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氨基乙基半胱氨酸酮亚胺脱羧二聚体在不抑制电子传递的浓度下可保护亚线粒体颗粒免受脂质过氧化作用。

Aminoethylcysteine ketimine decarboxylated dimer protects submitochondrial particles from lipid peroxidation at a concentration not inhibitory of electron transport.

作者信息

Pecci L, Fontana M, Montefoschi G, Cavallini D

机构信息

Dipartimento di Scienze Biochimiche A. Rossi Fanelli, Università di Roma La Sapienza, Italy.

出版信息

Biochem Biophys Res Commun. 1994 Nov 30;205(1):264-8. doi: 10.1006/bbrc.1994.2659.

DOI:10.1006/bbrc.1994.2659
PMID:7999034
Abstract

In contrast with other inhibitors of the NADH dehydrogenase of the respiratory chain, the decarboxylated dimer of aminoethylcysteine ketimine protects bovine heart submitochondrial particles (SMP) from the NADH-Fe(+3)-ADP-induced lipid peroxidation. This effect, measured as inhibition of malondialdehyde formation, is concentration-dependent in the range 0.02-0.2 mM. This range of concentration is not inhibitory on NADH-oxidase activity of SMP. Furthermore the dimer is able to counteract the malondialdehyde formation stimulated by the Complex I inhibitors rotenone and N-methyl-4-phenylpyridinium (MPP+).

摘要

与呼吸链NADH脱氢酶的其他抑制剂相比,氨基乙基半胱氨酸酮亚胺的脱羧二聚体可保护牛心亚线粒体颗粒(SMP)免受NADH-Fe(+3)-ADP诱导的脂质过氧化作用。以丙二醛形成的抑制作用来衡量,这种效应在0.02-0.2 mM范围内呈浓度依赖性。该浓度范围对SMP的NADH氧化酶活性没有抑制作用。此外,该二聚体能够抵消由复合物I抑制剂鱼藤酮和N-甲基-4-苯基吡啶鎓(MPP+)刺激产生的丙二醛形成。

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