Influence of xenobiotics on rainbow trout liver estrogen receptor and vitellogenin gene expression

ABSTRACT Rainbow trout hepatocyte primary culture was used to test the influence of some xenobiotics on the expression of two genes implicated in reproduction, those for the estrogen receptor (ER) and vitellogenin (Vg). We showed that chlordecone, nonylphenol, a polychlorobiphenol (PCB) mixture (Aroclor 1245) and lindane were able to induce ER and Vg mRNA accumulation. Antiestrogens, 4-hydroxytamoxifen and ICI 164,384, prevented the effects of the xenobiotics, indicating that the induction of gene expression is mediated by the ER. Among these four xenobiotics, only chlordecone and nonylphenol were able to displace the binding of [3H]estradiol to ER-enriched COS-1 extracts, and to activate an estrogen-dependent reporter gene (ERE-TK-CAT) cotransfected with an expression vector containing ER cDNA. The results suggest that chlordecone and nonylphenol are direct inducers of rainbow trout ER and Vg gene expression, whereas PCBs and lindane act through their hepatic metabolites. Moreover, pentachlorophenol acts as an antagonist of the induction by estradiol of rainbow trout ER and Vg gene expression.

Rainbow trout hepatocyte beta-adrenoceptors, catecholamine responsiveness, and effects of cortisol

Hepatocyte beta-adrenoceptors were characterized in trout with chronically raised plasma cortisol levels (132.1 +/- 14.8 ng/ml, n = 8, 11-12 days) and compared with shams (1.8 +/- 0.9 ng/ml, n = 8) using radioreceptor assay techniques. Hepatocytes prepared from sham trout possessed 1,696 +/- 179 beta-adrenoceptors/cell. These receptors were characterized as beta 2-adrenoceptors based on the potency order of specific inhibition of CGP binding. The number of putative surface beta 2-adrenoceptors significantly increased to 6,005 +/- 1,165 receptors/cell, in hepatocytes from trout exposed to the elevated plasma cortisol concentration. The physiological significance of the increase in hepatocyte surface receptors was assessed by the in vitro responsiveness of hepatocytes to a range of epinephrine concentrations (10-1,000 nmol/l). Both total glucose production and intracellular adenosine 3',5'-cyclic monophosphate content, indicators of epinephrine responsiveness, were enhanced as a result of chronically raised levels of plasma cortisol. We suggest that these cortisol-mediated alterations in the adrenergic responsiveness of trout hepatocytes may ultimately enhance the ability of the liver to supply glucose to the fish during acute stress after extended periods of chronic stress.