Effects of foetal and breastfeeding exposure to methylmercury (MeHg) and retinol palmitate (vitamin A) in rats : redox parameters and susceptibility to DNA damage in liver.

Abstract

Methylmercury (MeHg) is known to be a chemical that poses a risk to public health. Exposure to MeHg and

vitamin A (VitA) occurs through the ingestion of fish, present in the diet of most pregnant women. The ab- sorption of these elements generates oxidative stress and can generate adaptations for future stressful events.

Here, we assessed how exposure to VitA and/or MeHg during the fetal and breastfeeding period modulates the toxicity of MeHg reexposure in adulthood. We focus on redox systems and repairing DNA damage. Male rats (n = 50), were divided into 5 groups. Control received mineral oil; The VitA group received VitA during pregnancy, during breastfeeding and was exposed to MeHg in adulthood; VitA + MeHg received VitA and MeHg during pregnancy and breastfeeding and was exposed to MeHg in adulthood. The single exposure group (SE) was exposed to MeHg only in adulthood; and the MeHg group was pre-exposed to MeHg during pregnancy and breastfeeding and re-exposed to MeHg in adulthood. After treating the animals, we evaluated the redox status and the level of DNA damage in all rats. The results revealed that MeHg significantly decreased the activity of glutathione peroxidase (GPx) and sulfhydryl levels and increased the activity of superoxide dismutase (SOD), glutathione transferase, glutathione and carbonyl in all exposed groups. These results suggest that the second exposure to MeHg directly altered the effects of oxidation and that there were no specific effects associated with exposure during the fetal and breastfeeding periods. In addition, our findings indicate that MDA levels increased in MeHg and SE levels and no differences in MDA levels were observed between the VitA and MeHg + VitA groups. We also observed that animals pretreated exclusively with VitA showed residual damage similar to the control’s DNA, while the other groups showed statistically higher levels of damage. In conclusion, low doses of

MeHg and VitA during fetal and breastfeeding periods were unable to condition an adaptive response to sub- sequent exposure to MeHg in adulthood in relation to the observed levels of oxidative damage assessed after

exposure.