Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 2009-05-01

Effects of o,p'-DDE, heptachlor, and 17beta-estradiol on vitellogenin gene expression and the growth hormone/insulin-like growth factor-I axis in the tilapia, Oreochromis mossambicus.

Lori K Davis, Nancy Visitacion, Larry G Riley, Naoshi Hiramatsu, Craig V Sullivan, Tetsuya Hirano, E Gordon Grau

Index: Comp. Biochem. Physiol. C. Toxicol. Pharmacol. 149(4) , 507-14, (2009)

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Abstract

Effects of two endocrine disruptors, o,p'-DDE and heptachlor, and 17beta-estradiol (E(2)) on vitellogenin (Vg) and the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis were examined in male tilapia. In the first experiment, fish were given 5 weekly injections of either E(2), o,p'-DDE or heptachlor (5 microg/g). E(2) treatment increased plasma Vg and hepatic expression of three Vg genes (Vgs A, B, and C) and estrogen receptor alpha (ERalpha), while reducing plasma levels of IGF-I and suppressing the expression of IGF-I, the GH receptor (GHR2) and the putative somatolactin receptor (GHR1). Neither pesticide greatly affected the other parameters examined, except for a significant reduction in expression of GHR2 and increased plasma IGF-I. In the second experiment, fish were given a single injection of o,p'-DDE or heptachlor (100 microg/g), or E(2) (5 microg/g) and sacrificed 5 days post-injection. Treatment with E(2) stimulated expression of all three Vg genes. Both o,p'-DDE and heptachlor increased expression of VgB, whereas only o,p'-DDE increased VgA expression. There was no effect of o,p'-DDE or heptachlor on VgC expression or plasma Vg levels. Treatment with o,p'-DDE and heptachlor as well as E(2) increased ERalpha and ERbeta transcript levels. Similarly, both pesticides increased GHR1 and IGF-I expression, whereas no significant effect of E(2) was observed on GHR1, GHR2 or IGF-I expression. These results indicate that o,p'-DDE and heptachlor have varying temporal and dose effects on modulation of Vg and the GH/IGF-I axis that are distinct from E(2).