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硝苯地平对大鼠心脏和肝脏微粒体脂质过氧化的抑制作用。

Inhibition of rat heart and liver microsomal lipid peroxidation by nifedipine.

作者信息

Engineer F, Sridhar R

机构信息

Department of Basic Pharmaceutical Sciences, College of Pharmacy, University of South Carolina, Columbia 29208.

出版信息

Biochem Pharmacol. 1989 Apr 15;38(8):1279-85. doi: 10.1016/0006-2952(89)90334-1.

Abstract

Lipid peroxidation in rat heart and liver microsomes was induced by an NADPH-generating system or by ascorbate in the presence of an ADP-iron complex. Microsomal lipid peroxidation, as measured by malonaldehyde formation, was inhibited by nifedipine over a wide range of concentrations (47 microM to 6 mM). Nifedipine also decreased the oxygen consumption of cardiac and hepatic microsomes in a concentration-dependent manner. These results indicate that nifedipine may perturb microsomal electron transport systems. Nifedipine may have the potential to alter the sensitivity of cardiac and hepatic membranes to peroxidative damage.

摘要

在大鼠心脏和肝脏微粒体中,通过NADPH生成系统或在ADP - 铁复合物存在下由抗坏血酸诱导脂质过氧化。通过丙二醛形成测定的微粒体脂质过氧化在广泛的浓度范围(47 microM至6 mM)内受到硝苯地平的抑制。硝苯地平还以浓度依赖性方式降低心脏和肝脏微粒体的氧消耗。这些结果表明硝苯地平可能扰乱微粒体电子传输系统。硝苯地平可能有改变心脏和肝脏膜对过氧化损伤敏感性的潜力。

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