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放线菌素D或环己酰亚胺对聚肌苷酸:聚胞苷酸诱导的小鼠肝脏混合功能氧化酶抑制作用的影响

Inhibition of polyriboinosinic:polyribocytidylic acid-induced depression of mouse hepatic mixed function oxidases by actinomycin D or cycloheximide.

作者信息

Gorce P, Wade A E

出版信息

Biochem Biophys Res Commun. 1984 May 31;121(1):237-42. doi: 10.1016/0006-291x(84)90712-5.

DOI:10.1016/0006-291x(84)90712-5
PMID:6732804
Abstract

Administration of a single dose of the potent interferon inducer poly rI:rC to Swiss Webster mice depressed hepatic cytochrome P-450 to 75% of control, ethylmorphine N-demethylase to 56% of control and DMN N- demethylases I and II to about 80% of control. Although each enzyme responded in a unique manner, maximum depression occurred at 24 hours after poly rI:rC administration and the concurrent administration of inhibitors of protein synthesis (actinomycin D or cycloheximide) prevented this depression. These data suggest that poly rI:rC effects on the mixed function oxidases are not species specific although depression follows a time course shorter than that reported in the rat (maximum depression at 40 hours after poly rI:rC administration) and that depression occurs through the stimulation of a protein responsible for degrading cytochrome P-450.

摘要

给瑞士韦伯斯特小鼠单次注射强效干扰素诱导剂聚肌苷酸

聚胞苷酸(poly rI:rC)后,肝脏细胞色素P-450降至对照组的75%,乙基吗啡N-脱甲基酶降至对照组的56%,二甲基亚硝胺N-脱甲基酶I和II降至对照组的约80%。尽管每种酶的反应方式独特,但聚肌苷酸:聚胞苷酸给药后24小时出现最大程度的抑制,同时给予蛋白质合成抑制剂(放线菌素D或环己酰亚胺)可防止这种抑制。这些数据表明,聚肌苷酸:聚胞苷酸对混合功能氧化酶的作用并非物种特异性,尽管其抑制作用的时程比在大鼠中报道的要短(聚肌苷酸:聚胞苷酸给药后40小时出现最大抑制),并且这种抑制是通过刺激一种负责降解细胞色素P-450的蛋白质而发生的。

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1
Inhibition of polyriboinosinic:polyribocytidylic acid-induced depression of mouse hepatic mixed function oxidases by actinomycin D or cycloheximide.放线菌素D或环己酰亚胺对聚肌苷酸:聚胞苷酸诱导的小鼠肝脏混合功能氧化酶抑制作用的影响
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