The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Glutamate neurotoxicity, oxidative stress and mitochondria
Abstract
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.
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Cites
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Cited by
Molecular mechanisms of glutamate-dependent neurodegeneration in ischemia and traumatic brain injury
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Neurotoxicity of substituted amphetamines: Molecular and cellular mechanisms
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Metadata
- Authors
- Atlante, A., Calissano, P., Bobba, A., Giannattasio, S., Marra, E., & Passarella, S.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2001-05-18
- Volume
- 497
- Issue
- 1
- Pages
- 1-5
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W1984156662
- Cited by
- 360
- References
- 52
- FWCI
- 7.17
- Type
- journal article
- Language
- en
- Open access
- closed
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- Atlante, A., Calissano, P., Bobba, A., Giannattasio, S., Marra, E., & Passarella, S. (2001). Glutamate neurotoxicity, oxidative stress and mitochondria. FEBS Letters. https://doi.org/10.1016/s0014-5793(01)02437-1
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
