Impact of selenium on cerebellar injury and mRNA expression in offspring of rat exposed to methylmercury

Tao, Rui; Zhang, Chan-chan; Feng, Long-Hai; Huiqun, Wang; Wang, Wenjuan; Li, Ping

doi:10.1016/j.ecoenv.2021.112584

Cited by 4 publications

(1 citation statement)

References 34 publications

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“…More and more studies have manifested that Se has an antagonistic effect on brain dysfunction, OS, mitochondrial dysfunction, neuroinflammation, and apoptosis induced by various factors (Conrad & Proneth, 2020; Zhao et al, 2023). For example, Se reduced neuronal damage brought on by methylmercury exposure by changing the level of genes linked to neural communication and Ca 2+ pathways of signaling and improving learning and cognitive impairment in rat offspring (Tu et al, 2021). Tuo et al used a mouse model of cerebral ischemia‐reperfusion impairment to explain that the mechanism by which Se compounds prevent neuronal death is to increase the antioxidant capacity of the brain (Tuo et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

By regulating the IP3R/GRP75/VDAC1 complex to restore mitochondrial dynamic balance, selenomethionine reduces lipopolysaccharide‐induced neuronal apoptosis

Xu,

Wang,

Luo

et al. 2024

Journal Cellular Physiology

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Selenium (Se), as one of the essential trace elements, plays an anti‐inflammatory, antioxidation, and immune‐enhancing effect in the body. In addition, Se can also improve nervous system damage induced by various factors. Earlier studies have described the important role of mitochondrial dynamic imbalance in lipopolysaccharide (LPS)‐induced nerve injury. The inositol 1,4,5‐triphosphate receptor (IP3R)/glucose‐regulated protein 75 (GRP75)/voltage‐dependent anion channel 1 (VDAC1) complex is considered to be the key to regulating mitochondrial dynamics. However, it is not clear whether Selenomethionine (SeMet) has any influence on the IP3R/GRP75/VDAC1 complex. Therefore, the aim of this investigation was to determine whether SeMet can alleviate LPS‐induced brain damage and to elucidate the function of the IP3R/GRP75/VDAC1 complex in it. We established SeMet and/or LPS exposure models in vivo and in vitro using laying hens and primary chicken nerve cells. We noticed that SeMet reversed endoplasmic reticulum stress (ERS) and the imbalance in mitochondrial dynamics and significantly prevented the occurrence of neuronal apoptosis. We made this finding by morphological observation of the brain tissue of laying hens and the detection of related genes such as ERS, the IP3R/GRP75/VDAC1 complex, calcium signal (Ca2+), mitochondrial dynamics, and apoptosis. Other than that, we also discovered that the IP3R/GRP75/VDAC1 complex was crucial in controlling Ca2+ transport between the endoplasmic reticulum and the mitochondrion when SeMet functions as a neuroprotective agent. In summary, our results revealed the specific mechanism by which SeMet alleviated LPS‐induced neuronal apoptosis for the first time. As a consequence, SeMet has great potential in the treatment and prevention of neurological illnesses (like neurodegenerative diseases).

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