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Asian Journal of Andrology (2009) 11: 362-370. doi: 10.1038/aja.2009.2; published online 30 March 2009.
Green tea polyphenols inhibit testosterone production in rat Leydig cells
Marina S Figueiroa1, Juliany S B César Vieira1, Disleide S Leite1, Ruben C O Andrade Filho1, Fabiano Ferreira1, Patrícia S Gouveia1, Daniel P Udrisar1 and Maria I Wanderley1
1 Department of Physiology and Pharmacology, Federal University of Pernambuco, 50607-901 Recife, PE, Brazil
Correspondence: Dr Maria I. Wanderley, Department of Physiology and Pharmacology, Federal University of Pernambuco, 50607-901 Recife, PE, Brazil. Fax: +55-81-2126-8976 E-mail: ineswanderley@gmail.com
Received 16 November 2008; Revised 2 December 2008; Accepted 12 January 2009; Published online 30 March 2009.
| 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 17-hydroxysteroid dehydrogenase function.
Keywords: green tea polyphenols, Leydig cells, protein kinase A, protein kinase C, testosterone |
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