Smoking has multiple effects on hormone secretion, which is mainly mediated by the pharmacological actions of nicotine and other toxins such as thiocyanate. Smoking affects pituitary, thyroid, adrenal, testicular, and ovarian functions as well as the action of insulin 18. In pregnant women who smoke or use nicotine, nicotine crosses the placenta, concentrates in fetal blood and amniotic fluid, and is detectable in breast milk during lactation 7.
The changes observed in this study in the adrenal cortex may be due to impaired steroidogenesis 21 or impairments in the synthesis and secretion of corticosterone in the offspring of smoking mothers leading to accumulation of lipid droplets and appearance of cytoplasmic vacuolation, which were observed in the present study. These results are similar to those obtained with prenatal caffeine ingestion at a clinically toxic dose that retards the development of the fetal HPA axis function by directly injuring fetal adrenal steroidogenesis and by fetal overexposure to maternal GC levels 22. This may explain the results seen in the pituitary gland, which showed decreased activity of corticotrophs due to a negative feedback on the pituitary corticotrophs, which revealed a reduction in the number of cytoplasmic secretory granules.
The principle behind the production of GC by zona glomerulosa and zona fasciculata is the ACTH secreted by corticotrophs in the adenohypophysis of the anterior pituitary gland. Negative feedback control normally occurs when the elevated blood levels of cortisol act either on the hypothalamus, anterior pituitary, or both to cause a suppression of ACTH secretion 23.
They added that GC metabolic activation in the fetal hippocampus may account for the inhibition of the fetal HPA axis through negative feedback regulation. This was consistent with the results of some researchers who reported that nicotine administration leads to fetal overexposure to maternal GC, which eventually leads to fetal adrenocortical dysfunction 24.
Previous results demonstrated that prenatal nicotinic exposure can inhibit fetal adrenal steroidogenic acute regulatory (StAR) protein and gene expression in rats. Furthermore, nicotine reduced StAR gene expression and cortisol production in primary human fetal adrenal cortex cells, indicating that prenatal nicotinic exposure could inhibit fetal adrenal steroidogenic synthesis 19.
In this study, some zona fasciculata cells appeared with dark irregular nuclei and widened perinuclear space. These results are supported by Landais et al.25 and Yan et al.21, who found the same results.
The present study demonstrated that the most affected organelle in the adrenal cells in the nicotine-treated group was the mitochondria as they showed marked structural abnormalities and destruction. As a further validation of our results, another experiment proved that cigarette smoking may reduce the capacity of the mitochondria to metabolize cholesterol into pregnenolone 26. This is in agreement with other researchers who decided that there was increased oxidative damage specifically to mitochondrial proteins in the pancreas of nicotine- exposed neonates 27. Moreover, there was increased mitochondrial swelling by EM (electron microscope)in the pancreatic β cells of nicotine-exposed offspring 28. these results is that women who are pregnant should avoid exposure to tobacco smoke.
Cyanide is a potent toxic agent present in cigarette smoke that inhibits the activity of cytochrome oxidase and is metabolized to thiocyanate through sulfuration with thiosulfate by mitochondrial rhodanese enzyme 19. Human exposure to cyanide produces toxic effects by binding to the iron and copper in the active site of cytochrome c oxidase, thereby inhibiting the enzyme. Pituitary–adrenal activity in thiocyanate-treated rats was not changed 33.
Maternal exposure to cigarette smoke during pregnancy has deleterious effects on the pituitary–adrenal axis of the offspring, and these adverse health outcomes associated with maternal smoking may be attributable, at least in part, to nicotine alone. Therefore, the implication from
There are no conflicts of interest.
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