Kostyuk V A, Potapovich A I
Department of Biology, V.I. Lenin Byelorussian State University, Minsk, USSR.
Biochem Int. 1991 Sep;25(2):349-53.
Pretreatment of rats with 4-[4-N-sodium-N-(5-ethyl-1-thia-3,4-diazol-2-yl)sulfophenylamin o]-5- methoxy-1,2-benzoquinone (Q) before carbon tetrachloride intoxication inhibited lipid peroxidation by 85% but did not prevent cytochrome P-450 destruction, decrease of hydroxylase activity, and loss of the capability to bioactivate carbon tetrachloride in rat liver microsomes. Also no influence of Q on 10-day lethality was found. We conclude that covalent binding of free radical products of metabolic cleavage to various cellular structures is apparently the main damage factor of carbon tetrachloride hepatotoxicity rather than lipid peroxidation.
在四氯化碳中毒前用4-[4-N-钠-N-(5-乙基-1-硫杂-3,4-二唑-2-基)磺基苯基氨基]-5-甲氧基-1,2-苯醌(Q)预处理大鼠，可使脂质过氧化抑制85%，但不能防止细胞色素P-450的破坏、羟化酶活性的降低以及大鼠肝微粒体中四氯化碳生物活化能力的丧失。此外，未发现Q对10天致死率有影响。我们得出结论，代谢裂解的自由基产物与各种细胞结构的共价结合显然是四氯化碳肝毒性的主要损伤因素，而非脂质过氧化。
