期刊文献+

铜对大鼠肝细胞活性、自由基代谢及细胞膜电位的影响 被引量:2

The effects of copper on rat hepatocytes proliferation activity and its free radical metabolism and the membrane potential
原文传递
导出
摘要 通过建立大鼠肝细胞的铜胁迫模型,旨在讨论不同剂量的铜对大鼠肝细胞活性、自由基代谢及细胞膜电位的影响。以硫酸铜为试验铜源,6个不同铜质量浓度(以Cu2+计):0,50,100,200,400,800mg/L,分别加入培养液培养BRL-3A细胞24和48h后,测定不同Cu2+质量浓度、不同处理时间后细胞自由基产生、抗氧化酶活性及细胞膜电位变化。结果显示,处理质量浓度低于400 mg/L时,细胞增殖活性差异不显著(P>0.05),处理质量浓度为400,800mg/L时,细胞活性下降(P<0.05);处理质量浓度低于400 mg/L时,Cu2+质量浓度与细胞内T-SOD、GSH-Px、CP活性呈正相关,与MDA、NO含量呈负相关,质量浓度达400mg/L及以上质量浓度时,结果相反。随着Cu2+质量浓度的增加,细胞膜电位下降(P<0.05)。以上结果表明,适量的铜含量对细胞内的抗氧化酶活性具有促进作用,但高铜可能促使细胞活性下降,自由基产生增多,细胞膜电位下降。 In this research, copper poisoning model was established for further discussing different level of copper on rat hepatocyte proliferation activity, free radical metabolism and the membrane potential. The copper sulfate (CuSO4) was used as the source of copper, there were six levels of copper (Cu2+ ) : 0,50,100,200, 400,800 mg/L. In all of the groups, rat hepatocytes were cultured for 24 hours and 48 hours respectively, and the free radical produce,antioxidant enzyme activity and cell membrane potential were detected. The results showed that 400 and 800 mg/L copper decreased below 400 mg/L copper, the copper concentration obviously the cell proliferation activity(P〈0. 05). When and T-SOD,GSH-Px,CP activity were positively correla- ted,and that was negatively correlated with the content of MDA and NO. The results were reverse when the concentration of copper were 400 mg/L, with the increase of copper concentration,the membrane potential decreased(P〈0. 05). The above results showed that the proper concentration copper could promote the antioxidant enzyme activity of cells,but high copper might result in a decreasing of enzyme activity,more free radical production, and the decreasing of the hepatocyte membrane potential.
出处 《中国兽医学报》 CAS CSCD 北大核心 2016年第11期1939-1943,1948,共6页 Chinese Journal of Veterinary Science
基金 国家自然科学基金资助项目(30671550)
关键词 大鼠 肝细胞 氧化损伤 膜电位 copper rat liver cell oxidative damage membrane potential
  • 相关文献

参考文献11

二级参考文献80

共引文献255

同被引文献25

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部