Maternal exposure to nicotine causes oxidative stress and inflammatory changes in the ovaries of adult rats' offspring.

Nicotine is one of the most toxic substances found in cigarettes, but also found in chewing tobacco gum, patches and vaping products (electronic cigarettes). In addition to being a highly addictive chemical, it is capable of reducing fertility in men and women. In the ovaries, it can induce morphological changes and impair the formation of follicles, being a possible cause of changes in the reproductive cycle and anticipation of menopause in women whose mothers smoked during pregnancy. By increasing the generation of free radicals, nicotine can induce oxidation in biological samples and change the expression of inflammatory cytokines. It damages the immune system and many other cells of newborns exposed prenatally. Despite its teratogenic potential, many women continue to use this drug during pregnancy and breastfeeding. Thus, this work aims to analyze the effects of maternal exposure to nicotine on the ovaries of adult rats. To this end, 10 rats received nicotine throughout pregnancy and breastfeeding. Their offspring were euthanized around 90 days-old, in the metestrus phase, for ovary collection and analysis of oxidative stress and inflammation. The results showed that exposure to nicotine increased MDA level, but did not cause damage to the DNA of ovarian cells (8-OHdG). It also increased IL-1β and anti-inflammatory protein AnxA1 and receptor Fpr1, and reduced the mast cell population in ovaries. We concluded that maternal exposure to nicotine is capable of inducing oxidative stress and leading to inflammatory changes in the ovaries of adult offspring exposed during the intrauterine and breastfeeding phases.
Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests. Izabela Maria Mota de Freitas reports financial support was provided by State of Sao Paulo Research Foundation. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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