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- W4281954815 abstract "Methylmercury (MeHg) is a cumulative environmental pollutant that can easily cross the blood-brain barrier and cause damage to the brain, mainly targeting the central nervous system. The purpose of this study is to investigate the role of calcium ion (Ca2+ ) homeostasis between the endoplasmic reticulum (ER) and mitochondria in MeHg-induced neurotoxicity. Rat primary cortical neurons exposed to MeHg (0.25-1 μm) underwent dose-dependent cell damage, accompanied by increased Ca2+ release from the ER and elevated levels of free Ca2+ in cytoplasm and mitochondria. MeHg also increased the protein and messenger RNA expressions of the inositol 1,4,5-triphosphate receptor, ryanodine receptor 2, and mitochondrial calcium uniporter. Ca2+ channel inhibitors 2-aminoethyl diphenylborinate and procaine reduced the release of Ca2+ from ER, while RR and 4,4'-diisothiocyanatostilbene-2,2'-disulfonate inhibited Ca2+ uptake from mitochondria. In addition, pretreatment with Ca2+ chelator BAPTA-AM effectively restored mitochondrial membrane potential levels, inhibited over opening of mitochondrial permeability transition pore, and maintained mitochondrial function stability. Meanwhile, the expression of mitochondrial apoptosis-related proteins recovered to some extent, along with the reduction of the early apoptosis ratio. These results suggest that Ca2+ homeostasis plays an essential role in mitochondrial damage and apoptosis induced by MeHg, which may be one of the important mechanisms of MeHg-induced neurotoxicity." @default.
- W4281954815 created "2022-06-13" @default.
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- W4281954815 date "2022-06-09" @default.
- W4281954815 modified "2023-09-30" @default.
- W4281954815 title "Unbalanced ER‐mitochondrial calcium homeostasis promotes mitochondrial dysfunction and associated apoptotic pathways activation in methylmercury exposed rat cortical neurons" @default.
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- W4281954815 doi "https://doi.org/10.1002/jbt.23136" @default.
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