Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study

• Published in: Toxicology reports Vol. 9; pp. 563 - 574
• Main Authors: Fagundes, Beatriz Helena Fernandes, Nascimento, Priscila Cunha, Aragão, Walessa Alana Bragança, Chemelo, Victória Santos, Bittencourt, Leonardo Oliveira, Eiró-Quirino, Luciana, Silva, Marcia Cristina Freitas, Freire, Marco Aurelio M., Fernandes, Luanna Melo Pereira, Maia, Cristiane do Socorro Ferraz, Crespo-Lopez, Maria Elena, Lima, Rafael Rodrigues
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 2022; Elsevier
• Subjects: Central nervous system; Cerebellum; Hippocampus; Methylmercury; Neurotoxicology; Regular; Cerebellum; Hippocampus; Methylmercury; Neurotoxicology; Central nervous system
• ISSN: 2214-7500; 2214-7500
• DOI: 10.1016/j.toxrep.2022.02.014

The environmental contamination by methylmercury (MeHg) is a major concern for public health. The effects of MeHg in the central nervous system (CNS) of adult animals have been extensively investigated; however, little is known about the effects of MeHg exposure during intrauterine and lactation periods on motor and cognitive functions of adolescent rats. Therefore, this study aimed to investigate the effect of MeHg exposure during intrauterine life and lactation on both motor and cognitive functions of offspring rats. Ten female Wistar rats were exposed to 40 μg/kg/day of MeHg through cookie treats from the first day of pregnancy until the last day of breastfeeding. Both motor and cognitive functions of offspring male rats were assessed by open field, rotarod, and step-down inhibitory avoidance tests. Forty-one days after birth, the hippocampus and cerebellum were collected to determine total Hg content, antioxidant capacity against peroxyl radicals (ACAP), reduced glutathione (GSH) levels, lipid peroxidation (LPO), and nitrite levels. MeHg exposure during CNS development increased Hg levels in both hippocampal and cerebellar parenchymas, triggered oxidative stress throughout ACAP and GSH decrease, increased LPO and nitrite levels. These alterations resulted in reduced spontaneous and stimulated locomotion and short- and long-term memory deficits. Therefore, damages triggered by MeHg exposure during intrauterine life and lactation had detrimental effects on oxidative biochemistry and motor and cognitive functions of offspring rats.
•The MeHg exposure during CNS development increased mercury levels in hippocampal and cerebellar parenchyma.•The MeHg intoxication during pregnancy and lactation impairs the redox status of hippocampus and cerebellum of the offspring.•MeHg exposure causes behavioral effects in motor ability and cognition of offspring rats.