南方鲇对水体Cd暴露的急性中毒效应  

The Acute Toxicological Response of the Southern Catfish to Water-Borne Cadmium

作　　者：李健 罗其勇[3] 闫玉莲 谢小军[2] 

机构地区：[1]钦州学院海洋学院广西北部湾海洋生物多样性养护重点实验室,广西钦州535011 [2]西南大学生命科学学院水生生物及水环境研究所,重庆400715 [3]广西科技大学招生就业中心,广西柳州545006

出　　处：《重庆师范大学学报（自然科学版）》2018年第1期36-42,共7页Journal of Chongqing Normal University:Natural Science

基　　金：国家自然科学基金(No.31300338);重庆市自然科学基金(No.cstc2013jjB80008);中央高校基本科研业务费专项基金(No.XDJK2016C156);钦州学院校级科研项目(No.2017KYQD107);广西北部湾海洋生物多样性养护重点实验室项目(No.2018ZB03)

摘　　要：【目的】考查南方鲇(Silurus meridionalis)对Cd胁迫的毒理反应。【方法】以人工繁育获得的体质量为(20.80±0.51)g的南方鲇当年幼鱼为研究对象,在水体硬度为25mg·L^(-1)(以CaCO3质量浓度计)、水温为(27.5±0.5)℃、水体Cd^(2+)质量浓度分别为0,4.0,5.0,6.0,7.0,8.0mg·L^(-1)条件下进行了96h急性暴露实验,测定了该物种96h半致死浓度(LC50)、肝线粒体状态3呼吸率、细胞色素C氧化酶(CCO)活性以及脑组织乙酰胆碱酯酶(AChE)活性。【结果】水体中Cd^(2+)对南方鲇的96hLC50为5.46mg·L^(-1);在水体中质量浓度分别为0,4.0,5.0,6.0,7.0 mg·L^(-1)的Cd^(2+)暴露处理下,实验鱼的肝脏线粒体状态3呼吸率随着水体Cd^(2+)的质量浓度增加而降低,分别为(42.20±2.50),(34.97±1.61),(32.29±1.40),(31.63±1.82),(28.69±1.69)nmol·min-1·mg-1,且不同质量浓度Cd^(2+)暴露处理组的测得值均比对照组的更低,与后者的差异均具有统计学意义(p<0.05);肝脏线粒体的呼吸控制率(RCR)随着水体Cd^(2+)的质量浓度升高而呈降低趋势,且不同质量浓度Cd^(2+)暴露处理组肝脏线粒体的RCR均比对照组的更低,与后者的差异均具有统计学意义(p<0.05);实验鱼肝线粒体CCO的活性随着水体Cd^(2+)暴露质量浓度的增加而降低,且质量浓度为7.0mg·L^(-1)的Cd^(2+)暴露处理组的这一指标值比对照组的更低,差异具有统计学意义(p<0.05);不同质量浓度Cd^(2+)暴露处理组实验鱼脑组织AChE活性均比对照组的更低,与后者的差异均具有统计学意义(p<0.05)。【结论】南方鲇对水体Cd^(2+)暴露的耐受能力相对较强;受到Cd^(2+)暴露的实验鱼肝脏线粒体状态3呼吸率、CCO活性和RCR降低结果提示:在Cd^(2+)急性胁迫下线粒体功能受到损伤,呼吸代谢能力减弱;急性水体Cd^(2+)暴露抑制了实验鱼的脑组织AChE活性,使鱼体神经系统功能损伤,导致鱼体行为异常。[Purposes]It aims to investigate the acute toxicological response of the Silurus meridionalis to water-borne cadmium.[Methods]The juveniles of the S.meridionalis（body mass：（20.80±0.51）g）which were bred using artificial fertilization were exposed to different concentrations of cadmium（Cd（2＋））（0,4.0,5.0,6.0,7.0 and 8.0 mg·L（-1））in artificial soft water（CaCO325 mg·L（-1））at 27.5 ℃.After a 96-hour exposure,the median lethal concentration（96 hLC50）,state 3 respiration rate and cytochrome C oxidase（CCO）activity of mitochondria isolated from liver,and the activity of acetylcholine esterase（AChE）in brain were assessed.[Findings]Acute 96 hLC50 value of the test fish for Cd（2＋）toxicity was 5.46 mg·L（-1）.State 3 respiration rate was strongly inhibited by the addition of Cd（2＋）.The value in the groups of 4.0,5.0,6.0,and 7.0 mg·L（-1） were（34.97±1.61）,（32.29±1.40）,（31.63±1.82）,and（28.69±1.69）nmol·min-1·mg-1,respectively,which were significantly lower compared with the control group（42.20±2.50）nmol·min-1·mg-1（p〈0.05）.The respiratory control ratio（RCR）decreased with the increasing Cd（2＋）concentration and the value in the control group was significantly higher than that in other groups（p〈0.05）.The CCO activity decreased along the Cd（2＋）concentration gradient,significant inhibition of CCO activity by Cd（2＋）compared to controls was achieved only at the highest concentration tested（p〈0.05）.The activity of AChE in group of 4.0,5.0,6.0 and 7.0 mg·L（-1） were significantly lower than that of the control group（p〈0.05）.[Conclusions]S.meridionalis have higher tolerance for Cd（2＋）toxicity.The decrease in state 3 respiration rates,RCR,and CCO activity suggest that the mitochondrial impairment might be caused by waterborne Cd（2＋）,and which lead to the inhibition of the aerobic capacities in liver.The inhibition of AChE activity and abnormal behavior of the fish in the acute expos

关 键 词：水体Cd暴露 急性毒性 线粒体呼吸率 细胞色素C氧化酶 乙酰胆碱酯酶 南方鲇 

分 类 号：Q175[生物学—水生生物学]