作者: Thomas M. Burbacher , Rafael Ponce , Kimberly S. Grant
DOI: 10.1016/B978-0-12-800228-5.00006-6
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摘要: Catastrophic episodes of high-dose prenatal exposures have revealed the clear risk posed by methylmercury (MeHg) to developing nervous system. Effects in-utero MeHg exposure include abnormal reflexes, intellectual disability, deficits in vision and hearing, cerebral palsy paralysis, a constellation clinical signs termed Fetal Minamata Disease. More recent longitudinal studies high-fish-eating populations with low-dose identified subtle adverse changes key childhood outcomes, including memory, language, attention psychomotor abilities. Studies effects using animal models replicated many sub-clinical observed humans. These also important molecular, cellular organ-based mechanisms neurotoxicity based on its high affinity for protein sulphydryl groups selenium. Mechanistically, has range targets that underlie neurotoxicity. mitochondrial function, calcium regulation redox potentiation appear contribute impacts during neurodevelopment, impaired cell proliferation, migration neurotransmission