Astaxanthin supplementation may be effective for some types of normal tension glaucoma in which glutamate neurotoxicity and oxidative stress are involved. - GreenMedInfo Summary
The protective effect of astaxanthin on the ganglion cell complex in glutamate/aspartate transporter deficient mice, a model of normal tension glaucoma, analyzed by spectral domain-optical coherence tomography.
Biochem Biophys Rep. 2020 Sep ;23:100777. Epub 2020 Jun 29. PMID: 32637659
Takayuki Tanaka-Gonome
Astaxanthin (AST), a natural marine carotenoid, possess a wide variety of biological functions. In particular, as a strong antioxidant, AST effectively scavenges oxygen free radicals and reduces oxidative stress. In addition, recentstudies have suggested that AST attenuates glutamate-induced apoptosis and cytotoxicity. The glutamate/aspartate transporter (GLAST) deficient (GLAST) mouse is a mouse model of normal tension glaucoma (NTG) caused by both the glutamate neurotoxicity and oxidative stress in the retina. In the present study, we investigated the effects of AST on the ganglion cell complex, indicator of glaucomatous structural damage, using spectral domain-optical coherence tomography. As a result, AST significantly attenuated the thinning of ganglion cell complex in GLASTmice in comparison to an AST-free control group. Our results suggest the possibility that AST has protective effects against glutamate neurotoxicity and oxidative stress in the retina. At present, the only treatment for NTG that is available in the clinical setting is to reduce the IOP as much as possible. Thus, our results suggest that AST supplementation may be effective for some types of NTG in which glutamate neurotoxicity and oxidative stress are involved.