Steroidogenesis by the immature rhesus monkey ovary in vitro

• Published in: Journal of endocrinological investigation Vol. 9; no. 2; p. 171
• Main Authors: Bruot, B C, Gearing, M, Musey, P I, Wilson, M E, Collins, D C
• Format: Journal Article
• Language: English
• Published: Italy 01.04.1986
• Subjects: Androstenedione - pharmacology; Animals; Bucladesine - pharmacology; Cholesterol - isolation & purification; Cholesterol - pharmacology; Estradiol - biosynthesis; Female; Lipoproteins - analysis; Luteinizing Hormone - pharmacology; Macaca mulatta; Ovary - metabolism; Progesterone - biosynthesis; Sexual Maturation
• ISSN: 0391-4097; 1720-8386
• DOI: 10.1007/BF03348091

Primates are believed to have a low level of ovarian steroidogenic activity during prepubertal development. In order to study the rate limiting factors associated with the low level of steroidogenesis, ovaries from prepubertal rhesus monkeys were quartered and incubated for 48 h at 37 C in minimum essential medium. These ovaries secreted 687 +/- 347 pg estradiol/mg ovary and 299 +/- 35 pg progesterone/mg ovary during 48 h of incubation. The addition of 100 ng luteinizing hormone (LH) or 1 mM dibutyryl (Bu)2 cAMP failed to increase significantly estradiol or progesterone secretion. Furthermore, the addition of either progesterone or androstenedione failed to augment estradiol secretion. The presence of either LH or (Bu)2 cAMP with the steroidal substrates also failed to augment estradiol secretion. In contrast, the addition of (Bu)2 cAMP with lipoprotein-derived cholesterol significantly stimulated a two-fold increase in progesterone secretion. The presence of LH in the lipoprotein-supplemented medium failed to augment progesterone secretion. These results suggest that prepubertal monkey ovaries lack the ability to respond to LH, probably due to a lack of gonadotropin receptors or failure of the receptor to stimulate cAMP synthesis. Furthermore, the failure of progesterone and androstenedione to augment estradiol secretion suggests that some cellular components needed to induce aromatase activity are not functional in the prepubertal primate ovary.