2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin toxicity in yellow perch(Perca flavescens)

Publisher Website
Google Scholar
Abstract
Growth, mortality and morphologic lesions in juvenile, hatchery‐reared yellow perch, Perca flavescens, were studied after treatment with graded single doses of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD, 1–125 μg/kg, intraperitoneally). TCDD doses of 25 and 125 μg/kg caused 95% mortality by 28 d after treatment, without decreasing body weight. A TCDD dose of 5 μg/kg resulted in progressive loss of body weight with cumulative mortality of 80% by 80 d posttreatment. Periodic handling stress did not affect the time course of mortality or cumulative percent lethality in TCDD‐treated perch. Fin necrosis, petechial cutaneous hemorrhage, and ascites occurred in perch treated with 5 μg/kg or more of TCDD. Thymic atrophy, decreased hematopoiesis in the head kidney, fibrinous pericarditis, focal myocardial necrosis, submucosal gastric edema, and hyperplasia of the epithelium of gill filaments and lamellae occurred in perch dosed with 25 or 125 μg/kg. Dose‐related splenic lymphoid depletion occurred in perch receiving 5 μg/kg or more TCDD, and hepatocyte lipidosis occurred in groups treated with doses of 1 μg/kg or more TCDD. Thus yellow perch are as responsive to the acute toxic effects of TCDD as some of the more sensitive mammalian species, and neither loss of body weight nor histologic lesions in TCDD‐treated perch are sufficient to explain mortality.