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Glutamate neurotoxicity, oxidative stress and mitochondria
Author(s) -
Atlante Anna,
Calissano Pietro,
Bobba Antonella,
Giannattasio Sergio,
Marra Ersilia,
Passarella Salvatore
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02437-1
Subject(s) - neurotoxicity , mitochondrion , glutamate receptor , oxidative stress , reactive oxygen species , microbiology and biotechnology , cytochrome c , programmed cell death , chemistry , oxidative phosphorylation , biochemistry , neurodegeneration , biology , neuroscience , apoptosis , medicine , toxicity , receptor , disease , organic chemistry
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.