Abstract
Pregnenolone-16α-carbonitrile (PCN), a potent steroidal microsomal enzyme inducer, increased liver weight, depleted glycogen content, and markedly enhanced hepatic ethylmorphine N-demethylase activity in nonpregnant as well as in 18- and 21-day pregnant rats. Electron microscopy revealed extensive smooth-surfaced endoplasmic reticulum (SER) proliferation in the liver. Mitochondrial abnormalities were noted when the steroid was administered in the last stage of pregnancy. 14C-PCN or its derivative(s) was transported to the fetal liver. The steroid caused glycogen depletion without any detectable change in weight, ultrastructure, or ethylmorphine N-demethylation in the embryo's liver. PCN treatment of neonates produced SER proliferation and significantly increased hepatic weight and enzyme activity. The steroid affected the hepatic tissue of nonpregnant, pregnant, and newborn rats but, except for its effect on glycogen content, it did not act upon the embryonic liver.
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