【摘要】 目的:探明氯化镉（CdCl2）暴露对背角无齿蚌肝脏中抗氧化酶活力及脂质过氧化的影响。方法:根据背角无齿蚌96 h镉离子(Cd²⁺)半致死剂量设置1个对照组和2个处理组（0.1和0.5 mg/L）,分别检测镉暴露4周及镉清除4周期间背角无齿蚌肝脏中抗氧化酶[超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）]的活力和脂质过氧化物丙二醛（MDA）的含量。结果:不同浓度Cd²⁺暴露对背角无齿蚌抗氧化酶活力及脂质过氧化产生不同程度的影响,低浓度Cd²⁺暴露的毒性效应较弱,高浓度Cd²⁺暴露可显著抑制肝脏SOD活力,诱导GPx活力升高,在暴露后期显著抑制CAT活力,MDA含量随着暴露时间的延长而显著升高。结论:慢性Cd²⁺暴露可影响背角无齿蚌肝脏抗氧化酶活力,引起脂质过氧化损伤,且作用机制与急性毒性不同。更多还原

【Abstract】 Objective:To explore the changes of antioxidant enzyme activities and lipid peroxidation in the liver of the freshwater museel Anodonta woodiana after chronic exposure to cadmium chloride（CdCl2）.Methods:The freshwater mussels were exposed to different concentrations of Cd²⁺（0, 0.1 and 0.5 mg/L） for 4 weeks, then they were removed to clean water and cultured for another 4 weeks. Activities of antioxidant enzymes[superoxide dismutase（SOD）, glutathione peroxidase（GPx） and catalase（CAT）] and content of malondialdehyde（MDA） in the liver of the freshwater mussels were measured.Results:Different concentrations of Cd²⁺ exposure induced various changes of antioxidant enzyme activities and caused lipid peroxidation in the liver of the freshwater mussels. Toxic effect of low-dose Cd²⁺was lower. While, high-dose Cd²⁺exposure could induce severe oxidative stress such as inhibition of SOD activity, induction of GPx activity and increase in MDA content. Moreover, the persistent toxic effects were also found in the cleaning period.Conclusion:Chronic exposure of Cd²⁺affected the activities of antioxidant enzymes and caused lipid peroxidation damage in the liver of the freshwater mussels. The chronic toxicity mechanism of pollutants was different from the acute toxicity which should not be ignored.更多还原