铅镉联合暴露对大鼠肾脏的氧化损伤

采用饮水对大鼠进行铅(Pb)300 mg/L、镉(Cd)50 mg/L单独和联合(Pb+Cd)300 mg/L+50 mg/L染毒8周,通过检测肾脏皮质组织抗氧化指标和超微结构的变化来探讨铅镉对大鼠肾脏的毒性损伤及其机理.结果表明,Pb、Cd单独或联合染毒使肾脏皮质组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和还原型谷胱甘肽(GSH)含量显著或极显著低于对照组(P<0.05或P<0.01),以铅镉联合组降低幅度最大(P<0.01);3个染毒组丙二醛(MDA)含量显著或极显著高于对照组(P<0.05或P<0.01),联合组升高幅度最大而极显著高于单独染毒组(P<0.01).超微结构发现,铅镉染毒导致线粒体肿胀、膜损伤、嵴断裂或消失,联合组损伤程度重于单独染毒组.表明氧化损伤是Pb、Cd肾脏毒性的机制之一,其联合毒性表现为协同效应.

Effects of exposure to lead and cadmium on the oxidative damage of kidney in rats

Lead acetate(300 mg/L)and/or cadmium chloride(50 mg/L)were administered as drinking water to rats for eight weeks.Antioxidant indices and uhrastructural findings in the renal cortex were detected to investigate the toxicological effects of the heavy metals on the kidney of rats.It indicated that activities of superoxide dismutase (SOD)and glutathione peroxidase(GSH-Px),contents of reduced glutathione(GSH)in the exposed groups were significantly lower than those in the coadministrated group(P<0.05 or P<0.01)and the most remarkable changes occurred in the coadministrated group(P<0.01).Meanwhile,contents of malondialdehyde(MDA)in these exposed groups increased remarkably(P<0.05 or P<0.01),which content in the combined group was markedly higher than that in the single group(Pb or Cd),respectively(P<0.01).Ultrastructurally,mitoehondria damaged with swelling,vacuole-like changes,lesions of mitochondrial membrane,disappearance and fragmentation of carina following the exposure of lead and/or cadmium were observed.Also,the lesion of the(Pb+Cd)group was severer than that in the single(Pb or Cd)group.Thus it can be seen that oxidative damage is one of Pb/Cd-induced nephrotoxicity and synergistic effect lied in the coadministration.