Abstract
Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions. Nicotine exposure can increase oxidative stress levels, which could lead to thyroid dysfunction. However, the mechanism by which nicotine exposure during breastfeeding leads to thyroid gland dysfunction remains elusive. We aimed to investigate the long-term effects of maternal nicotine exposure on redox homeostasis in thyroid gland, besides other essential steps for thyroid hormone synthesis in rats from both sexes. Lactating Wistar rats were implanted with osmotic minipumps releasing nicotine (NIC, 6 mg/kg/day) or saline (control) from postnatal day 2 to 16. Offspring were analyzed at 180-day-old. NIC males showed lower plasma TSH, T3 and T4 while NIC females had higher T3 and T4. In thyroid, NIC males had higher sodium-iodide symporter protein expression, whereas NIC females had higher thyroid-stimulating hormone receptor (TSHr) and thyroperoxidase (TPO) protein expression. TPO activity was lower in NIC males. Hydrogen peroxide generation was decreased in NIC males. Activities of superoxide dismutase, catalase and glutathione peroxidase were compromised in NIC animals from both sexes. 4-Hydroxynonenal was higher only in NIC females, while thiol was not affected in NIC animals from both sexes. NIC offspring also had altered expression of sex steroid receptors in thyroid gland. Both sexes showed similar thyroid morphology, with lower follicle and colloid size. Thyroid from female offspring exposed to nicotine during breastfeeding developed oxidative stress, while the male gland seemed to be protected from redox damage. Thyroid dysfunctions seem to be associated with redox imbalance in a sex-dependent manner.
Highlights
Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions
This study demonstrated for the first time that maternal nicotine exposure during breastfeeding leads to thyroid redox imbalance in offspring of both sexes
Epidemiological and experimental studies have shown that prenatal nicotine exposure induces obesity and increases the risk of diseases later in life[18]
Summary
Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions. We aimed to investigate the long-term effects of maternal nicotine exposure on redox homeostasis in thyroid gland, besides other essential steps for thyroid hormone synthesis in rats from both sexes. Thyroid from female offspring exposed to nicotine during breastfeeding developed oxidative stress, while the male gland seemed to be protected from redox damage. As already demonstrated by our group, maternal nicotine exposure in rats during breastfeeding induces short- and long-term hypothyroidism associated with thyroid dysfunctions in male o ffspring[9,10,11]. Our hypothesis is that maternal exposure to nicotine during breastfeeding impact directly the redox homeostasis of the thyroid gland, impairing the thyroid hormonogenesis process in the offspring and imprinting thyroid dysfunctions later in life. We hypothesized that these dysfunctions would occur in a sex dependent manner
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