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

• Published in: Mutation research Vol. 858-860; p. 503239
• Main Authors: Rosa-Silva, Helen Tais da, Panzenhagen, Alana Castro, Espitia-Pérez, Pedro, Teixeira, Alexsander Alves, Roitman, Alice, Almeida, Roberto Farina, Heimfarth, Luana, Moreira, José Cláudio Fonseca
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2020
• Subjects: Animals; Breast Feeding; DNA Damage; DNA-repair; Female; Glutathione Peroxidase - metabolism; Humans; Liver - drug effects; Liver - metabolism; Male; Malondialdehyde - metabolism; Methylmercury; Methylmercury Compounds - administration & dosage; Methylmercury Compounds - toxicity; Oxidation-Reduction - drug effects; Oxidative stress; Oxidative Stress - drug effects; Pregnancy; Prenatal Exposure Delayed Effects - chemically induced; Prenatal Exposure Delayed Effects - diagnosis; Prenatal Exposure Delayed Effects - metabolism; Rats, Wistar; Vitamin A; Vitamin A - administration & dosage; Vitamins - administration & dosage; Vitamin A; Oxidative stress; DNA-damage; Methylmercury; DNA-repair
• ISSN: 1383-5718; 1879-3592; 1873-135X
• DOI: 10.1016/j.mrgentox.2020.503239

[Display omitted] •Exposure to MeHg promotes redox imbalance and damage to macromolecules.•Vitamin A has no protective effect on MeHg exposure in adulthood.•MeHg generates DNA damage and damage in repairing that damage.•Exposure to MeHg is genotoxic and mutagenic and its effects are intensified in the presence of Vitamin A. 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 absorption 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 subsequent exposure to MeHg in adulthood in relation to the observed levels of oxidative damage assessed after exposure.