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[实验性动脉粥样硬化中心肌含氮化合物脱氨基作用的紊乱]

[Disorders of the deamination of nitrogenous compounds in the heart muscle in experimental atherosclerosis].

作者信息

Khuzhamberdiev M, Saĭdullaev T, Mamadiev M, Gorkin V Z

出版信息

Biull Eksp Biol Med. 1984 Dec;98(12):678-80.

PMID:6509196
Abstract

The development of alimentary hypercholesterolemia in rabbits (confirmed by morphometric, electrophysiological and biochemical data) was accompanied by a decrease of the serotonin, benzylamine and tyramine deamination rates in heart muscle mitochondria. At the same time a qualitatively new reaction of cadaverine deamination could be seen in the mitochondria. The data obtained suggest that impairment of deamination of the nitrogenous compounds in atherosclerosis may be due to reversible qualitative modification (transformation) of mitochondrial monoamine oxidase activity. Some of the drugs which decrease the level of lipids in blood serum of hypercholesterolemic rabbits abolished and prevented the impairment of deamination of nitrogenous compounds.

摘要

家兔食饵性高胆固醇血症的发展(形态测量学、电生理学和生化数据证实)伴随着心肌线粒体中血清素、苄胺和酪胺脱氨率的降低。与此同时,在线粒体中可观察到尸胺脱氨出现了一种性质上全新的反应。所获得的数据表明,动脉粥样硬化中含氮化合物脱氨受损可能是由于线粒体单胺氧化酶活性发生可逆的性质改变(转化)所致。一些能降低高胆固醇血症家兔血清脂质水平的药物消除并预防了含氮化合物脱氨的损害。

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