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Ischemia‐reperfusion decreases hydrogen sulfide production in the kidney
Author(s) -
Karmin O,
Prathapasinghe Gamika,
Wu Nan,
Siow Yaw L.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.639.3
Hydrogen sulfide (H2S) is a gaseous molecule that plays an important role in many physiological and pathological processes. Cystathionine‐â‐synthase (CBS) is a key enzyme that regulates H2S production in our body. CBS enzyme is present in several organs including the kidney. Ischemia‐reperfusion (IR) injury is one of the common causes for delayed function of renal allograft and is associated with poor long‐term renal function The aim of the present study was to examine the effect of IR on cystathionine‐beta‐synthase (CBS)‐mediated H2S production in the kidney and its impact on kidney function. The left kidney of SD rat was subjected to 45 min ischemia followed by 6 h reperfusion. IR caused renal lipid peroxidation, cell death and renal dysfunction. Renal CBS enzyme activity and H2S levels were reduced in the IR group. Partial restoration of CBS activity not only enhanced the level of H2S in the kidney but also reduced IR‐induced cell death. Administration of exogenous H2S donor (NaHS) to rats alleviated IR‐induced oxidative stress and cell death as well as improved kidney function. These results suggest that regulation of H2S homeostasis may have therapeutic potential to protect against renal ischemia‐reperfusion injury.