Journal
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
Volume 46, Issue -, Pages 165-171Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2014.10.005
Keywords
Heat stress; Hydrogen sulfide; Testicular germ cell; Apoptosis; Infertility; Antioxidant
Categories
Funding
- NUHS B2B research [NUHSRO/2011/012/STB/B2B-08]
Ask authors/readers for more resources
Objective: The present study was designed to investigate whether H2S can protect testicular germ cells against heat exposure induced injury and the underlying mechanisms. Results: It was found that all three H2S generating enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lysase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST), were expressed in mouse testicular tissue. Three episodes of heat exposure (42 degrees C, 30 min/day, 3 days) significantly decreased endogenous H2S production and down-regulated the expression of CBS and CSE in testes. In primary cultured testicular germ cells, exogenous application of NaHS (an H2S donor) attenuated heat stress (42 degrees C, 30 min) induced cell death and apoptosis. This was mediated by the inhibitory effects of H2S 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 H2S in testicular germ cells. Exogenous application of H2S may protect germ cells by preservation of mitochondrial function and stimulation of anti-oxidant activity. (C) 2014 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available