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首页> 外文期刊>Environmental toxicology and chemistry >IS OXIDATIVE STRESS THE MECHANISM OF BLUE SAC DISEASE IN RETENE-EXPOSED TROUT LARVAE?
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IS OXIDATIVE STRESS THE MECHANISM OF BLUE SAC DISEASE IN RETENE-EXPOSED TROUT LARVAE?

机译：氧化应激暴露于鳟鱼幼虫中的蓝囊病是机制吗？

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摘要

Retene (7-isopropyl-1 -methylphenanthrene) causes blue sac disease (BSD) in early life stages of fish, an effect similar to that of 2,3,7,8-tetrachlorodibenzo(p)dioxin. The signs of BSD include cytochrome P450 (CYP1A) induction, edema, hemor-rhaging, and craniofacial deformities, indicating membrane damage, circulatory failure, and impaired development. To test if the underlying cause was oxidative stress, rainbow trout (Oncorhynchus mykiss} larvae were exposed to waterborne retene or to known prooxidants (paraquat, f-butyl hydroperoxide, and carbon tetrachloride) in the presence or absence of vitamin E, an antioxidant. Fish exposed to retene showed an increased prevalence of BSD, reduced tissue concentrations of vitamin E and total glutathione, and a lower percentage of glutathione in a reduced form. Coexposure to vitamin E reduced the prevalence of BSD and restored tissue concentrations of vitamin E, but it did not affect retene uptake or tissue concentrations of glutathione. These responses are consistent with oxidative stress as a mode of action of retene. However, retene did not affect whole-body lipid peroxide concentrations, and prooxidants did not affect the prevalence of BSD and had only minimal effects on tissue glutathione and vitamin E. Possible explanations for these conflicting results include prooxidant exposures were insufficient to generate oxidative stress; lipid peroxidation may not be measurable in whole-body homogenates of retene-exposed fish if effects are localized to endothelial cells, where CYP1A enzymes are most induced; or retene may have an alternate mode of action (e.g., adduction of retene metabolites to lipids, protein, or DNA).
机译：retene（7-异丙基-1-甲基菲）在鱼类的生命早期阶段引起蓝囊病（BSD），其作用类似于2,3,7,8-四氯二苯并（p）二恶英。 BSD的体征包括细胞色素P450（CYP1A）诱导，水肿，出血和颅面畸形，表明膜损伤，循环衰竭和发育受损。为了测试根本原因是否是氧化应激，在存在或不存在抗氧化剂维生素E的情况下，将虹鳟鱼（Oncorhynchus mykiss}幼虫暴露于水性retene或已知的抗氧化剂（百草枯，叔丁基过氧化氢和四氯化碳）。暴露于retene的鱼显示出BSD的患病率增加，维生素E和总谷胱甘肽的组织浓度降低，而谷胱甘肽的百分比降低，而维生素E的共同暴露降低了BSD的患病率并恢复了维生素E的组织浓度，但是这些反应与氧化应激作为一种视黄酮的作用方式是一致的，但这些反应与氧化应激是一致的，但是，视黄醛并不影响全身脂质过氧化物的浓度，而促氧化剂并没有影响BSD和BSD的患病率。对组织谷胱甘肽和维生素E的影响很小。对这些矛盾结果的可能解释包括暴露于促氧化剂不足以产生氧化应激；如果影响集中在内皮细胞（其中CYP1A酶最易诱导），脂质过氧化可能无法在暴露于retene的鱼的全身匀浆中测量到；视黄醇或视黄烯可以具有替代的作用方式（例如，视黄醇代谢物与脂质，蛋白质或DNA的内酰胺化）。

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