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硫胺素缺乏大鼠的肝脏药物代谢和脂质过氧化

Hepatic drug metabolism and lipid peroxidation in thiamine deficient rats.

作者信息

Galdhar N R, Pawar S S

出版信息

Int J Vitam Nutr Res. 1976;46(1):14-23.

PMID:816749
Abstract

In vitro metabolism of aminopyrene, ethylmorphine (Type I substrates), N-methylaniline and acetanilide (Type II substrates) in liver microsomal fraction from thiamine deficient male and female rats was studied. No significant change in microsomal protein content was noticed during the period of thiamine deficiency. However, a significant increase in the in vitro oxidation of aminopyrene, ethylmorphine, N-methylaniline and hydroxylation of acetanilide was observed. The NADPH linked and ascorbate induced lipid peroxidation was also increased during thiamine deficiency. The levels of NADPH cytochrome c-reductase, cytochrome b5 and heme were noticeably increased in thiamine deficient animals as compared to normal rats. Phenobarbital treatment induced the activities of all drug enzymes and inhibited the lipid peroxidation in either sex during the period of thiamine deficiency. It appears that thiamine intake is an important determination in drug metabolism and lipid peroxidation.

摘要

研究了硫胺素缺乏的雄性和雌性大鼠肝脏微粒体组分中氨基芘、乙基吗啡(I型底物)、N-甲基苯胺和乙酰苯胺(II型底物)的体外代谢。在硫胺素缺乏期间,微粒体蛋白含量未观察到显著变化。然而,观察到氨基芘、乙基吗啡、N-甲基苯胺的体外氧化以及乙酰苯胺的羟基化有显著增加。硫胺素缺乏期间,NADPH相关的以及抗坏血酸诱导的脂质过氧化也增加。与正常大鼠相比,硫胺素缺乏动物体内NADPH细胞色素c还原酶、细胞色素b5和血红素水平显著升高。在硫胺素缺乏期间,苯巴比妥处理诱导了两种性别所有药物酶的活性并抑制了脂质过氧化。看来硫胺素的摄入是药物代谢和脂质过氧化的一个重要决定因素。

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