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脂质过氧化作用及其被替诺立定抑制,II. 抗坏血酸诱导的大鼠肝线粒体脂质过氧化作用

Lipid peroxidation and its inhibition by tinoridine, II. Ascorbic acid-induced lipid peroxidation of rat liver mitochondria.

作者信息

Shimada O, Yasuda H

出版信息

Biochim Biophys Acta. 1979 Mar 29;572(3):531-6.

PMID:582014
Abstract

Incubation of rat liver mitochondrial suspension with ascorbic acid and Fe2+ resulted in the formation of malondialdehyde and a decrease in the turbidity of the suspension. The maximum amount of malondialdehyde formed during the peroxidation reaction was estimated to be 1 mol per approximately 6 mol of mitochondrial phospholipids. Tinoridine and alpha-tocopherol at the concentration of 5 micron and 1 mM, respectively, completely inhibited the peroxidative disintegration of mitochondria. From the relationship between the concentration of tinoridine and the amount of malondialdehyde formed, it was demonstrated that 1 mol of tinoridine prevents the formation of about 6 mol of malondialdehyde. These findings suggest that there is a limit in the chain reaction of the lipid peroxidation of mitochondria and that the limit is the membrane sphere which is capable of releasing 6 molecules of malondialdehyde and contains about 36 molecules of the constitutive phospholipids.

摘要

用抗坏血酸和Fe2+孵育大鼠肝脏线粒体悬浮液,导致丙二醛的形成以及悬浮液浊度的降低。据估计,过氧化反应过程中形成的丙二醛最大量约为每6摩尔线粒体磷脂1摩尔。分别以5微米和1毫摩尔的浓度使用替诺立定和α-生育酚,可完全抑制线粒体的过氧化解体。从替诺立定浓度与形成的丙二醛量之间的关系可以证明,1摩尔替诺立定可防止约6摩尔丙二醛的形成。这些发现表明,线粒体脂质过氧化的连锁反应存在一个限度,这个限度就是能够释放6个丙二醛分子且含有约36个组成性磷脂分子的膜球。

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