Vitamin E 400 mg 30 capsules

•prevention and treatment of vitamin E hypovitaminosis;

Capsules 400 mg: adults take 1 capsule daily.
The duration of treatment for vitamin E deficiency is individual and depends on the severity of the condition. If necessary, the dose can be increased to 1 g per day.
It is not recommended to prescribe for an extended period in conjunction with other multivitamin preparations, as there is a possibility of vitamin E overdose.

1 capsule contains: active ingredient: alpha-tocopherol acetate – 400 mg; excipients: sunflower oil sufficient quantity to obtain a capsule mass of 600 mg.
Shell composition: gelatin - 119.74 mg; glycerol - 54.83 mg; purified water - 15.2 mg; sodium benzoate E 211 - 0.23 mg.

soft gelatin capsules with a seam of light yellow color.

hypersensitivity;
acute myocardial infarction;
children under 12 years of age.

It is essential to strictly adhere to the dosage regimen.
A diet high in selenium and sulfur-containing amino acids reduces the need for vitamin E.
In congenital bullous epidermolysis, white hair may begin to grow in areas affected by alopecia.
With prolonged use of the medication and/or the need for repeated courses of therapy, it is recommended to periodically monitor blood coagulation parameters, as well as blood cholesterol levels.

Allergic reactions. When taking large doses - diarrhea, epigastric pain, creatinuria. If side effects occur, the dose of the medication should be reduced or the medication should be discontinued.

Increases the effectiveness of anticonvulsants in patients with epilepsy who have elevated levels of lipid peroxidation products in the blood.
Enhances the effect of steroid and non-steroidal anti-inflammatory drugs, antioxidants.
Increases the effectiveness and reduces the toxicity of cardiac glycosides, as well as vitamins A and D. Administration of vitamin E in high doses may cause a deficiency of vitamin A in the body.
Simultaneous use of vitamin E at doses greater than 400 mg/day with anticoagulants (coumarin and indandione derivatives) increases the risk of hypoprothrombinemia and bleeding.
Cholestyramine, colestipol, and mineral oils reduce the absorption of alpha-tocopherol acetate.
High doses of iron enhance oxidative processes in the body, increasing the need for vitamin E.
When alpha-tocopherol acetate is used simultaneously with cyclosporine, the absorption of the latter increases.

Vitamin E is an antioxidant agent that participates in cell proliferation processes, tissue metabolism, prevents hemolysis of erythrocytes, and inhibits increased permeability and fragility of capillaries. The preparation prevents the development of atherosclerosis, degenerative-dystrophic changes in the heart muscle and skeletal musculature, improves nutrition and contractile ability of the myocardium, and reduces oxygen consumption by the myocardium. It slows down free radical reactions, prevents the formation of peroxides that damage cellular and subcellular membranes. It stimulates the synthesis of heme and heme-containing enzymes - hemoglobin, myoglobin, cytochromes, catalase, peroxidase.

It is involved in the metabolism of nucleic acids and prostaglandins, in the cellular respiration cycle, and in the synthesis of arachidonic acid.

It improves tissue respiration, stimulates protein synthesis (collagen, enzyme, structural, and contractile proteins of skeletal and smooth muscles, myocardium), protects vitamin A from oxidation, inhibits cholesterol synthesis, and contributes to the normalization of lipid levels in blood plasma. It slows down the oxidation of unsaturated fatty acids and selenium (a component of the microsomal electron transport system). It activates phagocytosis and is used to maintain normal resistance of erythrocytes. In high doses, it prevents platelet aggregation. It has a pronounced positive effect on the human reproductive system.

In the absence of vitamin E in the body (avitaminosis E), degenerative changes develop in the skeletal muscles of the heart, capillary permeability and fragility increase, and the epithelium of the seminiferous tubules of the testes undergoes degeneration. In embryos, hemorrhages occur, leading to intrauterine death. Degenerative changes have also been established in nerve cells and damage to the parenchyma of the liver.

In vitamin E deficiency, a decrease in protein concentration in blood serum and nucleic acid content in the liver and testes is observed.

Vitamin E deficiency in humans may be related to dietary factors (for example, the absence of vegetable fats in the diet) or caused by various diseases, such as liver, pancreas, and others.

Approximately 50% of the administered dose is absorbed from the gastrointestinal tract, with peak blood levels reached after 4 hours. Absorption requires the presence of bile acids, fats, and normal pancreatic function. During absorption, it forms a complex with lipoproteins, which are intracellular carriers of vitamin E. It primarily enters the lymphatic system, then into the systemic circulation, where it mainly binds to alpha1 and beta-lipoproteins, and partially to serum albumin. In cases of protein metabolism disorders, transport is hindered. It is deposited in all organs and tissues, especially in adipose tissue. It undergoes metabolism in the liver to derivatives with a quinone structure (some of which have vitamin activity). It is excreted in bile (over 90%) and urine (about 6%) in unchanged form and as metabolites.

It crosses the placenta in insufficient amounts: 20-30% of the concentration in the maternal blood reaches the fetal blood. It penetrates into breast milk.