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Therefore, homocysteine-induced apoptosis and DNA damage could be potential mechanisms for the development and progression of PD in patients with hyperhomocysteinemia
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These results suggest that upon depletion of GSH, tissues undergo reprogramming to hyperactivate NRF2, possibly as a mechanism to upregulate adjacent antioxidant pathways and buffer oxidative stress induced upon GSH depletion
(D) Top metabolites generated by RF analysis resulted in predictive accuracy of 52% (compared to 33% expected by random chance alone)
Protein disulfide-isomerase, a folding catalyst and a redox-regulated chaperone
Each group included 612 animals
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