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Regulation of Microsomal P450, Redox Partner Proteins, and Steroidogenesis in the Developing Testes of the Neonatal Pig

Department of Population Health & Reproduction (F.M.M., C.J.C., S.M.P., A.J.C.), School of Veterinary Medicine, University of California, Davis, California 95616-8743; United States Department of Agriculture (J.J.F.), Agricultural Research Service, Roman L. Hruska United States Meat Animal Research Center, Clay Center, Nebraska 68933; and Department of Pharmacology & Therapeutics (A.M.B., V.C.N.), University of Maryland School of Medicine, Baltimore, Maryland 21201-1559

Address all correspondence and requests for reprints to: Alan J. Conley, University of California at Davis, Veterinary Medicine—Population Health and Reproduction, School of Veterinary Medicine, Davis, California 95616-8743.

Testicular growth and plasma androgen concentrations increase markedly in the first weeks of neonatal life of pigs. The regulation of steroidogenesis through this period was examined by measuring total microsomal cytochromes P450 (P450), 17-hydroxylase/17,20-lyase P450 (P450c17) and aromatase P450 (P450arom) enzyme activities, and the redox partner proteins nicotinamide adenine dinucleotide phosphate, reduced form (NADPH)-cytochrome P450 reductase (reductase) and cytochrome b₅ in testicular microsomes. Testes were collected from 1–24 d of age, and testicular development was suppressed by a GnRH antagonist in some animals from d 1–14. Both 17/20-lyase and aromatase activities increased from d 1–7 but not thereafter, and 17–20-lyase activity was always at least 200-fold higher than aromatase activity. Reductase decreased in wk 1, then increased to d 24. No changes were seen in cytochrome b₅ expression. GnRH antagonist treatment suppressed plasma LH, testosterone and testes growth to d 14. 17,20-Lyase and aromatase activities in testicular microsomes were reduced by 20% and 50%, respectively. Total microsomal P450 concentration was reduced by 50% on d 7, but there was no effect of treatment on reductase or cytochrome b₅ expression. These data support the hypothesis that the rise in neonatal testicular androgen secretion is more likely due to gonadotropin-stimulated gonadal growth, rather than specific P450c17 expression. Neither P450c17 nor P450arom can account for the decline in total microsomal P450. Reductase and cytochrome b₅ expression appears to be constitutive, but reductase levels saturate both P450c17 and P450arom.

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