitamin is also abundantly present in the green leaves and grass, and hence, this name folic acid (folium denotes leaf) has been given to it. F.a. is a yellow substance which is only slightly soluble in water. It is stable to heat in slightly alkaline medium, however it is destroyed on heating in acidic medium. Sunlight destroys it. On storage at room temperature, its activity is gradually lost.

Folic acid is made up of pteridine, p-aminobenzoic, glutamic acid. The portion of folic acid molecule which contains pteridine and paraaminobenzoic acid is known as pteroic acid.

There some vitamers f.a. – vitamin M, Bc, U, R and lactobacillus casei factor, they differ each from other by quantity molecule of glutamic acid

Sources this vitamin occurs widely in nature and is rich in the leafy plants. Besides leaves, the other important sources are cauliflower, yeast, liver and kidney. Small amounts of this vitamin are present in the tomatoes, bananas, rice, corn, sweet-potatoes, pork and meat.

Functions: folic acid is involved in the metabolism of 1-carbon moieties in various ways. In such reactions folic acid is first reduced to tetrahydrofolic acid in the presence of reduced NADPH and ascorbic acid.

THFA – is coenzyme of different transferases and transfers formyl, formimine, methylene, methynil, methyl, hydroxymethyl. This vitamin takes part in the biosynthesis serine from glycine, methionine from homocysteine, thymine from uracile, synthesis pyrimidines, tryptophan. THFA plays important role in the processes of the methylation – synthesis adrenaline from noradrenaline, creatinine from guanidineacetate. Folacin takes part in the activation of growth and the development of organism, stimulates process of blood formation, synthesis of hemoglobin and formation of leucocytes and erythrocytes.

Deficiency symptomps. Folic acid deficiency in man is polyavitaminos vB12 and vBc because cyanocobalamine receives methylgroups from methylTHFA and posses its to different substrates:

THFA + CH3«methylTHFA (with taking part of vB12, which is transformed to methylvB12 and passes methyl group on different substrates, by this way is resulted methylcompounds).

This deficiency of folic acid in man and chiks causes megaloblastic anemia, glossitis, disorder of gastrointestinal tract, leucopenia, edema and lesions of mouth. In rats deficiency of this vitamin leads to graying of hairs. Folic acid deficiency might be created by use of folic acid antogonists, such as, aminopterin, amethopterin. Administration of aminopterin produces anaemia and leucopenia in guinea-pigs and rats. In children, administration of aminopterin has been recommended for lowering acute leukemia.

Requirement about 15mg folic acid intake per day has been found to be adequate. In megaloblastic anemia its requirements is increased several hundred folds (from 10-30mg intravenously and about 50-60mg if taken orally.

Переглядів: 379