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Modulation of the ageing process by dietary restriction (DR) across multiple taxa is well established. While the exact mechanism through which DR acts remains elusive, the gasotransmitter hydrogen sulphide (H 2 S) may play an important role. We employed a comparative-type approach using females from three ILSXISS recombinant inbred mouse strains previously reported to show differential lifespan responses following 40% DR. Following long-term (10 months) 40% DR, strain TejJ89-reported to show lifespan extension under DR-exhibited elevated hepatic H 2 S production relative to its strain-specific ad libitum (AL) control. Strain TejJ48 (no reported lifespan effect following 40% DR) exhibited significantly reduced hepatic H 2 S production, while H 2 S production was unaffected by DR in strain TejJ114 (shortened lifespan reported following 40% DR). These differences in H 2 S production were reflected in highly divergent gene and protein expression profiles of the major H 2 S production and disposal enzymes across strains. Increased hepatic H 2 S production in TejJ89 mice was associated with elevation of the mitochondrial H 2 S-producing enzyme 3-mercaptopyruvate sulfurtransferase (MPST). Our findings further support the potential role of H 2 S in DR-induced longevity and indicate the presence of genotypic-specificity in the production and disposal of hepatic H 2 S in response to 40% DR in mice.

Strain-specificity in the hydrogen sulphide signalling network following dietary restriction in recombinant inbred mice