15th National and 1st International Congress of Histology and Embryology, Antalya, Türkiye, 26 - 28 Mayıs 2022, ss.80
Introduction: Varicocele is a common cause of male infertility, and lead to oxidative stress. Various studies of
testicular tissues of males with varicocele have shown that apoptosis is increased in developing germ cells. The
P53 plays a role in DNA repair mechanism and induces apoptosis. Nir (novel INHAT repressor) which inhibits
P53-mediated gene transactivation by blocking histon acetylation controls cell proliferation and apoptosis.
Purpose: The apoptotic processes of varicocele still are not known exactly. Currently, there is no evidence of Nir
protein expression in varicocele-induced testicular tissues in any studies. The aim of this study was to investigate
associated of Nir and P53 on testicular damage caused by varicocele.
Material-Method: Thirty male wistar rats were randomly divided into three groups as control, sham and
varicocele (VC). The VC model was established by partial ligation of the left renal vein, and the left testes were
taken from all groups after 13 weeks of varicocele formation. First of all, the obtained sections were stained with
Hematoxylin-Eosin and the degrees of seminiferous tubule degeneration were evaluated under the light
microscope. The TUNEL assay was used to detect apoptotic cells. Nir, p53 and HIF-1α expressions were
determined using Immunohistochemistry and Western blot techniques. One-way ANOVA was used to determine
the statistical significance between the results obtained from the groups.
Results: The expressions of Nir, P53, and HIF-1 were significantly increased (P < 0.05) in the varicocele group
according to the results of Immunohistochemistry and Western blot analysis. In addition, an increase in both
apoptotic germ cell number and seminiferous tubule degeneration was observed in the varicocele group.
Conclusion: In conclusion, increased expression of P53 (as Nir interacting partner) in varicocele group, appears
as a result of varicocele-induced apoptosis. HIF-1α protein which increased with hypoxia in rats with varicocele,
regulates apoptosis-related downstream gene, P53. Increased Nir expression can block P53 activity and therefore
the Nir signaling can play a protective role in this process.