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Titolo:
Prenatal exposure to dexamethasone alters Leydig cell steroidogenic capacity in immature and adult rats
Autore:
Page, KC; Sottas, CM; Hardy, MP;
Indirizzi:
Bucknell Univ, Dept Biol, Lewisburg, PA 17837 USA Bucknell Univ LewisburgPA USA 17837 , Dept Biol, Lewisburg, PA 17837 USA Populat Council, New York, NY 10021 USA Populat Council New York NY USA 10021 lat Council, New York, NY 10021 USA Rockefeller Univ, New York, NY 10021 USA Rockefeller Univ New York NY USA10021 eller Univ, New York, NY 10021 USA
Titolo Testata:
JOURNAL OF ANDROLOGY
fascicolo: 6, volume: 22, anno: 2001,
pagine: 973 - 980
SICI:
0196-3635(200111/12)22:6<973:PETDAL>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERMITTENT IMMOBILIZATION STRESS; PLASMA LUTEINIZING-HORMONE; RECEPTOR MESSENGER-RNA; PITUITARY-ADRENAL AXIS; GLUCOCORTICOID RECEPTOR; TESTICULAR STEROIDOGENESIS; DEHYDROGENASE-ACTIVITY; MATERNAL STRESS; 11-BETA-HYDROXYSTEROID DEHYDROGENASE; DEVELOPMENTAL-CHANGES;
Keywords:
testis; neuroendocrine; luteinizing hormone; testosterone; corticosterone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Page, KC Bucknell Univ, Dept Biol, 7th St, Lewisburg, PA 17837 USA Bucknell Univ 7th St Lewisburg PA USA 17837 wisburg, PA 17837 USA
Citazione:
K.C. Page et al., "Prenatal exposure to dexamethasone alters Leydig cell steroidogenic capacity in immature and adult rats", J ANDROLOGY, 22(6), 2001, pp. 973-980

Abstract

This study examines the effects of prenatal exposure to dexamethasone (DEX) on postnatal testosterone production in male rats. Pregnant female rats were treated on gestation days 14-19 with DEX (100 mug/kg body weight per day; n = 9) or vehicle (n = 9). Results show that 35-day-old male offspring from DEX-treated pregnant females (n = 42) had decreased levels of serum testosterone (45.6% lower, P < .05) compared with control offspring (n = 43), although serum luteinizing hormone (LH) levels were not significantly altered. These findings suggest that a direct programming of developing gonadal cells occurs in response to high levels of maternal glucocorticoid. Indeed,testosterone production was significantly reduced in Leydig cells isolatedfrom immature offspring of DEX-treated pregnant females compared with controls (48.3%, P < .001), and LH stimulation of these cells did not compensate for the lowered steroidogenic capacity. The hypothalamic-pituitary-adrenal axis was also affected, because significant reductions in both serum adrenocorticotropic hormone (ACTH; 26.2%, P < .001) and corticosterone (CORT; 32.3%, P < .001) were measured in DEX-exposed immature male offspring. In contrast, adult male offspring from DEX-treated dams had significantly higherlevels of serum ACTH (39.2%, P < .001) and CORT (37.8%, P < .001). These same animals had higher serum testosterone (31.6%, P less than or equal to .05) and a significant reduction in serum LH (30.8%, P < .001). Moreover, Leydig cells isolated from these adult offspring exhibited an increased capacity for testosterone biosynthesis under basal (38.6%, P < .001) and LH-stimulated conditions (33.5%, P < .001). In summary, sustained changes in steroidogenic capacity were observed in male rats exposed to high levels of glucocorticoid during prenatal development. More specifically, DEX exposure, inutero perturbed Leydig cell testosterone production in both pubertal and adult rats.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 18:28:56