[THE UNESTERIFIED FATTY ACIDS IN BLOOD PLASMA AND INTERCELLULAR MEDIUM: EFFECT OF INSULIN AND ALBUMIN (THE LECTURE)].

The high content of palmitic saturated fatty acid, palmitic triglycerides in food, the large amount of lipoproteins of very low density of the same name in blood, obvious insufficient amount of unesterified fatty acids releasing under lipolysis in blood to meet in vivo requirements in biotransforming energy of ATP are the causes of biological malfunction of homeostasis. As a rule, for every cell in vivo everything is always to be enough. The deficiency of synthesis of ATP by reason of non-optimal substratum for acquirement of ATP by mitochondria is followed by activation also phylogenetically earlier biological function of adaptation, biological reaction of stress. Thus, surplus of palmitic unesterified fatty acid after every food intake forms in vivo biological reaction of "metabolic" stress, deficiency of energy by reason of realization by mitochondria in vivo non-optimal exogenous substratum-palmitic unesterified fatty acid, deficiency of acyl- and acetyl-KoA and prognostically formation of potentially ineffective palmitic alternative of metabolism of fatty acids. The deficiency of palmitic unesterified fatty acids in biological reaction of exotrophy after every intake of food compensates biological reaction of stress, activation of releasing of palmitic unesterified fatty acids from visceral fatty cells of gland as it physiologically occurs in biological reaction of endotrophy. At that, adrenalin increases lipolysis in visceral fatty cells of gland and physiologically late insulin can't inhibit lipolysis in phylogenetically early visceral fatty cells. Increasing of content of unesterifed fatty acids in blood plasma, as it always occurs in vivo, stops absorption of glucose by cells initiating hyperglycemia, hyperinsulinemia, and syndrome of resistance to insulin. The result of such a compensation of biological reaction of exotrophy is biological reaction of endotrophy, condition of "metabolic" stress, depletion of function of ß-cells of islets with formation of diabetes mellitus type I, deficiency in vivo of insulin synthesis. The biological role of albumin - transfer of fatty acids in intercellular medium inform of unesterifed fatty acids and prevention of formation of pool of free fatty acids effecting aphysiologically.

[The role of lipoprotein-associated enzyme paraoxonase 1 and its polymorphisms in the pathogenesis of endothelial dysfunction and somatic complications in patients with alcoholism: Review ].

A review of recent data on the role of the multifunctional enzyme, associated with high density lipoproteins - paraoxonase 1 (PON1) in maintaining healthy endothelial function by detoxifying both oxidized low density lipoproteins and homocysteine thiolactone. The additional contribution to the protection of the endothelium against damage makes organophosphatase activity of PON1 involved in the detoxification products of tobacco smoke. The reduction of antioxidant activity of PON1 promotes the differentiation of monocytes into macrophages and the development of inflammation. The reduction of thiolactonase activity of PON1 is accompanied by a decrease of methionine re-synthesis from homocysteine causing DNA- hypomethylation and alteratioin of the expression patterns of pro- and anti-atherogenic genes. Global hypomethylation of the genome is regarded as one of the three most important mechanisms of the increased risk of somatic complications of alcoholism. The accumulation of homocysteine thiolactone serving agonist of glutamate receptors and antagonist of dopamine receptors is a prerequisite to increased alcohol abuse. Clinical observations focusing on gene polymorphisms of PON indicate that three different genotypes of polymorphism PON1Q192R have unequal degrees atheroprotective properties.

[Mechanisms of the liver anti-endotoxin defence].

Current knowledge of immunocellular and lipoprotein mechanisms of the liver-induced anti-endotoxin tolerance has been summarized. The role of T regulatory cells, different macrophage phenotypes, high density lipoproteins, oxidized low density lipoproteins and their receptors as the key players in mechanism of tolerance to endotoxin has been discussed.

[A simple method for quantification of modified low-density lipoproteins].

A simple method for quantification of modified low-density lipoproteins (mLDL) in the blood serum containing 8.9% polyvinylpyrrolidone solution 12600 +/- 2700 has been developed. The results show that 10 min incubation of serum in a buffer containing 8.9% PVP leads to complete aggregation mLDL. Atherogenicity of aggregated mLDLs is experimentally confirmed by two independent tests (mLDLs bind and activate the complement system of a guinea pig (pro-inflammatory effect) and cause platelet hyperaggregation (thrombogenic effect)). The proposed method is simple and involves only two steps: mixing the serum with a solution of PVP and recording the turbidity. The method allows to register the presence of mLDL directly in serum without its prior fractionation.

[Modified method for determining circulating immune complexes in the complement fixation test with polyethylene glycol precipitate].

The authors have modified a method for determining circulating immune complexes in the complement fixation test. It is shown that with the 7% concentration of polyethylene glycol (PEG)-6000, there is a more complete precipitation of low- and medium-molecular weight immune complexes. The time and temperature of serum incubation were optimized when PEG-6000 was obtained. The use of the soluble circulating immune complexes (sCIC) prepared from human serum as a standard for the construction of a standard plot could substantially enhance the sensitivity of the method (0.325 microg/ ml). The content of circulating immune complexes was studied in donors and in patients with connective tissue dysplasia (CTD) by the improved procedure. In the group of donors, the mean level of sCIC was 0.62 +/- 0.24 mg/ml. In the CTD group, that was 2.32 +/- 0.93 mg/ml; the serum concentrations of sCIC ranging from 1.1 to 5.0 mg/ml. In the donors and patients, the detection rate of serum sCIC was 100%. The proposed method may be clinically used to measure the human serum levels of sCIC.