甲基汞体负荷对肝脏再生的影响。

W Chen, N K Mottet
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摘要

采用肝再生模型研究甲基汞负荷量对细胞增殖的影响。结果表明,慢性甲基汞负荷阻碍了DNA合成过程中胸腺嘧啶的掺入速度。肝部分切除后24小时,汞暴露大鼠胸苷的掺入率为对照组的53%。放射自显影制剂中标记肝细胞的计数也支持这一观察结果。24小时DNA合成活性的显著差异也反映在部分肝切除术后72小时的DNA含量和肝脏重量上(肝脏重量2.36 +/- 0.21 gm/100 gm b.w. vs. 2.67 +/- 0.31 gm/100 b.w., P < 0.05;DNA含量160.78 +/- 36.76 μ g /gm vs. 214.80 +/- 37.908 μ g /gm, P < 0.05)。两周后,肝脏重量、DNA含量和合成活性无显著差异。另一方面,在所有研究期间,甲基汞负荷大鼠肝脏中的蛋白质含量和生物合成与对照组没有显著差异。从这些数据可以得出结论,在细胞增殖最活跃的再生早期,甲基汞处理组肝细胞的分裂率降低。
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The effect of a body burden of methylmercury on hepatic regeneration.

The model of hepatic regeneration is chosen to study the effect of methylmercury burden on cell proliferation. The results show that chronic methylmercury burden impedes the rate of thymidine incorporation during the process of DNA synthesis. At 24 hours after partial hepatectomy, thymidine incorporation in the mercury exposed rats is 53% of the controls. Counts of labeled hepatocytes in radioautographic preparations also support this observation. This remarkable difference in DNA synthetic activity at 24 hours also reflects in the DNA content and liver, weights at 72 hours after partial hepatectomy (Liver weights 2.36 +/- 0.21 gm/100 gm B. W. vs. 2.67 +/- 0.31 gm/100 B. W., P < 0,05; DNA contents 160.78 +/- 36.76 microgram/gm vs. 214.80 +/- 37.908 microgram/gm, P < 0.05). After two weeks, no significant difference is noted in liver weight, DNA content and synthetic activity. On the other hand, protein content and biosynthesis in the liver of methylmercury burdened rats shows no significant difference from the controls in all the periods studied. From these data it is concluded that the dividing fraction of hepatocytes is reduced in methylmercury-treated group at an early stage of regeneration when cell proliferation is most active.

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