SUN-547 Hydrogen Sulfide (H2S) Inhibition Of Reducing Sugar Induced Oxidative Stress In Pancreatic β Cells.

Abstract Disclosure: K.N. Islam: None. R.K. Islam: None. A.H. Penn: None. Diabetes is a major cause of morbidity and mortality. Elevation of oxidative stress is associated with diabetic patients because of increased levels of blood sugar concentration. Hydrogen Sulfide (H2S) is a gasotransmitter and antioxidant with many health benefits for many disease conditions. The pancreatic β cells are insulin-secreting. The present study investigated the effects of H2S on reducing sugar-induced oxidative stress in pancreatic β cells (HIT) from a Chinese hamster. Here, we determined the effects of reducing sugar on the induction of oxidative stress, as it was measured by the formation of thiobarbituric acid reactive substances (TBARS) and protein carbonyl (CO) formation in serum-starved β cells. We observed marked oxidative stress in the serum-starved β cells after treatment with reducing sugar. We tested the effects of H2S on reducing sugar-induced oxidative stress in serum-starved β-cells, and we found that H2S markedly inhibited sugar-induced oxidative stress in serum-starved β cells. Treatment with H2S caused significant induction of cell viability and a marked reduction of cellular cytotoxicity in β cells under serum starvation incubated without or with sugar. H2S treatment of starved β cells antagonized expression levels of inflammatory cytokines, TNF-α and inhibited the activation of the transcription factor, NF-κB signaling pathway. In addition, H2S treatment increased antioxidant activity and activated the Nrf2 signaling pathway in stressed β cells. Our findings suggest that H2S/its donors may be used as therapy to cure diabetes by inhibiting oxidative stress, thereby decreasing blood sugar levels in diabetic patients. Presentation: Sunday, July 13, 2025