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[巴比妥类药物毒性作用的可能生化机制]

[Possible biochemical mechanism of the toxic effects of barbiturates].

作者信息

Ratnikova L A, Cheistiakov V V

出版信息

Biokhimiia. 1978 Nov;43(11):1989-93.

PMID:737214
Abstract

Administration of amytal or phenobarbital to rats results in inhibition of liver respiration determined by oxygen uptake in isolated tissue preparations. Increasing doses of phenobarbital cause an increase of inhibition of liver respiration. In vitro addition of vitamin K3 to liver preparations from rat treated by amytal or administration of vitamin K3 after barbiturate-induced intoxication reverses the inhibition of respiration. It is also shown that the lethal effects of amytal are significantly lowered after administration of vitamin K3. It is concluded that the toxic effects of barbiturates are partially due to the inhibition of mitochondrial respiration at the level of NADH-dehydrogenase.

摘要

给大鼠注射异戊巴比妥或苯巴比妥会导致通过分离组织制剂中的氧摄取所测定的肝脏呼吸受到抑制。增加苯巴比妥的剂量会导致肝脏呼吸抑制作用增强。在体外,向经异戊巴比妥处理的大鼠肝脏制剂中添加维生素K3,或在巴比妥类药物诱导中毒后给予维生素K3,可逆转呼吸抑制。还表明,给予维生素K3后,异戊巴比妥的致死作用会显著降低。得出的结论是,巴比妥类药物的毒性作用部分归因于在NADH脱氢酶水平上对线粒体呼吸的抑制。

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