Retinoids, LRAT and REH activities in eggs of Japanese quail following maternal and in ovo exposures to 3,3',4,4'-tetrachlorobiphenyl.

Environmental monitoring for the effects of organochlorine contaminants has identified changes in egg yolk retinoid concentrations, however underlying mechanisms are unknown. Breeding female Japanese quail, Coturnix coturnix japonica, received 3 bimonthly injections of a low dose (5 microg/g) of the coplanar polychlorinated biphenyl (PCB) 3,3',4,4'-tetrachlorobiphenyl. No overt maternal toxicity or embryotoxicity was detected. For the exposed females, oocytes (yolk deposition nearly completed) and freshly laid eggs contained higher concentrations of retinol. For PCB-exposed female quail, freshly laid eggs and fertile eggs incubated for 6 days contained higher concentrations of retinyl palmitate. These results suggest that the PCB congener caused greater deposition of retinoids in yolks during late oogenesis or greater net esterification in the yolk-sac membrane. Retinyl ester hydrolase (REH) activity, assayed in the microsomal fraction of the yolk-sac membrane, was significantly inhibited in the PCB-exposed group. Therefore, the higher retinyl palmitate concentrations may be explained by less retinyl palmitate conversion to retinol. In a second experiment, fertile quail eggs were injected with 2, 10 or 20 microg of the PCB congener and incubated for 6 days. In contrast to the maternal exposure, yolk retinol decreased and retinyl ester hydrolase increased in the PCB-injected eggs. The difference in the results of adult versus egg injections may be related to several factors including adult transformation of the PCB to toxic metabolites and differences in post-transcriptional regulation of REH expression.