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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.

Author information

1
Center for Convergence Bioceramic Materials, Korea Institute of Ceramic Engineering and Technology, Chungcheongbuk-do 28160, Korea.
2
Department of Avian Diseases Laboratory, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea.
3
Viral Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
4
The Institute for the 3Rs & Department of Laboratory Animal Medicine, College of Veterinary Medicine and Veterinary Science Research Institute, Konkuk University, Seoul 05029, Korea.

Abstract

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.

KEYWORDS:

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

PMID:
30319134
DOI:
10.4103/aja.aja_76_18
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