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雄性小鼠急性暴露于氯甲烷后肾脏中DNA损伤的形成与修复

Formation and repair of DNA lesions in kidneys of male mice after acute exposure to methyl chloride.

作者信息

Ristau C, Bolt H M, Vangala R R

机构信息

Institut für Arbeitsphysiologie, Universität Dortmund, FRG.

出版信息

Arch Toxicol. 1990;64(3):254-6. doi: 10.1007/BF02010734.

Abstract

The time-course of DNA lesions (DNA-protein cross-links, single-strand breaks) induced by high concentrations of methyl chloride (1000 ppm) was measured in renal tissue of male mice by means of the alkaline elution assay in order to gain an insight into repair processes. DNA-protein cross-links were removed at a fast rate, whereas single-strand breaks appeared to accumulate, even during repair of DNA-protein cross-links. However, 48 h after exposure to methyl chloride, neither of these lesions were detectable in mouse kidney. Both types of DNA damage were ascribed to the action of formaldehyde, an intermediate in methyl chloride metabolism which may react with nucleic acids and protein and interfere with DNA repair.

摘要

为深入了解修复过程,通过碱性洗脱试验测定了高浓度氯甲烷(1000 ppm)诱导的雄性小鼠肾组织中DNA损伤(DNA-蛋白质交联、单链断裂)的时间进程。DNA-蛋白质交联以快速速率被去除,而单链断裂似乎会累积,即使在DNA-蛋白质交联修复过程中也是如此。然而,在接触氯甲烷48小时后,小鼠肾脏中均未检测到这些损伤。这两种类型的DNA损伤均归因于甲醛的作用,甲醛是氯甲烷代谢的中间产物,可能与核酸和蛋白质发生反应并干扰DNA修复。

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