| Abstract |
- Persistent organochlorines (OCs) bioaccumulate in aquatic biota and potentially impair reproduction via endocrine disruption. The present research evaluated estrogenic effects of the OCs, chlordecone (CD) and o,p'-DDT/DDE, and the antiestrogenicity of 3,4,5,3',4',5'-hexachlorobiphenyl (345-HCB) in juvenile rainbow trout, utilizing vitellogenesis as a biomarker. Vitellogenesis, estrogen regulated hepatic production of the yolk protein precursor, vitellogenin (Vg), served as an indicator of estrogenic or antiestrogenic actions relevant to reproductive toxicity or hepatocarcinogenesis. In an estrogen-dose response experiment, plasma Vg was the most sensitive biomarker of vitellogenesis induction, compared to changes in plasma lipids, hepatic estrogen receptor (ER) concentrations or liver somatic index (%LSI). Vitellogenesis was weakly induced by chronic dietary CD exposure (0.4 mg/kg/day) and was associated with relatively high hepatic CD concentrations (15 mg/kg) but was not correlated to the observed mild promotion of hepatocarcinogenesis. In vitro binding assays confirmed CD was weakly estrogenic as CD exhibited low binding affinity for trout hepatic ER (1000-fold less than the synthetic estrogen, moxestrol). A second group of xenoestrogens, o,p'-DDT and o,p'-DDE, demonstrated very weak in vitro trout ER binding affinity (156,000-fold less than moxestrol) and p,p'-DDE was inactive. In vivo, plasma Vg and hepatic ER concentrations were significantly elevated by o,p'-DDT and o,p'-DDE, but not p,p'-DDE, (total dose 45 to 90 mg/kg via ip injection) in trout at mg/kg hepatic concentrations. Co-planar PCBs such as 345-HCB may act as antiestrogens by decreasing ER or plasma estradiol concentrations or by altering estrogen regulated gene expression. However, results demonstrated 345-HCB (0.25 to 100 mg/kg via ip injection) did not antagonize estrogen induced increases in hepatic ER, plasma Vg or %LSI but significantly elevated CYP1A protein and mRNA content and depressed plasma estradiol. We concluded vitellogenesis modulation in trout was a less sensitive 345-HCB exposure biomarker than CYP1A induction and plasma estradiol suppression by 345-HCB did not significantly influence plasma Vg. Collectively, results indicated vitellogenesis was a suitable biomarker for assessing weak estrogenic effects of OCs in juvenile rainbow trout but was not responsive to potential antiestrogenic effects of 345-HCB.
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