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目的探讨氯化镉(CdC l2)在肝脏内蓄积及其引起肝脏毒性的氧化性损伤机制,为防治镉危害提供依据。方法雌性BALB/c小鼠随机分成3组,每组7只,体重(18±2)g。染毒组分别腹腔注射10μmol/kg(高镉组)和2.5μmol/kg(低镉组)CdC l2溶液,每周3次,连续14周;对照组腹腔注射生理盐水。测定体重变化、脏器系数、肝脏镉含量及脂质过氧化产物丙二醛(MDA)和超氧化物歧化酶(SOD)含量,HE染色观察肝、肾组织形态学。结果高镉组体重降低,肝脾脏器系数高于对照组,肝脏镉含量、MDA和SOD水平均增高(P<0.05);肾脏的组织形态学发生变化。低镉组仅见肝、心、脾、肾的脏器系数高于对照组(P<0.05)。结论CdC l2可在小鼠肝脏蓄积,氧化性损伤可能是其肝脏毒性的机制之一。
Objective To investigate the accumulation of cadmium chloride (CdC12) in the liver and the oxidative damage mechanism of its causing liver toxicity, to provide evidence for the prevention of cadmium damage. Methods Female BALB / c mice were randomly divided into 3 groups with 7 mice in each group and weighing 18 ± 2 g. Rats in the exposure group were intraperitoneally injected with 10μmol / kg (high cadmium group) and 2.5μmol / kg (low cadmium group) CdC12 solution three times a week for 14 weeks. The control group was intraperitoneally injected with normal saline. The changes of body weight, organ coefficient, hepatic cadmium content and the contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The morphological changes of liver and kidney were observed by HE staining. Results The body weight of high cadmium group decreased and the coefficient of liver and spleen organs was higher than that of the control group. The content of cadmium, the content of MDA and SOD in the liver increased (P <0.05). The histomorphology of kidney changed. The organ coefficient of liver, heart, spleen and kidney in low cadmium group was higher than that in control group (P <0.05). Conclusion CdC12 can accumulate in the liver of mice, and oxidative damage may be one of the mechanisms of liver toxicity.