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Lipid dynamics in goldfish (Carassius auratus) during a period of gonadal recrudescence: Effects of beta-sitosterol and 17beta-estradiol exposure.

Sharpe RL, MacLatchy DL

Canadian Rivers Institute and Department of Biology, University of New Brunswick, Saint John, NB, Canada E2L 4L5. rainie.sharpe@unb.ca

The potential for contaminants to alter lipid or cholesterol dynamics in fish is rarely investigated and may include critical physiological endpoints that are impacted by exposure to endocrine-active substances. The current study investigated plasma and tissue lipid dynamics over a period of recrudescence in goldfish, while also examining the potential for beta-sitosterol (beta-sit), a phytosterol and 17beta-estradiol (E(2)), an endogenous estrogen, to alter lipid homeostasis. Goldfish were exposed to 0 microg/g (no chemical; control), 200 microg/g beta-sit (72.3% sitosterol mixture) or 10 microg/g 17beta-estradiol (E2) via Silastic implants for a period of five months. Plasma lipids peaked in control fish coincident with maximum liver size, while gonadal cholesterol concentration was highest concomitant with maximum gonad size. Plasma lipid concentrations were highly affected by E2 but not beta-sit exposure; E2 elevated total cholesterol (p<0.001) and triglyceride (TG; p<0.001) and decreased high-density lipoprotein (HDL) concentration (p<0.001) in male fish. Tissue cholesterol concentrations were minimally affected by beta-sit exposure, while hepatic cholesterol concentrations were increased in E2 exposed females (p=0.041), indicating elevated liver lipogenesis in response to E2, but not beta-sit, exposure. The present study demonstrates differential effects by beta-sit and E2 on plasma lipoprotein profile and TG concentration and indicates estrogen-specific effects on hepatic lipid metabolism during gonadal development.

Published 4 May 2007 in Comp Biochem Physiol C Toxicol Pharmacol, 145(4): 507-17.
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