Xenobiotics in gametes of Lake Michigan lake trout (Salvelinus namaycush) induce hepatic monooxygenase activity in their offspring.
Xenobiotics in gametes of Lake Michigan lake trout (Salvelinus namaycush) induce hepatic monooxygenase activity in their offspring.
复制标题
密歇根湖鳟鱼（Salvelinus namaycush）配子中的异生物质诱导其后代的肝单加氧酶活性。
DOI：
10.1016/0272-0590(84)90244-6
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Lech,JJ
中科院分区：
文献类型：
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作者：
Binder,RL;Lech,JJ
密歇根湖鳟鱼（Salvelinus namaycush）配子中的外源物质诱导其后代肝脏单加氧酶活性。宾德河L.，Lech，J. J.（1984）. Fundamental.应用毒理学4，1042-1054。产自密歇根湖的湖鳟的卵含有许多有害生物化合物，包括多氯联苯（PCB）。为了评估这种污染是否足以诱导肝细胞色素P-450依赖性单加氧酶（MO）活性在早期发展，肝MO系统的实验室培养的后代密歇根湖，格林湾，和马奎特孵化湖鳟鱼进行了比较。此外，诱导肝cytochromeP-450系统在开发湖鳟鱼的商业PCB混合物，Aroclor 1254（A1254），其特征在于。在胚胎发育后期和上游阶段，野生湖鳟后代的肝MO系统出现诱导，芳烃羟化酶（AHH）活性水平的基础上，是3.5- 8.6倍，高于孵化控制水平。此外，在上游阶段，野生鳟鱼后代类似于A1254处理的孵化场鱼苗，α-萘甲酮对肝脏AHH活性的抑制程度，以及肝微粒体中存在可诱导的Mr = 58，000多肽。与孵化场对照水平相比，密歇根湖和格林湾上游鱼苗的氨基比林N-脱甲基酶活性水平相对较低，对诱导剂反应相对较弱。经过7个月的孵化后实验室培养，当受精时存在的外源性物质残留物被生长大大稀释时，密歇根湖和孵化场鳟鱼后代的肝MO系统在许多参数方面基本上没有区别。这些结果表明，在早期阶段的孵化场和野生鳟鱼后代之间观察到的差异不太可能有一个遗传基础，而是由于异源型诱导。剂量反应实验和残留物分析数据表明，商用多氯联苯混合物的残留物至少是造成本文所述影响的部分原因。总的来说，这些数据提供了非常有力的证据表明，污染的密歇根湖湖鳟鱼配子的多氯联苯和其他外源性物质引起诱导肝MO活性在其后代。具有诱导MO系统的鱼胚胎和鱼苗可能对某些环境污染物的毒性敏感性增加，这些污染物由细胞色素P-450代谢活化。
Xenobiotics in Gametes of Lake Michigan Lake Trout (Salvelinus namaycush) Induce Hepatic Monooxygenase Activity in Their Offspring. BINDER, R. L., AND LECH, J. J. (1984).Fundam. Appl. Toxicol. 4, 1042–1054. Eggs spawned from Lake Michigan lake trout contain a number of xcnobiotic compounds, including polychlorinated biphenyls (PCBs). To assess whether this contamination is sufficient to induce hepatic cytochromeP-450-dependent monooxygenase (MO) activity during early development, the hepatic MO systems of laboratory-cultured offspring of Lake Michigan, Green Bay, and Marquette Hatchery lake trout were compared. Additionally, the induction of hepatic cytochromeP-450 systems in developing lake trout by the commercial PCB mixture, Aroclor 1254 (A1254), was characterized. During late embryonic development and at the swim-up stage, the hepatic MO systems of the feral lake trout offspring appeared induced, based on levels of aryl hydrocarbon bydroxytase (AHH) activity that were 3.5- to 8.6-fold higher than the hatchery control levels. Furthermore, at the swim-up stage the feral trout offspring resembled A1254-treated hatchery fry with regard to the degree of inhibition of hepatic AHH activity by α-naphthoflavone, and the presence of an inducibleMr= 58,000 polypeptide in hepatic microsomes. The levels of aminopyrineN-demethylase activity, which was relatively unresponsive to inducers, were moderately lower in the Lake Michigan and Green Bay swim-up fry compared to the hatchery control levels.After 7 months of posthatching laboratory culture, when residues of xenobiotics present at fertilization were greatly diluted by growth, the hepatic MO systems of the Lake Michigan and hatchery trout offspring appeared essentially indistinguishable with regard to a number of parameters. These results indicate that the differences observed between the hatchery and feral trout offspring at earlier stages were not likely to have a genetic basis, but rather were due to a xenobiotic-type induction. Dose-response experiments and residue analysis data indicated that residues of commercial PCB mixtures were at least partially responsible for the effects described here. Overall, these data provide very strong evidence that contamination of Lake Michigan lake trout gametes by PCBs and possibly other xenobiotics caused induction of hepatic MO activity in their progeny. Fish embryos and fry with induced MO systems may have an increased sensitivity to the toxicity of certain environmental contaminants that are metabolically activated by cytochromeP-450.