Abstract
SUMMARY The oxidation of cholester01-26-C~~, sodium propionate-1, -2, or -3-C14, and sodium octan0ate-1-U~ by liver mitochondrial preparations from intact and gonadectomized rats of both sexes, and from intact and gonadectomized rats of both sexes treated with androgens and estrogens, has been studied. Mitochondria from intact female rats and mice consistently oxidized added cholesterol to a greater extent than mitochondria from intact males. There were no significant sex differences in the oxidation of sodium propionate (a possible intermediate in the oxidation of the cholesterol side chain to carbon dioxide). Surgical or chemical castration of male rats enhanced cholesterol oxidation. Androgen treatment of female rats slightly depressed cholesterol oxidation but ovariectomy had no effect. Cholesterol oxidation by preparations of normal male or female rat liver mitochondria was inhibited by sex hormones added in vitro. These sex differences in cholesterol oxidation suggest that circulating androgen, rather than estrogen, levels determine the efficiency of cholesterol oxidation. Octanoate oxidation by liver mitochondria was not influenced by prior castration or treatment of male rats with androgens or estrogens. Androgen treatment of female rats slightly inhibited octanoate oxidation while estrogen treatment enhanced octanoate oxidation.
Highlights
We compared the oxidation of cholesteroland octanoate-l-CI4 by mitochondrial preparations from the livers of four groups of female rats: normal (F),gonadectomized (FG), normal but treated with androgen (FA), and gonadectomized treated with androgen (FGA)
Androgen treatment of either intact or gonadectomized female rats reduced the percentage oxidized of both substrates
To ensure that the effects observed following androgen and estrogen administration were not due to residual hormone in the liver preparations, we carried out a series of iiicubations with liver mitochondria from intact male and female rats to which were added 30 pmoles of the sex hormones or some of their hepatic metabolites
Summary
The oxidation of cholester01-26-C~~s,odium propionate-1, -2, or -3-C14, and sodium octan0ate-1-U~by liver mitochondrial preparations from intact and gonadectomized rats of both sexes, and from intact and gonadectomized rats of both sexes treated with androgens and estrogens, has been studied. Cholesterol oxidation by preparations of normal male or female rat liver mitochondria was inhibited by sex hormones added in vitro. These sex differences in cholesterol oxidation suggest that circulating androgen, rather than estrogen, levels determine the efficiency of cholesterol oxidation. W e have repeatedly observed that suitably fortified preparations of liver mitochondria from normal male rats are less active in oxidizing added cholesterol in vitro than liver mitochondria from female rats of the same age or weight [1, 2]. We have shown [3] that liver mitochondria from male rats that have been castrated either surgically or with estrogens exhibit enhanced cholesterol oxidation activity. The oxidation of sodium octanoate by these mitochondrialpreparations was studied to provide some indication d nonspecific changes in the oxidative capacity of the mitochondria as a consequence of gonadectomyor hormoneadministration
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