Increased testicular 8-hydroxy-2'-deoxyguanosine (8-OHdG) and inducible nitric oxide synthetase (iNOS) and nuclear factor κB (NF-κB) expressions in experimental rat varicocele
To assess nuclear factor-kappaB (NF-kappaB), inducible NO synthase (iNOS) immunohistochemically, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) biochemically, which are sensitive biological markers of oxidative damage and stress, in testes with experimental varicocele. Adult rats were randomly divide...
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Published in | Archivio italiano di urologia, andrologia Vol. 82; no. 4; p. 148 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Italy
01.12.2010
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Subjects | |
Online Access | Get more information |
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Summary: | To assess nuclear factor-kappaB (NF-kappaB), inducible NO synthase (iNOS) immunohistochemically, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) biochemically, which are sensitive biological markers of oxidative damage and stress, in testes with experimental varicocele.
Adult rats were randomly divided into three groups. Control group (n: 10), sham group (n: 10), varicocele group (n: 10). Of 14 rats undergoing partial ligation of the left renal vein, 10 rats had developed dilation of the left spermatic vein when evaluated 3 months after varicocele-inducing surgery. The rats were sacrificed after 3 months of the varicocele-inducing surgery. Ipsilateral and contralateral testes were examined for 8-hydroxy-2'-deoxyguanosine (8-OHdG) biochemically, inducible NO synthase (iNOS) and nuclear factor-kappaB (NF-kappaB) expression immunohistochemically.
Inducible NO synthase (iNOS), nuclear factor-kappaB (NF-kappaB) expressions and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in both testes of varicocele group were markedly higher compared with control and sham groups (p < 0.01). There was no difference between control and sham groups (p > 0.05).
Regarding to our results, we suggest that varicocele may produce oxidative stress in both of testes, and we believe that this stress may play a role in male fertility. |
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ISSN: | 1124-3562 |