FEBS Letters | |
Glutamate neurotoxicity, oxidative stress and mitochondria | |
Passarella, Salvatore3  Atlante, Anna1  Calissano, Pietro2  Marra, Ersilia1  Giannattasio, Sergio1  Bobba, Antonella1  | |
[1] Centro di Studio sui Mitocondri e Metabolismo Energetico, CNR, Via G. Amendola 165/A, 70126 Bari, Italy;Istituto di Neurobiologia e Medicina Molecolare, CNR, Viale K. Marx 15, 00137 Rome, Italy;Dipartimento di Scienze Animali, Vegetali e dell'Ambiente, Università del Molise, Via De Sanctis, 86100 Campobasso, Italy | |
关键词: Glutamate neurotoxicity; Reactive oxygen species; Mitochondrion; Oxidative stress; Cytochrome c; | |
DOI : 10.1016/S0014-5793(01)02437-1 | |
学科分类:生物化学/生物物理 | |
来源: John Wiley & Sons Ltd. | |
【 摘 要 】
The excitatory neurotransmitter glutamate plays a major role in determining certain neurological disorders. This situation, referred to as ‘glutamate neurotoxicity’ (GNT), is characterized by an increasing damage of cell components, including mitochondria, leading to cell death. In the death process, reactive oxygen species (ROS) are generated. The present study describes the state of art in the field of GNT with a special emphasis on the oxidative stress and mitochondria. In particular, we report how ROS are generated and how they affect mitochondrial function in GNT. The relationship between ROS generation and cytochrome c release is described in detail, with the released cytochrome c playing a role in the cell defense mechanism against neurotoxicity.
【 授权许可】
Unknown
【 预 览 】
Files | Size | Format | View |
---|---|---|---|
RO201912020310540ZK.pdf | 1247KB | download |