Zinc protects renal function during cadmium intoxication in the rat
Zinc protects renal function during cadmium intoxication in the rat
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DOI：
10.1152/ajprenal.00366.2004
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发表时间：
2006-01-01
影响因子：
4.2
通讯作者：
Poujeol, P
中科院分区：
文献类型：
--
作者：
Jacquillet, G;Barbier, O;Poujeol, P
锌对镉中毒大鼠肾功能的保护作用。美国肾脏生理学杂志290：F127-F137，2006年。首次发表于2005年6月7日; doi：10.1152/ajprenal.00366.2004。本研究探讨慢性CdCl_2中毒（500 μ g Cd ~（2+）/kg，每天ip，连续5天）对大鼠肾功能的影响，以及大鼠肾脏中紧密连接蛋白claudin-2、claudin-3和claudin-5的变化。我们还研究了在慢性CdCl 2中毒的共同管理的ZnCl 2（500 μ g Zn 2 +/ kg）的效果。结果表明：（1）大部分滤过的Cd ~（2+）在肾脏内被重吸收，（2）慢性Cd ~（2+）中毒可引起肾脏处理离子的改变，但不改变肾小球滤过率，（3）迟发性肾病，表现为Fanconi样特征，出现于Cd ~（2+）暴露结束后5天以上; 4）慢性Cd ~（2+）中毒改变了上皮细胞的完整性，影响了紧密连接蛋白的表达和定位;和5）与Zn 2+共处理保护免受Cd 2+的肾毒性作用，防止改变的claudin表达并抑制细胞凋亡。总之，这些结果表明，镉的毒性和细胞毒性机制是复杂的，可能影响膜转运蛋白和紧密连接蛋白。最后，锌2+补充可能为未来的治疗提供基础。
Zinc protects renal function during cadmium intoxication in the rat. Am J Physiol Renal Physiol 290: F127-F137, 2006. First published June 7, 2005; doi:10.1152/ajprenal.00366.2004.- This study investigates the effect in the rat of chronic CdCl2 intoxication (500 mu g Cd2+/kg, daily ip injection for 5 days) on renal function and the changes in tight junction proteins claudin-2, claudin-3, and claudin-5 present in rat kidney. We also studied the effect of coadministration of ZnCl2 (500 mu g Zn2+/ kg) during chronic CdCl2 intoxication. Our results indicate that 1) most of the filtered Cd2+ is reabsorbed within the kidney; 2) chronic Cd2+ intoxication can induce a change in renal handling of ions without altering glomerular filtration rate; 3) a delayed nephropathy, showing Fanconi-like features, appears more than 5 days after the end of CdCl2 exposure; 4) epithelial integrity is altered by chronic Cd2+ intoxication affecting the expression and localization of claudin tight junction proteins; and 5) cotreatment with Zn2+ protects against the renal toxic effects of Cd2+, preventing altered claudin expression and inhibiting apoptosis. In conclusion, these results show that Cd2+ toxicity and cellular toxic mechanisms are complex, probably affecting both membrane transporters and tight junction proteins. Finally, Zn2+ supplementation may provide a basis for future treatments.