采用亚慢性毒性实验研究了镉、锌对白氏文吕鱼(Branchiostoma belcheri)(简称文昌鱼)的毒性累积效应及体内超氧化物歧化酶(SOD)活性、乙酰胆碱酯酶(ACHE)活性、磷酸酶活性及脂质过氧化产物丙二醛(MDA)含量的影响,探讨了亚致死浓度镉、锌胁迫下文昌鱼的生理生化响应.研究结果表明,镉和锌对文昌鱼的96h半致死浓度(LC50)分别为4.60和2.26mg/L,相比之下锌对文昌鱼的毒性更大.实验采用理论上的镉、锌安全浓度(1/1096hLC50)对文吕鱼进行7d的亚慢性暴露,随着暴露时间的推移,镉在文昌鱼体内呈线性增加,而锌的含量则与对照组无显著性差异,表明文昌鱼对锌的调节能力大于镉.7d亚慢性毒性实验表明文昌鱼体内的AChE活性随着金属暴露时间的延长持续下降,至第7天时镉和锌对AChE活性的抑制率分别达65%和79%;脂质过氧化产物MDA水平在金属暴露初期即达到极显著水平,随后稍有下降且镉对文昌鱼体内活性氧的诱导作用大于锌;SOD活性在暴露中期受到显著抑制,可能是由于体内过氧化程度过高抑制其活性,之后逐渐恢复.文昌鱼体内的碱性磷酸酶(AKP)活性在镉或锌暴露的第1天被显著诱导,之后恢复至对照水平;酸性磷酸酶(ACP)活性随镉暴露时间延长,呈现先升高再下降的趋势,而锌对ACP活性无显著影响.实验结果表明即使是很低浓度的镉、锌都会对文昌鱼的神经系统及抗氧化等防御系统造成一定的损伤.
This study was quantified the effects of Cd and Zn on some selected enzymes activities of amphioxus after 7 d of sublethal exposure. The results of acute toxicity experiments showed that the 96 h LC50 of Cd and Zn for amphioxus were 4.60 and 2.26 mg/ L, respectively. After seven days of exposure tO sublethal Cd and Zn, the Cd concentration in the amphioxus increased linearly, where-as the Zn concentrations did not change, suggesting that amphioxus regulated Zn uptake from the ambient water. Compared to the control,the AchE of amphioxus decreased gradually and was inhibited by 65% and 79% for Cd and Zn, respectively, during seven days of exposure. The MDA level increased significantly at the beginning of exposure. SOD was significantly inhibited after three days of exposure to Cd and Zn,while AKP was induced within the first day of exposure and then decreased to the normal level. Zn had no significant effect on ACP of amphioxus,but Cd significantly increased its activity after one day of exposure. Even safet concentrations of Cd and Zn damged the defense system of amphioxus during the long term exposure.