title: Biosynthesis of testicular steroids in the immature, adult and senescent guinea-pig.
abstract: The potential biosynthetic capacity of testicular hormones was studied in immature, pubertal and aging guinea-pig. In their sexual development towards puberty, changes in the relationship of the steroids involved in the steroidogenic pathways were observed. The testosterone/androstenedione ratio changes markedly, showing an important increase with pubertal proximity. The testosterone in equilibrium androstenedione sequence, reversibly catalyzed by 17 beta-hydroxysteroid oxidoreductase (17 beta-oxido-reductase), clearly shifted towards androstenedione in immature animals irrespective of the precursor utilized. Post-pubertal animals showed a greater enzymatic activity in the 5-ene and 4-ene testicular synthesis pathways, testosterone production being greatest. In the aging animal, hormonal biosynthetic capacity falls. Reversion of the 17 beta-oxido-reductase activity could be one of the mechanisms responsible for the decrease in testosterone, as in immature guinea-pigs. In order to investigate the in vitro steroidogenic capacity of glands at different ages, minces of testicular tissue were incubated with labelled precursors. The studies were conducted in triplicate at 35 degrees C. For equal quantities of incubated tissue the non-metabolized amount of [3H]pregnenolone and [14C]progesterone, utilized as precursors, was different in post-pubertal and senescent animals: 55.7 +/- 3 vs 59.3 +/- 2.3% (P less than 0.01) for pregnenolone, and 50.1 +/- 3.3 vs 56.3 +/- 2.9% (P less than 0.01) for progesterone, respectively. Testosterone production was 12 +/- 2% in adult and 6.7 +/- 2.7% in senescent animals (P less than 0.01). The testosterone/androstenedione ratio was not significantly different in post-pubertal and senescent animals: 2.8 +/- 0.5 vs 2.4 +/- 0.4, but consistently higher than found in immature animals: 0.3 +/- 0.1. The lesser potential capacity of the aging tissue to synthesize testosterone could be explained by a decline in the glands capacity to metabolize the hormonal precursors.
authors.affiliation: Department of Clinical Biochemistry, Pharmacy and Biochemistry School, University of Buenos Aires, Argentina.
authors.forename: J C
authors.initials: JC
authors.lastname: Hoschoian
authors.forename: M E
authors.initials: ME
authors.lastname: Cardoso
authors.forename: D M
authors.initials: DM
authors.lastname: Coumroglon
authors.forename: J A
authors.initials: JA
authors.lastname: Andrada
mesh_terms: D000375:Aging; D000728:Androgens / Q000096:biosynthesis*; D000818:Animals; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D010088:Oxidoreductases / Q000378:metabolism*; D012741:Sexual Maturation; D013737:Testis / Q000201:enzymology / Q000378:metabolism*
chemical_list: D000728:Androgens; D010088:Oxidoreductases