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Growing evidence has demonstrated that, as an endogenous signaling gasotransmitter, hydrogen sulfide (H(2)S) plays an important role in regulating numerous biological functions. The role of H(2)S in hypoxia-induced radioresistance on hepatoma cells was investigated in the present work. Results showed that, when HepG2 cells were maintained in hypoxia circumstances for 4 h, the cellular radioresistance was extensively increased so that the oxygen enhancement ratio of the survival fraction approached 2.68. Under this hypoxic condition, when the cells were treated with DL-propargylglycine (PPG) and aminooxyacetic acid (AOAA), a specific inhibitor of H(2)S synthase of cystathionine-γ-lyase (CSE) and cystathionine-β-synthase (CBS) respectively, radiation responses including cell killing, micronuclei (MN) formation, and caspase-3 activity were significantly enhanced. However, treatment of cells with low concentrations of NaHS (≤ 100 µM) protected cells from these radiation damages. Western bolting assay showed that CSE and CBS were over-expressed in the irradiated hypoxic cells in a dose dependent manner. Moreover, when the hypoxic HepG2 cells were treated with NaHS together with glibenclamide, a specific inhibitor of K(+)(ATP) channels, the role of exogenous H(2)S in radioprotection was partly eliminated. This study demonstrated that H(2)S contributed to hypoxia-induced radioresistance probably via the opening of K(+)(ATP) channels, which suggests that the endogenous H(2)S synthase could be a potential radiotherapeutic target for a hypoxic tumor.

Hydrogen Sulfide Contributes to Hypoxia-induced Radioresistance on Hepatoma Cells