Occurrence of CYP1A activity and bluesac disease in relation to specific developmental stages in rainbow trout (Oncorhynchus mykiss ) exposed to retene.

摘要

The polycyclic aromatic hydrocarbon, 7-isopropyl-1-methylphenanthrene (retene) induces CYP1A activity in fish in both natural aquatic environments and laboratory settings. The most common symptoms of retene toxicity are a group of symptoms known as bluesac disease, which includes yolk sac and pericardial edema, hemorrhaging, craniofacial malformations, and arrested growth, which can lead to mortality or recruitment failure. To determine the effects of retene exposure in early life stages of rainbow trout, four separate experiments were set up to determine whether there is a sensitive ontogenic stage to retene toxicity, and if CYP1A induction is a forerunner to retene toxicity. CYP1A protein concentrations were measured through immunohistochemistry. Results indicate that CYP1A activity in retene exposed fish began during organogenesis, when organ and enzyme systems are first being developed, and steadily increased until swim-up. A rise in the prevalence of bluesac disease symptoms one week following a sharp increase in CYP1A activity at the completion of hatch indicates that CYP1A may be responsible for toxic effects. The high prevalence of CYP1A activity and bluesac disease symptoms during the yolk sac stage (post-hatch to swim-up) also indicates that this stage was the most sensitive to retene toxicity. The most common symptoms of bluesac disease were hemorrhaging, yolk sac edema, and mortality; hemorrhaging was the initial and most observed response to retene toxicity in larval rainbow trout. Tissue concentrations of retene indicate that concentrations were quite high in early development, but steadily decreased as fish neared the swim-up stage, most likely due to a greater rate of excretion of both retene and its metabolites at later developmental stages. All fish exposed to water controls showed no toxic effects.