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Asian J Androl. 2018 Oct 12. doi: 10.4103/aja.aja_76_18. [Epub ahead of print]

Sodium nitrite-derived nitric oxide protects rat testes against ischemia/reperfusion injury.

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Center for Convergence Bioceramic Materials, Korea Institute of Ceramic Engineering and Technology, Chungcheongbuk-do 28160, Korea.
Department of Avian Diseases Laboratory, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea.
Viral Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
The Institute for the 3Rs & Department of Laboratory Animal Medicine, College of Veterinary Medicine and Veterinary Science Research Institute, Konkuk University, Seoul 05029, Korea.


Testicular torsion, a common urologic emergency, is primarily caused by ischemia/reperfusion (I/R) injury of the testis. Nitric oxide (NO)-derived from nitrite (NO2-) has been reported to have prominent therapeutic effects on I/R injury in the heart, liver, and brain; however, its effects on testicular I/R injury have not been evaluated. This study, therefore, investigated whether NO from NO2- is beneficial in a rat model of testicular I/R injury which eventually results in impaired spermatogenesis. Male Sprague-Dawley rats were assigned to the following seven groups: group A, sham-operated control group; Group B, I/R with no treatment; Groups C, D, and E, I/R followed by treatment with three different doses of NO2-; Group F, I/R followed by administration of NO2- and NO scavenger (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt [C-PTIO]); and Group G, I/R followed by administration of nitrate (NO3-). NO2-, NO3-, and C-PTIO were intravenously administered. Histological examination of the testes and the western blot analysis of caspase-3 were performed. Levels of antioxidant enzymes and lipid peroxidation were measured. Germ cell apoptosis, oxidative stress, antioxidant enzymatic function, and lipid peroxidation in Group B were significantly higher than those in Group A. Group B exhibited an abnormal testicular morphology and impaired spermatogenesis. In contrast, testicular damages were attenuated in the NO2- treatment groups, which were caused by reduction in superoxide and peroxynitrite levels and an inhibition of caspase-3-dependent apoptosis. The results of this study suggest NO2- to be a promising therapeutic agent with anti-oxidant and anti-apoptotic properties in testicular I/R injury.


ischemia/reperfusion injury; nitric oxide; nitrite; rat; testis

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