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

Abstract EN

Aims.

The study was designed to explore whether hydrogen sulphide (H2S) and nitric oxide (NO) generation changed in D-galactose- (D-gal-) induced ageing, the possible effects of exogenous H2S supplementation, and related mechanisms.

Results.

In D-gal-induced senescent mice, both H2S 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 H2S donor (NaHS) treatment for 2 months elevated H2S 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 H2S-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 H2S can partially rescue ageing-related dysfunction by inducing endogenous H2S and NO production and reducing oxidative stress.

Restoring endogenous H2S production may contribute to healthy ageing, and H2S may have antiageing effects.