Green tea polyphenols inhibit testosterone production in rat Leydig cells.
- Author:
Marina S FIGUEIROA
1
;
Juliany S B César VIEIRA
;
Disleide S LEITE
;
Ruben C O Andrade FILHO
;
Fabiano FERREIRA
;
Patrícia S GOUVEIA
;
Daniel P UDRISAR
;
Maria I WANDERLEY
Author Information
- Publication Type:Journal Article
- MeSH: Androstenedione; pharmacology; Animals; Camellia sinensis; Chorionic Gonadotropin; pharmacology; Cyclic AMP-Dependent Protein Kinases; metabolism; Flavonoids; pharmacology; Gonadotropin-Releasing Hormone; pharmacology; Humans; Leydig Cells; drug effects; metabolism; Male; Phenols; pharmacology; Plant Extracts; pharmacology; Polyphenols; Protein Kinase C; metabolism; Rats; Rats, Wistar; Signal Transduction; drug effects; Testosterone; metabolism
- From: Asian Journal of Andrology 2009;11(3):362-370
- CountryChina
- Language:English
- Abstract: This study investigated the acute effects of green tea extract (GTE) and its polyphenol constituents, (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin (EC), on basal and stimulated testosterone production by rat Leydig cells in vitro. Leydig cells purified in a Percoll gradient were incubated for 3 h with GTE, EGCG or EC and the testosterone precursor androstenedione, in the presence or absence of either protein kinase A (PKA) or protein kinase C (PKC) activators. The reversibility of the effect was studied by pretreating cells for 15 min with GTE or EGCG, allowing them to recover for 1 h and challenging them for 2 h with human chorionic gonadotropin (hCG), luteinizing hormone releasing hormone (LHRH), 22(R)-hydroxycholesterol or androstenedione. GTE and EGCG, but not EC, inhibited both basal and kinase-stimulated testosterone production. Under the pretreatment conditions, the inhibitory effect of the higher concentration of GTE/EGCG on hCG/LHRH-stimulated or 22(R)-hydroxycholesterol-induced testosterone production was maintained, whereas androstenedione-supported testosterone production returned to control levels. At the lower concentration of GTE/EGCG, the inhibitory effect of these polyphenols on 22(R)-hydroxycholesterol-supported testosterone production was reversed. The inhibitory effects of GTE may be explained by the action of its principal component, EGCG, and the presence of a gallate group in its structure seems important for its high efficacy in inhibiting testosterone production. The mechanisms underlying the effects of GTE and EGCG involve the inhibition of the PKA/PKC signalling pathways, as well as the inhibition of P450 side-chain cleavage enzyme and 17beta-hydroxysteroid dehydrogenase function.
