Hydrogen sulfide (H2S) is known to act protectively during renal
ischemia/reperfusion injury (IRI). However, the role of the endogenous H2S in
acute kidney injury (AKI) is largely unclear. Here, we analyzed the role of
cystathionine gamma-lyase (CTH) in acute renal IRI using CTH-deficient
(Cth−/−) mice whose renal H2S levels were approximately 50% of control (wild-
type) mice. Although levels of serum creatinine and renal expression of AKI
marker proteins were equivalent between Cth−/− and control mice, histological
analysis revealed that IRI caused less renal tubular damage in Cth−/− mice.
Flow cytometric analysis revealed that renal population of infiltrated
granulocytes/macrophages was equivalent in these mice. However, renal
expression levels of certain inflammatory cytokines/adhesion molecules
believed to play a role in IRI were found to be lower after IRI only in Cth−/−
mice. Our results indicate that the systemic CTH loss does not deteriorate but
rather ameliorates the immediate AKI outcome probably due to reduced
inflammatory responses in the kidney. The renal expression of CTH and other
H2S-producing enzymes was markedly suppressed after IRI, which could be an
integrated adaptive response for renal cell protection