Bulger W H, Kupfer D
Res Commun Chem Pathol Pharmacol. 1976 Jul;14(3):497-13.
The oral administration of carbon tetrachloride (CC14) to ovariectomized rats markedly inhibited the elevation of uterine decarboxylase (ODC) by estradiol-17beta (E2) and by 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2,2-trichloroethane (o,p'DDT). The inhibition of ODC induction by CC14 does not appear to be mediated by the formation of an inhibitor of ODC activity. CC14 treatment caused no observable alteration in the uterine cytosolic E2 receptor. Namely, there was no alteration by CC14 in the number of E2 binding sites, in the affinity of the receptor for E2 or in the sedimentation constant of the 8S receptor. Furthermore, the possibility that CC14 inhibition of ODC induction is a resultant of an initial stimulation of this uterine enzyme by CC14 was excluded. The potential inhibitory effect of CC14 by direct of indirect route on uterine protein synthesis is discussed.
