ABSTRACT
The issue of MeHg contamination is a significant concern due to its detrimental impact on the environment. This study aimed to thoroughly investigate the effects of MeHg on neurodevelopmental biomarkers, as there is a lack of systematic reviews in this area. We conducted a comprehensive search of three databases (PubMed, Scopus, and Web of Science) and found 522 records, which were then meticulously reviewed by two independent reviewers. A total of 66 studies were included, with biomarkers related to oxidative stress, neurotransmission, inflammation, epigenetics, and apoptosis being the most prominent. The results of both in vitro and in vivo models indicate that antioxidant enzymes and other oxidative stress-related markers are indeed, altered following MeHg exposure. Moreover, MeHg exposure causes significant disruptions to neurotransmitter levels, activities of neurotransmitter synthesis enzymes, receptor densities, and proteins involved in synaptic function. Proinflammatory biomarkers are consistently overexpressed in both MeHg-treated cells and the brains of exposed rats. Furthermore, studies on DNA methylation and biomarker activity suggest that MeHg exposure may lead to neurotoxicity and neurodevelopmental issues via perturbations to epigenetic markers and the apoptosis pathway.
Subject(s)
Biomarkers , Methylmercury Compounds , Oxidative Stress , Methylmercury Compounds/toxicity , Biomarkers/metabolism , Animals , Humans , Oxidative Stress/drug effects , Neurotoxicity Syndromes/metabolism , Neurotoxicity Syndromes/etiology , Apoptosis/drug effects , Rats , Epigenesis, Genetic/drug effects , DNA Methylation/drug effects , Neurodevelopmental Disorders/chemically induced , Neurodevelopmental Disorders/metabolismABSTRACT
Methylmercury (MeHg) is an organic bioaccumulated mercury derivative that strongly affects the environment and represents a public health problem primarily to riparian communities in South America. Our objective was to investigate the hepatic and neurological effects of MeHg exposure during the phases foetal and breast-feeding and adult in Wistar rats. Wistar rats (n = 10) were divided into 3 groups. Control group received mineral oil; The simple exposure (SE) group was exposed only in adulthood (0.5 mg/kg/day); and double exposure (DE) was pre-exposed to MeHg 0.5 mg/kg/day during pregnancy and breastfeeding (±40 days) and re-exposed to MeHg for 45 days from day 100. After, we evaluated possible abnormalities. Behavioral and biochemical parameters in liver and occipital cortex (CO), markers of liver injury, redox and AKT/GSK3ß/mTOR signaling pathway. Our results showed that both groups treated with MeHg presented significant alterations, such as decreased locomotion and exploration and impaired visuospatial perception. The rats exposed to MeHg showed severe liver damage and increased hepatic glycogen concentration. The MeHg groups showed significant impairment in redox balance and oxidative damage to liver macromolecules and CO. MeHg upregulated the AKT/GSK3ß/mTOR pathway and the phosphorylated form of the Tau protein. In addition, we found a reduction in NeuN and GFAP immunocontent. These results represent the first approach to the hepatotoxic and neural effects of foetal and adult MeHg exposure.