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Aims . The study was designed to explore whether hydrogen sulphide (H 2 S) and nitric oxide (NO) generation changed in D-galactose- (D-gal-) induced ageing, the possible effects of exogenous H 2 S supplementation, and related mechanisms.  Results . In D-gal-induced senescent mice, both H 2 S and NO levels in the heart, liver, and kidney tissues were decreased significantly. A similar trend was observed in D-gal-challenged human umbilical vein endothelial cells (HUVECs). Sustained H 2 S donor (NaHS) treatment for 2 months elevated H 2 S and NO levels in these mice, and during this period, the D-gal-induced senescent phenotype was reversed. The protective effect of NaHS is associated with a decrease in reactive oxygen species levels and an increase in antioxidants, such as glutathione, and superoxide dismutase and glutathione peroxidase activities. Increased expression of the H 2 S-producing enzymes cystathionine  γ -lyase (CSE) and cystathionine- β -synthase (CBS) in the heart, liver, and kidney tissues was observed in the NaHS-treated groups. NaHS supplementation also significantly postponed D-gal-induced HUVEC senescence.  Conclusions . Endogenous hydrogen sulphide production in both ageing mice and endothelial cells is insufficient. Exogenous H 2 S can partially rescue ageing-related dysfunction by inducing endogenous H 2 S and NO production and reducing oxidative stress. Restoring endogenous H 2 S production may contribute to healthy ageing, and H 2 S may have antiageing effects.

H2S Donor NaHS Changes the Production of Endogenous H2S and NO in D-Galactose-Induced Accelerated Ageing

H₂S Donor NaHS Changes the Production of Endogenous H₂S and NO in D-Galactose-Induced Accelerated Ageing