Treatment of pregnant females with dexamethasone influences postnatal development of the adrenal medulla

Manojlović, Milica; Kalafatić, D.; Hristić, M; Plećaš, B.; Virag, Aleksandra; Čakić, Maja

doi:10.1016/s0940-9602(98)80010-1

Cited by 10 publications

(6 citation statements)

References 33 publications

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“…Evidence supporting the hypothesis that prenatal stress and its accompanying glucocorticoid excess results in a developmental delay has been reported (Barlow et al, 1978, Weinstock et al, 1988. Although glucocorticoid hormones are necessary for organogenesis, excessive exposure to DEX during adrenal development results in desensitization of the GRs and a consequent atrophy of both the medulla and cortex in immature 35-day-old offspring (Betito et al, 1993;Hristic et al, 1997;Manojlovic et al, 1998). Additional studies have shown that prenatal DEX exposure delays biochemical differentiation and cardiac development in rats.…”

Section: Discussionmentioning

confidence: 82%

Prenatal Exposure to Dexamethasone Alters Leydig Cell Steroidogenic Capacity in Immature and Adult Rats

Page

Sottas

Hardy

2001

Journal of Andrology

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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 microg/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 isolated from 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 higher levels of serum ACTH (39.2%, P <. 001) and CORT (37.8%, P < .001). These same animals had higher serum testosterone (31.6%, P < or = .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 in utero perturbed Leydig cell testosterone production in both pubertal and adult rats.

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Section: Discussionmentioning

confidence: 82%

Prenatal Exposure to Dexamethasone Alters Leydig Cell Steroidogenic Capacity in Immature and Adult Rats

Page

Sottas

Hardy

2001

Journal of Andrology

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“…Multiple dexamethasone doses applied during pregnancy exert a more potent inhibitory effect. A reduced number of chromaffin cells and significantly decreased adrenaline content in the adrenals were seen in 14-day-old neonatal offspring [181].…”

Section: Programming Of the Fetal Hypothalamic-pituitary-adrenal Axismentioning

confidence: 92%

“…Multiple dexamethasone exposure during pregnancy affects the ultrastructure of ACTH cells, which in the Golgi complex show much lower presence of specific granules as well as dilation of the endoplasmatic reticulum [180]. Decreased morphometric parameters of the ACTH cells and their changed ultrastructure resulted in significantly reduced plasma ACTH levels in fetuses and neonatal offspring after multiple dexamethasone administration during pregnancy [180,181]. On the contrary, a single dose of dexamethasone, given to pregnant rats on day 16 of gestation, suppressed the synthetic activity of fetal ACTH cells, but in the early neonatal period this suppression was followed by stimulation of ACTH secretion and increased circulating ACTH levels [182].…”

Section: Programming Of the Fetal Hypothalamic-pituitary-adrenal Axismentioning

confidence: 99%

Prenatal Glucocorticoids: Short-Term Benefits and Long-Term Risks

Manojlović‐Stojanoski¹,

Nestorović²,

Milošević³

2012

Glucocorticoids - New Recognition of Our Familiar Friend

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“…Five animals each from the control and SRIH-14 treated group received a single intraperitoneal injection of vincristine (Oncovin, Lek, Ljubljana, Slovenia with Eli Lilly-Co, Indianopolis, IN, USA) at a dose of 1 mg/kg b.w., 3 h before being killed (Manojlović et al, 1998). Granulosa and/or theca cell metaphases were counted in twenty small and ten large healthy follicles in each class per experimental group.…”

Section: Mitotic Index Determinationmentioning

confidence: 99%

Chronic somatostatin treatment affects pituitary gonadotrophs, ovaries and onset of puberty in rats

Nestorović¹,

Lovren²,

Sekulić³

et al. 2004

Life Sciences

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Treatment of pregnant females with dexamethasone influences postnatal development of the adrenal medulla

Cited by 10 publications

References 33 publications

Prenatal Exposure to Dexamethasone Alters Leydig Cell Steroidogenic Capacity in Immature and Adult Rats

Prenatal Exposure to Dexamethasone Alters Leydig Cell Steroidogenic Capacity in Immature and Adult Rats

Prenatal Glucocorticoids: Short-Term Benefits and Long-Term Risks

Chronic somatostatin treatment affects pituitary gonadotrophs, ovaries and onset of puberty in rats

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