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• W50276461 abstract "Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease that affects motor neurons of the brain and spinal cord. Many studies indicate that mitochondrial oxidative stress (MOS) is a principal mechanism underlying the pathophysiology of this and other devastating neurodegenerative diseases. Here, we investigated a unique whey protein supplement (Immunocal®) to determine its neuroprotective efficacy in several in vitro models of MOS and in an in vivo mouse model of ALS. This non-denatured whey supplement contains cystine which is an oxidized form of cysteine, an essential precursor for synthesis of the endogenous antioxidant, glutathione (GSH). In primary cultured rat cerebellar granule neurons (CGNs), pre-incubation with Immunocal® completely protected against MOS induced by HA14-1, an inhibitor of the pro-survival Bcl-2 protein. This effect was prevented by co-incubation with the gamma-glutamyl cysteine ligase inhibitor, buthionine sulfoximine, demonstrating that the de novo synthesis of GSH underlies the neuroprotective mechanism of Immunocal®. Additionally, Immunocal® displayed significant protection against an array of MOS-inducing agents, including sodium nitroprusside, copper, and aluminum, supporting its ability to upregulate mitochondrial antioxidant capacity. In accordance with these findings in CGNs, Immunocal® decreased cell death due to both H2O2 and glutamate toxicity in NSC34 motor neuron-like cells. Immunocal® also significantly protected CHO cells iii from MOS evoked by overexpression of amyloid precursor protein (APP). Immunocal® treatment in NSC34 motor neuron-like cells decreased cell death caused by both H2O2 and glutamate glycine. Most compelling are our findings in the hSOD1 G93A mouse model of ALS. These mice were given Immunocal® (3.33% solution in drinking water) ad libitum, beginning at 60-days-old. Although no effect on overall survival was observed, Immunocal®-treated mice displayed a significant (7 ±1.08 day) delay in disease onset, compared to mutant control mice. Importantly, Immunocal®-treated mice showed a highly significant decrease in the rate of decline in grip strength. Finally, using HPLCECD we found that whole blood and lumbar spinal cord GSH levels were each depleted by nearly 50% in end-stage hSOD1 G93A mice, and these reductions were essentially prevented in mutant mice receiving Immunocal®. These findings suggest that sustaining GSH by supplementation with Immunocal® may help to mitigate the progression of ALS through suppression of MOS. In addition to investigating Immunocal® for its neuroprotective efficacy, we also show that an anthocyanin-enriched fraction from strawberries delays disease onset and extends survival in the hSOD1 G93A mouse model of ALS. These cumulative data suggest that nutraceutical antioxidants hold promise in neurodegenerative disease." @default.
• W50276461 created "2016-06-24" @default.
• W50276461 creator A5083525103 @default.
• W50276461 date "2012-01-01" @default.
• W50276461 modified "2023-09-24" @default.
• W50276461 title "Nutraceutical Antioxidants and Their Therapeutic Potential in Neurodegeneration" @default.
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