Metabolism <I>in vitro</I> of 4-<SUP>14</SUP>C-Testosterone by Hepatic Microsomal and Soluble Fractions of Carbon Tetrachloride and Ethionine Injured Rats
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4-<SUP>14</SUP>C-testosterone was incubated with hepatic microsomal and soluble fractions of normal, CCl<SUB>4</SUB> and ethionine administered male rats in the presence of NADPH at 37° for 90minutes. The metabolites produced were detected by thin layer autoradiography and chemical transformation.<BR>In the microsomal metabolism by the CCl4-injured liver, a high amount of the unmetabolized substrate remained and hydroxytestosterones were remarkably lower than those by the normal liver. These findings indicate that hydroxylation of testosterone is impaired by the administration of CCl<SUB>4</SUB>. In the soluble fraction, most of the substrate was not metabolized by the CCl<SUB>4+</SUB>Injured liver and little hydroxytestosterone was found. The amount of 5β-androstane-3β, 17β-diol, which was the predominant metabolite by the normal liver, was significantly reduced. These findings indicate the impairment of Δ<SUP>4</SUP>-5β-hydrogenase.<BR>In the microsomal metabolism by the ethionine-injured liver, the amount of the unmetabolized substrate was less than that in the microsomal metabolism by the CCl<SUB>4</SUB>-injured liver, but the hydroxylation of testosterone was not significantly suppressed. In the metabolism by the soluble fraction, a slightly higher amount of the unmetabolized substrate was found, but no impairment of Δ<SUP>4</SUP>-5β-hydrogenase was observed.
- Endocrinologia Japonica
Endocrinologia Japonica 18(3), 227-234, 1971
The Japan Endocrine Society