汞、硒暴露对紫贻贝(Mytilus edulis)抗氧化酶系统的影响

为了研究重金属汞及微量元素硒对海洋贝类的毒性效应,揭示汞、硒在生物体内的相互作用机制,用汞和硒对指示生物紫贻贝(Mytilus edulis)进行单一及联合亚慢性暴露实验。设置对照组(0μg·L-1)、汞暴露组(25μg·L-1Hg2+)、硒暴露组(4μg·L-1Se4+)以及硒汞联合暴露组(25μg·L-1Hg2++4μg·L-1Se4+)4个实验组,并分别在暴露期间的第0、2、4和6天定时采集样本,测定紫贻贝鳃SOD、GPx及CAT3种抗氧化酶活性。将实验数据进行ANOVA分析处理后,结果表明:与对照组相比,汞暴露组SOD和GPx均呈现先显著升高(p<0.05或p<0.01)后降低(p<0.01或p<0.001)的趋势,CAT则从第4天开始显著降低(p<0.05);硒暴露组中SOD活性始终高于对照组(p<0.001),GPx活性在第2天也显著升高(p<0.001),CAT活性始终与对照组相近;硒汞联合作用与汞暴露组相比,SOD、GPx和CAT活性在不同时间点均有显著升高(p<0.05),而与硒暴露组相比,3种酶活性均低于硒单独暴露的水平。说明汞在短期能够诱导抗氧化酶活性,随着暴露时间的延长,则表现出明显的抑制作用;微量硒能够增强抗氧化酶系统活性,对汞导致的氧化损伤具有拮抗作用。

Exposure Effects of Mercury and Selenium on Antioxidant Enzymes of Blue Mussel Mytilus edulis

The toxic effects of mercury and selenium on blue mussels (Mytilus edulis) were investigated to illustrate the interaction mechanism by four group design including control (0 μg·L-1), Hg (25 μg·L-1Hg2+), Se (4 μg·L-1Se4+) and Hg+Se (25 μg·L-1 Hg2+ + 4 μg·L-1 Se4+). The activities of SOD, GPx and CAT in the gill tissue of M. edulis were measured after exposure for 0, 2, 4 and 6 days. The ANOVA analysis showed that: (1) In Hg treatment, the activities of SOD and GPx increased significantly at first (p<0.05 or p<0.01) and then decreased (p<0.01 or p<0.001), while CAT was significantly inhibited from the 4th day (p<0.05). (2) In Se treatment, the activities of SOD were higher than that of the control throughout the whole exposure, and GPx increased significantly from the 2nd day, while no significant change was found in CAT activities. (3) In the joint exposure of Hg and Se, higher levels of SOD, GPx and CAT were found than that in Hg treatment (p<0.05), while the levels of the three enzymes were significantly lower as compared with that in Se treatment. It was demonstrated that antioxidant enzymes activity in blue mussels could be induced in short time ranges and then be inhibited by mercury treatment with the extension of exposure time, and selenium could stimulate the activity of antioxidant enzymes and showed antagonistic effects on mercury-induced oxidative stress.