Journal
MARINE DRUGS
Volume 18, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/md18060335
Keywords
NMDA; astaxanthin; calcium; mitochondrial superoxide; excitotoxicity
Categories
Funding
- CORFO [13IDL2-18271]
- FONDECYT [11140580, 1150736, 1170053, 1201899, P-09-015, ANID/PIA/ACT192144]
- BNI [P-09-015]
- FONDAP [15130011]
- UBO/VVCM [1905]
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Astaxanthin (ASX) is a carotenoid pigment with strong antioxidant properties. We have reported previously that ASX protects neurons from the noxious effects of amyloid-beta peptide oligomers, which promote excessive mitochondrial reactive oxygen species (mROS) production and induce a sustained increase in cytoplasmic Ca(2+)concentration. These properties make ASX a promising therapeutic agent against pathological conditions that entail oxidative and Ca(2+)dysregulation. Here, we studied whether ASX protects neurons from N-methyl-D-aspartate (NMDA)-induced excitotoxicity, a noxious process which decreases cellular viability, alters gene expression and promotes excessive mROS production. Incubation of the neuronal cell line SH-SY5Y with NMDA decreased cellular viability and increased mitochondrial superoxide production; pre-incubation with ASX prevented these effects. Additionally, incubation of SH-SY5Y cells with ASX effectively reduced the basal mROS production and prevented hydrogen peroxide-induced cell death. In primary hippocampal neurons, transfected with a genetically encoded cytoplasmic Ca(2+)sensor, ASX also prevented the increase in intracellular Ca(2+)concentration induced by NMDA. We suggest that, by preventing the noxious mROS and Ca(2+)increases that occur under excitotoxic conditions, ASX could be useful as a therapeutic agent in neurodegenerative pathologies that involve alterations in Ca(2+)homeostasis and ROS generation.
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