Vitamin A in the serum

Reference values ​​of the concentration of vitamin A( retinol) in the blood serum: in children 1-6 years - 0.7-1.5 μmol / l, 7-12 years - 0.91-1.71 μmol / l, 13-19years - 0,91-2,51 μmol / l;in adults it is 1.05-2.09 μmol / l.

Vitamin A is fat-soluble and exists in two forms - actually vitamin A, or retinol( found only in animal products), and provitamin A, known as carotene( derived from animal and vegetable products) that can be converted to retinol inwalls of the digestive tract. Approximately 50-90% of the retinol taken with food is absorbed in the small intestine and transported in the complex bound to the chylomicrons into the liver, which is stored in the form of retinol palmitate. If necessary, it is released into the bloodstream in the form of retinol, which is in combination with vitamin A-binding protein. In the serum, the vitamin A-binding protein + retinol complex binds to transthyretin. Of the

serum of blood, retinol is captured by target cells, such as retinal photoreceptors and epithelium.

When the intake of vitamin A in an amount exceeding the requirements( 180-430 μg of retinol per day, depending on age, sex and physiological condition), its excess is deposited in the liver forming the depot of this vitamin. With a reduced intake of retinol from food, its liver stores are released into the bloodstream, maintaining the serum retinol concentration at a normal level( above 0.7 μmol / L).Other biologically active forms of vitamin A( retinal and retinoic acid) are present in the blood in very low concentrations( below 0.35 μmol / L);on the esters of retinol accounts for approximately 5% of total vitamin A( 0.1-0.1 μmol / l).

Vitamin A has an important role in oxidation-reduction processes. Retinol promotes the formation of glycogen in the liver and muscles, promotes an increase in the content of cholesterol in the blood, takes part in the synthesis of steroid and sex hormones. It is necessary for the growth and formation of the bone skeleton, the resynthesis of rhodopsin, and also contributes to the normal functioning of the mucous membranes and the integumentary epithelium of the skin, preventing its metaplasia, hyperkeratosis and excessive sloughing. Vitamin A helps strengthen hair, teeth and gums. In recent years, the multiple role of vitamin A in preventing cancer and regulating immunity has been shown( necessary for the completion of phagocytosis, increases Ig synthesis, stimulates the formation of T-killers, stimulates T helper type II, etc.).Vitamin A - an active antioxidant, mainly acting in the presence of vitamin E;it protects vitamin C from oxidation. Deficiency of vitamin A is regarded as a risk factor for malignant neoplasms. In experimental studies it was shown that an increase in the vitamin A content in the diet increases the median duration of life by 17.5% [Lishchuk VA, Mostkova EV, 1999].Zinc is an essential cofactor of vitamin A metabolism( necessary for the synthesis of vitamin A-binding protein).

The average daily requirement for retinol for adults( 20-50 years) is 1.2 mg( 4000 IU, 1 IU equivalent to 0.3 μg retinol), for pregnant women - 1.5 mg( 5000 IU), for breast-feeding - 1, 8 mg( 6000 IU), for people over 60 years - 2.5 mg( 10,000 IU) [Mindel E., 1997].At least a third of the daily requirement of retinol should be delivered to the body in ready-made form;the rest can be absorbed by the use of carotino-ida, from which the body forms retinol. It should be borne in mind that approximately 30% of retinol in foodstuffs is destroyed by their heat treatment. The activity of retinol is 2 times higher than carotene, in addition, the latter is only 30-40% absorbed into the intestine. Therefore, in assessing the dietary intake, it is considered that 1 mg of retinol approximately corresponds to 6 mg of carotenoids.

Vitamin A deficiency is a systemic disease that affects the cells and organs of the entire body. The resulting changes in the structure of the epithelium are called "keratonizing metaplasia."Keratonizing metaplasia of the epithelium of the respiratory and urinary tract and associated changes in the epithelium of the digestive tract develop in the relatively early periods of the disease, even before the appearance of clinically pronounced changes from the conjunctiva of the eyes, one

ko in most cases they proceed secretly. Typical clinical manifestations of vitamin A deficiency include reduced dark adaptation and twilight vision( hemostalopia), slower bone growth, hyperkeratosis, dryness of the cornea( xerophthalmia).As a result of these processes, the risk of developing inflammatory diseases of the skin and mucous membranes( dermatitis, rhinitis, bronchitis, etc.) increases. The physiological consequences of vitamin A deficiency, such as a violation of adaptation to darkness or an abnormal differentiation of the conjunctival epithelium( revealed by cytological examination of the conjunctival smear), usually begin to develop at a serum retinol concentration below 1 μmol / L.Obvious xerophthalmia usually appears at concentrations below 0.7 μmol / L and takes a more severe form at values ​​below 0.35 μmol / L( severe insufficiency and depletion of liver stores) [Sommer A., ​​1982].The risk of disruption of iron utilization and lethal outcome gradually increases as the concentration of vitamin A in the blood decreases.

Taking drugs that reduce the concentration of cholesterol in the blood, reduces the absorption of vitamin A in the intestine.

There are 2 forms of vitamin A deficiency in the body - primary( alimentary), associated with insufficient intake of retinol or karotinoids with food, and secondary, which occurs when the metabolism of vitamin A is disturbed, more often with diseases of the gastrointestinal tract, liver, pancreas.

Doses of vitamin A in excess of 100,000 IU / day in adults and 18,500 IU / day in children can be toxic for several months, resulting in decreased appetite, hair loss, insomnia, nausea, vomiting, diarrhea, yellow-redpigmentation of the skin and mucous membranes, pain in the bones, headache, enlargement of the liver. Symptoms of intoxication occur when the vitamin A content in the serum exceeds the ability of the vitamin A-binding protein to bind it. Normally, the molar ratio of vitamin-A / vitamin A-binding protein is 0.8-1, with intoxication it decreases. With the development of acute hypervitaminosis A, retinol esters can account for more than 30% of the total amount of vitamin A( 62.82 μmol / L).