Glutamate neurotoxicity, oxidative stress and mitochondria

被引:296
作者
Atlante, A
Calissano, P
Bobba, A
Giannattasio, S
Marra, E
Passarella, S
机构
[1] CNR, Ctr Studio Mitocondri & Metab Energet, I-70126 Bari, Italy
[2] CNR, Ist Neurobiol & Med Mol, I-00137 Rome, Italy
[3] Univ Molise, Dipartimento Sci Anim Vegetali & Ambiente, I-86100 Campobasso, Italy
关键词
glutamate neurotoxicity; reactive oxygen species; mitochondrion; oxidative stress; cytochrome c;
D O I
10.1016/S0014-5793(01)02437-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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, (C) 2001 Published by Elsevier Science B,V. on behalf of the Federation of European Biochemical Societies.
引用
收藏
页码:1 / 5
页数:5
相关论文
共 57 条
[1]   GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].
ANKARCRONA, M ;
DYPBUKT, JM ;
BONFOCO, E ;
ZHIVOTOVSKY, B ;
ORRENIUS, S ;
LIPTON, SA ;
NICOTERA, P .
NEURON, 1995, 15 (04) :961-973
[2]   Glutamate neurotoxicity in rat cerebellar granule cells: A major role for xanthine oxidase in oxygen radical formation [J].
Atlante, A ;
Gagliardi, S ;
Minervini, GM ;
Ciotti, MT ;
Marra, E ;
Calissano, P .
JOURNAL OF NEUROCHEMISTRY, 1997, 68 (05) :2038-2045
[3]   Rapid uncoupling of oxidative phosphorylation accompanies glutamate toxicity in rat cerebellar granule cells [J].
Atlante, A ;
Gagliardi, S ;
Minervini, GM ;
Marra, E ;
Passarella, S ;
Calissano, P .
NEUROREPORT, 1996, 7 (15-17) :2519-2523
[4]   A sensitive method to assay the xanthine oxidase activity in primary cultures of cerebellar granule cells [J].
Atlante, A ;
Valenti, D ;
Gagliardi, S ;
Passarella, S .
BRAIN RESEARCH PROTOCOLS, 2000, 6 (1-2) :1-5
[5]   Cytochrome c is released from mitochondria in a reactive oxygen species (ROS)-dependent fashion and can operate as a ROS scavenger and as a respiratory substrate in cerebellar neurons undergoing excitotoxic death [J].
Atlante, A ;
Calissano, P ;
Bobba, A ;
Azzariti, A ;
Marra, E ;
Passarella, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (47) :37159-37166
[6]   CARRIER THIOLS ARE TARGETS OF PHOTOFRIN-II PHOTOSENSITIZATION OF ISOLATED RAT-LIVER MITOCHONDRIA [J].
ATLANTE, A ;
PASSARELLA, S ;
QUAGLIARIELLO, E ;
MORENO, G ;
SALET, C .
JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 1990, 7 (01) :21-32
[7]   Glutamate neurotoxicity in rat cerebellar granule cells involves cytochrome c release from mitochondria and mitochondrial shuttle impairment [J].
Atlante, A ;
Gagliardi, S ;
Marra, E ;
Calissano, P ;
Passarella, S .
JOURNAL OF NEUROCHEMISTRY, 1999, 73 (01) :237-246
[8]   DO DEFECTS IN MITOCHONDRIAL ENERGY-METABOLISM UNDERLIE THE PATHOLOGY OF NEURODEGENERATIVE DISEASES [J].
BEAL, MF ;
HYMAN, BT ;
KOROSHETZ, W .
TRENDS IN NEUROSCIENCES, 1993, 16 (04) :125-131
[9]  
BEAL MF, 1997, MITOCHONDRIA FREE RA
[10]   Perspectives on the mitochondrial permeability transition [J].
Bernardi, P ;
Basso, E ;
Colonna, R ;
Costantini, P ;
Di Lisa, F ;
Eriksson, O ;
Fontaine, E ;
Forte, M ;
Ichas, F ;
Massari, S ;
Nicolli, A ;
Petronilli, V ;
Scorrano, L .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 1998, 1365 (1-2) :200-206