title: Effect of testicular ischemia-reperfusion on recruitment of neutrophils, E-selectin expression and germ cell apoptosis in the contralateral testis in a rat.
abstract: Recent evidence suggests that neutrophil recruitment may initiate germ cell apoptosis in the ischemic testis. The purpose of the present study was to examine the relationship between germ cell apoptosis and neutrophil recruitment in the contralateral testis following testicular ischemia-reperfusion (IR) injury in a rat. Adult male Sprague-Dawley rats were divided randomly into two experimental groups: Group A: Sham operated animals; Group B: IR rats underwent 90 min of unilateral testicular ischemia following by 96 h of reperfusion. The rats were sacrificed and testes were harvested. Johnsen's criteria and the number of germinal cell layers were measured to categorize the spermatogenesis. TUNEL assay was used to determine germ cell apoptosis in both the ischemic and contralateral testis. The recruitment of neutrophils was calculated per 100 venules. Expression of E-selectin was determined using immunohistochemical analysis. Statistical analysis was performed using Student's t test, with P less than 0.05 considered statistically significant. Germ cell apoptosis in both the ischemic and the contralateral testis increased significantly after IR. E-selectin expression was significantly greater in ischemic testis from IR rats compared to sham animals. The small increase in E-selectin expression and the concomitant increase in neutrophil recruitment in the contralateral testis of the IR rats (vs. sham animals) were not statistically significant. In conclusion, testicular ischemia causes an increase in germ cell apoptosis in the contralateral testis. Mechanisms other than neutrophil recruitment apparently initiate this process.
authors.affiliation: Department of Pediatric Surgery and Pathology, Bnai Zion Medical Center, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, 47 Golomb St., P.O.B. 4940, Haifa 31048, Israel.
authors.forename: Igor
authors.initials: I
authors.lastname: Sukhotnik
authors.forename: Katya
authors.initials: K
authors.lastname: Voskoboinik
authors.forename: Michael
authors.initials: M
authors.lastname: Lurie
authors.forename: Arnold G
authors.initials: AG
authors.lastname: Coran
authors.forename: Robert
authors.initials: R
authors.lastname: Greenblatt
authors.forename: Eitan
authors.initials: E
authors.lastname: Shiloni
authors.forename: Samuel
authors.initials: S
authors.lastname: Eldar
authors.forename: Jorge G
authors.initials: JG
authors.lastname: Mogilner
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D019040:E-Selectin / Q000096:biosynthesis*; D015870:Gene Expression; D005854:Germ Cells / Q000473:pathology*; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D020556:Neutrophil Infiltration; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D013091:Spermatogenesis; D013733:Testicular Diseases / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D013737:Testis / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology
chemical_list: D019040:E-Selectin