Hydrogen sulfide protects testicular germ cells against heat-induced injury.

Abstract Objective The present study was designed to investigate whether H 2 S can protect testicular germ cells against heat exposure induced injury and the underlying mechanisms. Results It was found that all three H 2 S generating enzymes, cystathionine β-synthase (CBS), cystathionine γ-lysase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST), were expressed in mouse testicular tissue. Three episodes of heat exposure (42 °C, 30 min/day, 3 days) significantly decreased endogenous H 2 S production and down-regulated the expression of CBS and CSE in testes. In primary cultured testicular germ cells, exogenous application of NaHS (an H 2 S donor) attenuated heat stress (42 °C, 30 min) induced cell death and apoptosis. This was mediated by the inhibitory effects of H 2 S on cytochrome C release and the ratio of the Bax/Bcl-2. NaHS also improved mitochondrial function by decreasing oxygen consumption and increasing ATP production. NaHS treatment also stimulated SOD activity and reduced ROS production. Conclusions Our results revealed both physiological and pharmacological roles of H 2 S in testicular germ cells. Exogenous application of H 2 S may protect germ cells by preservation of mitochondrial function and stimulation of anti-oxidant activity.