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细胞质铜对微粒体脂质过氧化和药物代谢的影响

Modification of microsomal lipid peroxidation and drug metabolism by cytoplasmic copper.

作者信息

Wittig M, Steffen C

出版信息

Res Commun Chem Pathol Pharmacol. 1984 Jun;44(3):477-93.

PMID:6463369
Abstract

NADPH-dependent microsomal lipid peroxidation (LPO) can be influenced by addition of cytoplasmic supernatant as was demonstrated by Gram and Fouts (Arch. Biochem. Biophys. 114, 331-335, 1966). Small quantities of hepatocellular supernatant stimulate LPO, higher concentrations are inhibitory. These opposed effects depend on the relative concentrations of copper and iron, either as ions or protein-bound. A mathematical model is given to predict the formation of malondialdehyde as indicator of LPO in dependence of these metals. The copper-containing superoxide dismutase was shown to be without effect on LPO, whereas coeruloplasmin was inhibitory. Inhibition of LPO by copper ions or by TRIS buffer increased the linearity of microsomal ethylmorphine demethylase.

摘要

如Gram和Fouts(《生物化学与生物物理学报》114, 331 - 335, 1966)所证明的,烟酰胺腺嘌呤二核苷酸磷酸(NADPH)依赖性微粒体脂质过氧化(LPO)可受到细胞质上清液添加的影响。少量肝细胞上清液刺激LPO,较高浓度则具有抑制作用。这些相反的作用取决于铜和铁作为离子或蛋白质结合形式的相对浓度。给出了一个数学模型来预测作为LPO指标的丙二醛的形成与这些金属的关系。含铜超氧化物歧化酶对LPO无影响,而血浆铜蓝蛋白具有抑制作用。铜离子或TRIS缓冲液对LPO的抑制增加了微粒体乙基吗啡脱甲基酶的线性。

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引用本文的文献

1
Promotion of iron-induced rat liver microsomal lipid peroxidation by copper.铜对铁诱导的大鼠肝微粒体脂质过氧化的促进作用。
Lipids. 1988 Jun;23(6):559-63. doi: 10.1007/BF02535597.