Nicotine-induced prenatal overexposure to maternal glucocorticoid and intrauterine growth retardation in rat

Sep 21, 2007Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie

Nicotine during pregnancy linked to high stress hormone levels and slowed growth before birth in rats

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Abstract

Prenatal chronic nicotine exposure causes intrauterine growth retardation (IUGR) in rats (P<0.01).

Maternal serum corticosterone levels were elevated during mid- and late-gestation in response to nicotine exposure (P<0.05).
mRNA expressions of adrenal steroidogenic proteins increased in maternal adrenals but decreased in fetal adrenals.
Placental levels of 11 beta-hydroxysteroid dehydrogenase type 2 were reduced during both mid- and late-gestation (P<0.05).
The findings suggest that nicotine-induced IUGR may be linked to disruptions in glucocorticoid regulation in both mothers and fetuses.

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Overexposure to glucocorticoid during fetal development can result in intrauterine growth retardation (IUGR) as well as other diseases after birth. The purpose of this study is to investigate the possibility of glucocorticoid disturbance-mediated nicotine-induced IUGR after chronic prenatal exposure. Nicotine at 1.0mg/kg twice a day was administered subcutaneously to pregnant rats from gestational day (GD) 8 to GD 15 (mid-gestation) or GD 21 (late-gestation). Placental weights and fetal developmental parameters were recorded. Corticosterone levels were determined by radioimmunoassay. The mRNA expressions of adrenal steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side chain cleavage (P450scc) and placental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD-2) were determined using real-time quantitative RT-PCR. The results showed that prenatal chronic nicotine exposure causes IUGR in rats (P<0.01); in response to nicotine exposure, maternal serum corticosterone levels were elevated at mid- and late-gestations (P<0.05); mRNA expressions of StAR and P450scc increased in maternal adrenals (P<0.05 or 0.01) but decreased in fetal adrenals (P=0.16 or 0.11). Furthermore, the mRNA levels of placental 11 beta-HSD-2 were reduced at mid- and late-gestations (P<0.05). These results suggest that nicotine-induced IUGR is associated with the disturbances of glucocorticoid homeostasis in maternal and fetal rats. A possible underlying mechanism is that long term nicotine administration leads to fetal overexposure to maternal glucocorticoid by the combined effect of increased maternal glucocorticoid level and impaired placental barrier to it, all of which eventually leads to the fetal adrenocortical dysfunction and IUGR.

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Nicotine-induced prenatal overexposure to maternal glucocorticoid and intrauterine growth retardation in rat

Abstract

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