Figure 2.

Cellular function of H₂S as an antioxidant in DPN.

The beneficial action of H₂S through mediating superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) in hyperglycemia-induced oxidative stress. Superoxide dismutase (SOD) binds with alpha lipoic acid (ALA) to exert antioxidant effects by increasing GSH level. On the other hand, GSH is reduced by H₂O₂ formation and it is converted into oxidized GSSH. The ratio of nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) to nicotinamide adenine dinucleotide phosphate (NADP) is altered by polyol pathway. Glutathione peroxidase (Gpx) can attenuate the balance to provide antioxidant function. In the case of CAT, it also provides similar antioxidant mechanism by removing H₂O₂ formation. As a consequence, oxidized GSSH is decreased and GSH is increased. DPN: Diabetic peripheral neuropathy; H₂S: hydrogen sulfide; NADPH: nicotinamide adenine dinucleotide phosphate; PKC: protein kinase C; ROS: reactive oxygen species.