title: Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells.
abstract: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.
  
  
  
  We find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.
  
  
  
  These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.
authors.affiliation: Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, 750004, People's Republic of China.
authors.forename: Yan-Mei
authors.initials: YM
authors.lastname: Ma
authors.affiliation: Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, Durham, NC, 27707, USA.
authors.forename: Gordon
authors.initials: G
authors.lastname: Ibeanu
authors.affiliation: Department of Pathology, Shanxi Traditional Chinese Medicine Hospital, Xi'an, Shanxi, People's Republic of China.
authors.forename: Li-Yao
authors.initials: LY
authors.lastname: Wang
authors.affiliation: Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, 750004, People's Republic of China.
authors.forename: Jian-Zhong
authors.initials: JZ
authors.lastname: Zhang
authors.affiliation: Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, 750004, People's Republic of China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Chang
authors.affiliation: Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, 750004, People's Republic of China.
authors.forename: Jian-Da
authors.initials: JD
authors.lastname: Dong
authors.affiliation: Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, Durham, NC, 27707, USA. pli@nccu.edu.
authors.forename: P Andy
authors.initials: PA
authors.lastname: Li
authors.affiliation: Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia, 750004, People's Republic of China. 1203220205@qq.com.
authors.forename: Li
authors.initials: L
authors.lastname: Jing
mesh_terms: D000818:Animals; D053477:Apoptotic Protease-Activating Factor 1 / Q000378:metabolism; D001343:Autophagy / Q000187:drug effects / Q000502:physiology; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D004353:Drug Evaluation, Preclinical; D018698:Glutamic Acid / Q000633:toxicity*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D063154:Mitochondrial Dynamics / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D012643:Selenium / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism
chemical_list: C506593:Apaf1 protein, mouse; D053477:Apoptotic Protease-Activating Factor 1; C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D018696:Neuroprotective Agents; D013481:Superoxides; D018698:Glutamic Acid; C505409:Casp3 protein, mouse; C506434:Casp9 protein, mouse; D053148:Caspase 3; D053453:Caspase 9; D012643:Selenium
keywords: Autophagy; Glutamate toxicity; Mitochondrial fission; Selenium