Does maternal exposure to nicotine affect the oocyte quality and reproductive capacity in adult offspring?

Toxicol Appl Pharmacol. 2021 Sep 1:426:115638. doi: 10.1016/j.taap.2021.115638. Epub 2021 Jul 6.

Abstract

Gonadal development begins in the intrauterine phase and females from most species are born with an established oocyte reserve. Exposure to drugs during gestation can compromise the offspring health, also affecting the gametes quality. Nicotine, the main component of cigarettes, is an oxidant agent capable of altering the fertility in men and women. As female gametes are susceptible to oxidative stress, this drug can damage the oolemma and affect oocyte maturation, induce errors during chromosomal segregation and DNA fragmentation. Oocyte mitochondria are particularly susceptible to injuries, contributing to the oocyte quality loss and embryonic development disruption. Thus, considering the high number of women who smoke during pregnancy, while significant events are occurring in the embryo for future fertility of offspring, we seek to verify the quality of the oocytes from adult rats exposed to nicotine during intrauterine phase and breastfeeding. Pregnant Wistar rats received nicotine by osmotic mini-pumps and the female progenies were evaluated in adulthood for oocyte quality (viability, lipid peroxidation, generation of reactive oxygen species and mitochondrial integrity) and reproductive capacity. Embryos (3dpc) and fetuses (20dpc) generated by these rats were also evaluated. The results showed that the dose of 2 mg/kg/day of nicotine through placenta and breast milk does not affect the number of oocytes and the fertility capacity of adult rats. However, it causes some morphological alterations in oocytes, mitochondrial changes, embryonic fragmentation and disruption of fetal development. The malformations in fetuses generated from these gametes can also indicate the occurrence of epigenetic modifications.

Keywords: Embryo; Female Reproduction; Nicotine; Oocyte; Rat.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Female
  • Fetal Development / drug effects
  • Lactation
  • Lipid Peroxidation / drug effects
  • Male
  • Maternal-Fetal Exchange
  • Mitochondria / drug effects
  • Nicotine / toxicity*
  • Oocytes / drug effects*
  • Oocytes / metabolism
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Reproduction / drug effects*

Substances

  • Reactive Oxygen Species
  • Nicotine