Oikari A, Jimenez B
Department of Biology, University of Joensuu, Finland.
Ecotoxicol Environ Saf. 1992 Feb;23(1):89-102. doi: 10.1016/0147-6513(92)90024-w.
Effects of chemically induced hepatic injury on biotransformation enzymes in fish were studied. Sunfish hybrids (Lepomis macrochirus x L. cyanellus) were dosed per os with allyl formate (ALF) and carbon tetrachloride (CCl4), and the induction of liver EROD (7-ethoxyresorufin O-deethylase) activity was subsequently challenged by injections of beta-naphthoflavone (BNF) and benzo[a]pyrene (B[a]P). Hepatotoxicity of chemical treatments was assessed using blood enzymes (ASAT, ALAT, and LDH) along with other biochemical variables. Both hepatotoxicants partially abolished the induction of EROD (maximally by 76-89%), and the decrease in induction was dose related. The cytosolic activity of glutathione S-transferase (GST) in the liver decreased in parallel with the decrease in EROD induction. Fish receiving high doses of ALF exhibited significantly less microsomal and blood plasma proteins and, occasionally, were jaundiced. These symptoms, however, were less sensitive indicators of hepatotoxicity than alterations in liver EROD and GST. Both ALF and CCl4 increased the activities of hepatic enzymes in the blood plasma, indicating cytotoxicity. In addition B[a]P, unlike BNF, also increased plasma activities of LDH and ALAT at a dose inducing liver EROD, implying simultaneous hepatotoxicity at high sublethal levels of this xenobiotic. These data suggest that hepatotoxic chemicals absorbed by fish may act antagonistically by decreasing the degree of induction of the cytochrome P450 system relative to the inherent capacity of inducing xenobiotic chemicals present in the environment. Therefore, when assessing the toxicological status of water using fish health biomarkers, it is advisable to measure a concert of metabolic and biochemical variables instead of any single biomarker.
研究了化学诱导的肝脏损伤对鱼类生物转化酶的影响。给太阳鱼杂交种（大鳍鳞鳃太阳鱼×蓝鳃太阳鱼）经口投喂甲酸烯丙酯（ALF）和四氯化碳（CCl4），随后通过注射β-萘黄酮（BNF）和苯并[a]芘（B[a]P）来激发肝脏EROD（7-乙氧基异吩唑酮O-脱乙基酶）活性的诱导。使用血液酶（谷草转氨酶、谷丙转氨酶和乳酸脱氢酶）以及其他生化变量评估化学处理的肝毒性。两种肝毒性物质都部分消除了EROD的诱导（最大消除率为76%-89%），诱导的降低与剂量相关。肝脏中谷胱甘肽S-转移酶（GST）的胞质活性与EROD诱导的降低平行下降。接受高剂量ALF的鱼微粒体和血浆蛋白显著减少，偶尔会出现黄疸。然而，这些症状作为肝毒性指标不如肝脏EROD和GST的变化敏感。ALF和CCl4都增加了血浆中肝脏酶的活性，表明存在细胞毒性。此外，与BNF不同，B[a]P在诱导肝脏EROD的剂量下也增加了血浆中乳酸脱氢酶和谷丙转氨酶的活性，这意味着在这种外源性物质的高亚致死水平下同时存在肝毒性。这些数据表明，鱼类吸收的肝毒性化学物质可能通过相对于环境中存在的诱导外源性化学物质的固有能力降低细胞色素P450系统的诱导程度而产生拮抗作用。因此，在使用鱼类健康生物标志物评估水的毒理学状态时，建议测量一系列代谢和生化变量，而不是任何单一的生物标志物。
