Mamadiev M, Khuzhamberdiev M, Gorkin V Z
Vopr Med Khim. 1983 Mar-Apr;29(2):83-9.
Appearance of cadaverine deaminating activity in mitochondrial fractions of liver and kidney of rabbits with experimental alimentary hypercholesterolaemia was prevented by an antioxant diludin (2,6-dimethyl-3,5-diethoxycarbonyl-1,4-dihydropyridine) which also decreased the abnormally elevated AMP-deaminating activity and elevated the decreased monoamine oxidase activity (substrates: serotonin, benzylamine, tyramine). In heart and brain tissues as compared with liver and kidney the impairments caused by hypercholesterolaemia and the normalizing effect of diludin were less distinct. The effects of diludin could be reproduced by nucleophylic reagents sodium thiosulphate or ascorbate. The normalization of impairments in deamination of nitrogenous compounds in hypercholesterolaemia was accompanied by improvement in morpho-physiological manifestations of atherosclerosis (injury of aortal intima, alteration in heart rhythm, changes in content of cholesterol, triglycerides and lipoproteins in blood serum). The data obtained are in agreement with the hypothesis on the significance of qualitative alteration (transformation) in catalytic properties of mitochondrial monoamine oxidases in the mechanism of impairments in deamination of nitrogenous compounds in atherosclerosis.
抗氧化剂敌草快（2,6-二甲基-3,5-二乙氧基羰基-1,4-二氢吡啶）可防止实验性食饵性高胆固醇血症家兔肝脏和肾脏线粒体部分尸胺脱氨活性的出现，该抗氧化剂还可降低异常升高的AMP脱氨活性，并提高降低的单胺氧化酶活性（底物：5-羟色胺、苄胺、酪胺）。与肝脏和肾脏相比，在心脏和脑组织中，高胆固醇血症引起的损害以及敌草快的正常化作用不太明显。硫代硫酸钠或抗坏血酸等亲核试剂可重现敌草快的作用。高胆固醇血症中含氮化合物脱氨损伤的正常化伴随着动脉粥样硬化形态生理表现的改善（主动脉内膜损伤、心律改变、血清中胆固醇、甘油三酯和脂蛋白含量变化）。获得的数据与关于线粒体单胺氧化酶催化特性的定性改变（转化）在动脉粥样硬化含氮化合物脱氨损伤机制中的意义的假说一致。
