Autor: |
K, Dubey Tiwari, G, Sharma, M M, Prakash, M S, Parihar, V, Dawane |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
Annales Pharmaceutiques Françaises. 81:457-465 |
ISSN: |
0003-4509 |
DOI: |
10.1016/j.pharma.2022.10.003 |
Popis: |
The excess amount of glutamate in neurons is associated with the excitotoxicity and neurodegenerative diseases. Glutamate induces neurotoxicity primarily by immense influx of CaHere, we have shown that the higher concentration of glutamate treatment caused a significant elevation in the N-methyl-D-aspartate (NMDA) receptors expression and elevated the intra-mitochondrial calcium accumulation in SHSY5Y neuronal cells. As a result of an accumulation of intra-mitochondrial calcium, there is a concentration-dependent elevation in ROS in the mitochondria. Tyrosine nitration of several mitochondrial proteins was increased while the mitochondrial membrane potential was dissipated. Furthermore, glutamate treatments also resulted in mitochondrial membrane permeability transition.These findings suggest that treatment of high glutamate concentration causes impairment of mitochondrial functions by an increase in intra-mitochondrial calcium, ROS production, dissipation of mitochondrial membrane potential and mitochondrial permeability transition pore opening in human neuroblastoma SHSY5Y cells. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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