TSEG-2基因在小鼠睾丸扭转复位模型中的表达特征

目的 探讨睾丸特异表达基因2(testis specific expressed gene 2,TSEG-2)在小鼠睾丸扭转复位模型中的表达特征.方法 昆明小鼠36只,随机分组为对照组(6只)、假手术组(6只)、单侧睾丸扭转复位实验组(24只).实验组分为2组,每组12只,左侧睾丸扭转720°维持2 h,分别于复位后1、7 d取扭转侧睾丸.采用HE染色、原位末端标记技术(TUNEL)观察睾丸组织形态改变;黄嘌呤氧化酶法、硫代巴比妥酸比色法测定超氧化物歧化酶(SOD)、丙二醛(MDA)活性;原位杂交法观测TSEG-2在睾丸生精细胞内的表达定位;实时定量PCR法检测TSEG-2基因在睾丸组织中的表达水平.结果 对照组和假手术组生精上皮排列规则,扭转复位后1、7 d的睾丸组织内生精上皮结构松散,出现生精细胞凋亡,Johnsen's评分分别降低23.4%、64.1%(P<0.01),SOD活性降低11.6%、22.2%(P<0.05),MDA活性升高69.6%、93.2%(P<0.01).TSEG-2基因表达定位于小鼠睾丸生精小管的精原细胞和精母细胞.与对照组比较,扭转复位1、7 d后睾丸组织内TSEG-2表达水平分别上调2.2倍、6.6倍(P<0.01).结论 成功建立小鼠睾丸扭转复位模型,TSEG-2表达上调可能与抗氧化酶活性下降、生精细胞凋亡有关.     

硫氧还蛋白对大鼠睾丸缺血再灌注损伤保护作用的研究

目的 探讨硫氧还蛋白对大鼠睾丸缺血再灌注损伤的保护作用.方法 选取雄性SD大鼠60只,随机分为4组:假手术对照组(A组);睾丸扭转/复位组(B组);睾丸扭转/复位+腹腔内注射生理盐水组(C组);睾丸扭转/复位+腹腔内注射硫氧还蛋白组(D组).无菌条件下制作左侧睾丸扭转模型,扭转持续4h,复位4h后取睾丸标本(D组在复位前15 min腹腔内注射硫氧还蛋白).对标本进行病理组织学检查;检测睾丸组织中超氧化物歧化酶(SOD)和丙二醛(MDA)的含量.结果 睾丸扭转/复位后可见生精小管退变,间质出现水肿及出血,腹腔注射硫氧还蛋白使睾丸扭转/复位诱发的组织学改变明显改善.B组及C组睾丸损伤评分(8.3±0.96;8±0.87)明显高于A组(0.78±0.36)(P＜0.01),而腹腔注射硫氧还蛋白可以使睾丸损伤分值(3.1±0.42)显著降低(P＜0.05).B组及C组MDA含量(4.39±0.21;4.42±0.17)升高,SOD活性(269±27.1;271±21.3)降低,与对照组(MDA:1.61±0.18;SOD:317±22.3)相比,差别具有显著性意义(P＜0.01).而腹腔注射硫氧还蛋白能有效降低MDA含量(2.03±0.03)并升高SOD活性(315±24.2)(P＜0.01).结论 本实验为硫氧还蛋白作为治疗睾丸扭转继发损害的有效物质提供了组织学及生化依据.为临床预防和治疗睾丸缺血再灌注损伤提供了理论依据.     

西地那非对大鼠单侧睾丸扭转后对侧睾丸的影响及作用研究

目的 探讨大鼠单侧睾丸扭转后对侧睾丸的损伤以及西地那非（万艾可）的保护机理.方法 将72只健康雄性SD大鼠,随机分为假手术组、安慰剂组、西地那非组.3组分别在假手术/左侧睾丸扭转复位术后4 h、24 h、2周时,各组各处死8只大鼠.分别观察右侧睾丸组织病理学变化、测定右侧睾丸组织中MDA、NO/NOS含量.结果 术后4 h,各组间组织病理学变化、MDA、NOS含量无明显差异,睾丸组织未见损伤,但NO在两地那非组较假手术组、安慰剂组明显增加（P〈0.05）.术后24 h,假手术组右侧睾丸组织损伤最小,西地那非组较严重,安慰剂组最为严重;与假手术组比,其余两组MDA、NO/NOS含量明显升高（P〈0.05）;西地那非组NO/NOS含量与安慰剂组相比明显下降（P〈0.05）;术后2周时,睾丸组织损伤有不同程度恢复,但仍以安慰剂组最为严重;与假手术组比,其余两组MDA、NO/NOS含量仍然升高（P〈0.05）;西地那非组NO/NOS含量与安慰剂组相比明显下降（P〈0.05）.结论 大鼠单侧睾丸扭转复位后,对侧睾丸组织术后4 h时.睾丸组织未见损伤.12 h后睾丸组织明显损伤,并且持续至2周后.早期应用适量西地那非（万艾可）可促局部NO增加,扩血管作用加强,拮抗交感神经缩血管作用,进而保护对侧睾丸.     

褪黑激素对大鼠睾丸扭转缺血和再灌注损伤的保护作用

目的 探讨褪黑激素对大鼠睾丸扭转的治疗作用.方法 选取青春期雄性SD大鼠48只,随机分为3组:空白对照组(A组);扭转复位组(B组);扭转复位+褪黑激素组(C组).B组和C组大鼠建立睾丸扭转复位模型,对照组不扭转.扭转4h后复位睾丸,复位前15 min B组腹腔注射生理盐水1 ml:C组腹腔注射褪黑激素1ml(17 mg/kg).复位后4h处死所有动物取睾丸待测.以原位缺口末端标记法(TUNEL)检测生精细胞凋亡指数;化学比色法测定睾丸组织内总抗氧化能力(T-AOC).结果 B组T-A0C( 20.31±2.55)U/mg比A组(33.62±3.29) U/mg明显降低,差异有统计学意义(P＜0.01).而C组T-AOC(30.05±2.08)U/mg较B组明显升高(P＜0.05).B组凋亡指数(42.2±3.21)％明显高于A组(5 7±0.67)％(P＜0.01),而C组凋亡指数(12.2±1.34)％较B组显著下降(P＜0.05).结论 褪黑激素具有明显对抗睾丸扭转复位后的氧化损伤,对因睾丸扭转导致的缺血再灌注损伤具有保护作用.     

大鼠睾丸扭转复位及减压治疗对睾丸的影响

目的 研究睾丸扭转复位及减压治疗对睾丸的影响,为睾丸扭转的预后判断、治疗方法的选择等提供新的理论依据.方法 将30只SD雄性大鼠随机分成5组,制成睾丸扭转复位及复位+减压治疗的模型.分别设立空白对照组及实验A～D组,睾丸扭转/复位组(A组)、睾丸扭转/复位+减压治疗组(B组)喂养至术后1 d处死;睾丸扭转/复化组(C组)、睾丸扭转/复位+减压治疗组(D组)喂养至术后1个月处死.应用化学检测和组织学分析方法,观察睾丸大体标本的变化、睾丸组织内丙二醛(MDA)含量的变化及睾丸组织Johnsen's评分.结果 五组睾丸MDA分别为3.18±0.22(空白对照组)、9.54±2.05(A组)、7.92±1.38(B组)、6.67±0.61(C组)、4.30±1.81(D组),实验组术侧睾丸的MDA含量显著高于自身对侧(P<0.05).D组MDA含量比C组明显下降(P<0.05).单纯复位组的术后睾丸标本比自身对侧和减压治疗组有明显萎缩;五组Johnsen's评分分别为10±0、7.2±0.18、8.2±0.19、2.2±0.19、9.2±0.18.D组比C组明显提高(P<0.05).结论 睾丸扭转复位+减压治疗能明显减少扭转侧睾丸生殖细胞凋亡,减轻脂质过氧化程度,可能有利于睾丸组织结构与功能的恢复.     

不同日龄隐睾复位大鼠睾丸组织结构观察

目的 观察不同13龄隐睾复位大鼠睾丸组织结构的变化.方法 72只21 d雄性SD大鼠随机分为单侧隐睾组、双侧隐睾组、假手术对照组各24只.建立单、双侧隐睾动物模型.2周后行隐睾大鼠睾丸下降固定术,于日龄40、60 d处死取睾丸,采用苏木素.伊红染色光镜下观察各组大鼠精曲小管生育力指数(TFI)和平均精曲小管直径(MTD);生物素-dUTP/酶标亲和素法(TUNEL法)检测睾丸生殖细胞凋亡情况.结果 隐睾侧睾丸MTD、TFI显著低于阴囊内睾丸,而隐睾生殖细胞凋亡指数(AI)明显增高于阴囊内睾丸(P＜0.05);单侧隐睾组阴囊内睾丸TFI低于相应日龄的假手术对照组,但无统计学意义(P＞0.05).40 d时单侧隐睾组隐睾侧睾丸生殖细胞AI较双侧隐睾组低(P＜0.05),日龄60 d,各组隐睾侧睾丸AI较40 d时明显降低(P＜0.05),但单侧隐睾和双侧隐睾AI比较无统计学差异(P＞0.05).结论 实验隐睾复位大鼠睾丸AI升高,同时单侧隐睾鼠对侧睾丸组织存在不同程度的损害.随着复位时间的延长,隐睾组织的病理损害有恢复的趋势.     

血栓通注射液对大鼠小肠缺血再灌注损伤的作用

目的采用肠系膜上动脉(SMA)缺血再灌注(I/R)模型,观察血栓通注射液对大鼠小肠I/R损伤的防治作用。方法将30只大鼠随机分为假手术组、I/R组、治疗组。治疗组于SMA再灌注前15分钟静脉注射血栓通注射液,I/R组按同样方式注射生理盐水,假手术组除不夹闭SMA外,其余操作同I/R组。分别观察平均动脉压(MABP)、血浆一氧化氮(NO)、小肠粘膜出血程度、肠组织湿/干重比值、丙二醛(MDA)浓度和超氧化物歧化酶(SOD)活性。结果与假手术组比较,I/R组再灌注后60分钟MABP、血浆NO含量显著下降,肠组织湿/干重比值、MDA浓度明显升高(P<0.01),而SOD活性无变化(P>0.05)。治疗组,则能明显减缓这种趋势,各项指标改善,小肠粘膜损伤程度明显减轻(P<0.01)。结论血栓通注射液对大鼠小肠I/R损伤有一定保护作用,其作用机制与抑制脂质过氧化和NO含量增加有关。     

兔睾丸扭转复位后睾丸细胞凋亡的观察

目的　观察兔睾丸扭转复位后睾丸细胞凋亡情况及药物减轻睾丸凋亡的效果。方法　选用青春期雄性日本大耳白兔 2 0只 ,体重 90 0～ 110 0g ,月龄 2～ 3个月 ,随机分为 4组 ,每组 5只。手术制作幼兔睾丸扭转模型 (72 0° ,2h) ,对部分扭转组应用抗氧化剂 (抗坏血酸 )或钙离子通道拮抗剂 (维拉帕米 )。 2d后取出睾丸 ,TUNEL法观查各组动物睾丸组织细胞凋亡情况 ,HE染色检查睾丸病理组织学改变。结果　幼兔睾丸扭转复位后 ,精原细胞发生凋亡 ,而睾丸支持细胞及间质细胞未见凋亡现象。单纯扭转组精原细胞平均凋亡指数 (AI) (7.92± 1.2 9)‰ ,较对照组 (2 .6 0± 1.0 1)‰显著升高 ;睾丸扭转前后应用抗坏血酸及维拉帕米组的睾丸细胞平均AI ,分别为 (4.12± 0 .73)‰ ,(4.0 8± 0 .88)‰ ,较单纯扭转组 (7.92± 1.2 9)‰显著下降。HE染色的组织学改变与TUNEL法类似。结论　睾丸扭转损伤后可致使生精细胞凋亡。应用抗氧化剂及钙离子通道拮抗剂可以减轻扭转睾丸的精原细胞凋亡     

青春期前大鼠睾丸扭转生精功能损伤与Fas/FasL mRNA的表达

单侧睾丸扭转（unilateral testicular totsion,UTT）好发于青春期前小儿，即使手术复位后仍可能出现生精功能长期受损，并造成成年男子不育。单侧睾丸扭转影响生精功能的机制较为复杂，缺血／再灌注损伤是患侧睾丸生精功能受损的主要原因之一，凋亡调控基因亦参与其中。本实验通过建立青春期前大鼠睾丸扭转模型，研究大鼠睾丸扭转复位后患侧睾丸生精功能损伤的分子机制。     

不同缝线行睾丸固定复位术对隐睾模型大鼠生精能力的影响

目的建立内分泌型双侧隐睾大鼠模型,通过手术复位睾丸,检测、对比应用不同缝线固定睾丸对隐睾模型大鼠生精能力的影响。方法取孕SD大鼠10只,自然分娩产仔鼠,随机选取新生雄性仔鼠40只为正常对照组,并选取80只为双侧隐睾模型组。双侧隐睾模型组大鼠从出生第3天起皮下注射17-β雌二醇,第26天观察双侧睾丸均未降入阴囊内为隐睾模型制作成功。将双侧隐睾大鼠随机分为1号丝线手术组(采用1号丝线固定睾丸)和6-0可吸收线手术组(采用6-0可吸收线固定睾丸),各40只。于日龄45 d、56 d时采集血清后处死。采用ELISA间接法测定其血清抗精子抗体(AsAb)水平。睾丸切片苏木精-伊红染色光镜下观察曲细精管生育力指数(TFI)、平均曲细精管直径(MTD)。结果 1号丝线手术组隐睾大鼠45 d、56 d时TFI、MTD水平均低于6-0可吸收线手术组(Pa<0.05);45 d、56 d时1号丝线手术组大鼠血清AsAb IgG、IgA、IgM水平均显著高于6-0可吸收线手术组(Pa<0.01)。结论采用6-0可吸收线固定睾丸可以减少AsAb的产生。     

The protective effect of selenium on ipsilateral and contralateral testes in testicular reperfusion injury

This study was designed to investigate the effect of selenium on ipsilateral and contralateral testicular damage after unilateral testicular torsion/detorsion (T/D). Thirty-two male rats were divided into four groups, each containing eight rats. Torsion was created by rotating the right testis 720° in a clockwise direction. Group 1 underwent sham operation to determine basal values for biochemical and histopathological evaluation. Sham operation was performed in group 2, and sodium selenate (0.2 mg/kg) was given intraperitoneally. Group 3 served as a T/D group, receiving 4-h torsion and 4-h detorsion. Similarly, in group 4 sodium selenate (0.2 mg/kg) was injected intraperitoneally 20 min before detorsion. Bilateral orchiectomies were performed for measurement of tissue malondialdehyde (MDA) levels and superoxide dismutase (SOD) activities and histopathologic examination. The results were compared statistically. The highest MDA and the lowest SOD values were determined in both testes in group 3. There were statistically significant differences in MDA levels and SOD activities in group 3 compared with group 4. Specimens from group 3 had a significantly greater histologic injury than other groups. These results suggest that ischemia-reperfusion injury occurred in both testes after unilateral testicular T/D and that selenium administration before detorsion prevents reperfusion injury in testicular torsion.     

Effects of gabexate mesilate on ischemia-reperfusion-induced testicular injury in rats

The aim of this study was to determine the effects of a synthetic serine protease inhibitor, gabexate mesilate (GM), in rats with ischemia-reperfusion (I-R) damage due to unilateral testicular torsion. Thirty male Sprague-Dawley rats were separated into three groups, each containing ten rats. A sham operation was performed in group 1 (control). In group 2 (I-R/untreated), 1 h detorsion of the testis was performed after 6 h of unilateral testicular torsion. In group 3 (I-R/GM), after performing the same surgical procedures as in group II, gabexate mesilate was given intravenously. In all experimental rats, ipsilateral orchiectomies were performed for histological examination and measuring the tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). MDA values and the testicular injury score decreased and SOD, CAT and GSH-Px values increased in the GM-treated group compared to the I-R/untreated group. The Tc-99m pertechnetate uptake ratio and the perfusion index were significantly decreased in the group 2 compared to the group 1 and 3 rats. In group 3, these values were significantly increased compared to group 2. Most of the specimens in the GM-treated group showed grade-I testicular injury. However, the injuries in the I-R/untreated rats varied between grade-III and grade-IV. The results of this study show that GM may play a role in reducing the injury caused by I-R.     

PAF antagonist BN-52021 reduces intercellular adhesion molecule-1 expression and oxidative stress in rats with reperfusion damage due to unilateral testicular torsion

The aim of this study was to determine the effects of specific platelet-activating factor (PAF) antagonist BN-52021 on intercellular adhesion molecule-1 (ICAM) expression and oxidative stress in rats with reperfusion damage due to unilateral testicular torsion. Thirty male Sprague–Dawley rats were separated into three groups, each containing ten rats. A sham operation was performed in group 1 (control). In group 2 [ischemia-reperfusion (I-R)/untreated], 1-h detorsion of the testis was performed after 6 h of unilateral testicular torsion. In group 3 (I-R/BN-52021), after performing the same surgical procedures as in groups II, BN-52021 was given intravenously at the starting time of reperfusion. In all experimental rats, ipsilateral orchiectomies were performed for histological examination and measuring the tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). MDA values and the testicular injury score decreased and SOD, CAT and GSH-Px values increased in the I-R/BN-52021 treated group compared to in the I-R/untreated group. Most of the specimens in the I-R/BN-52021 treated group showed grade-I testicular injury. However, the injuries in the I-R/untreated rats varied between grades III and IV. An ICAM-1 expression was intensive in the interstitial spaces and basement membrane of the tubuli seminiferi, of testicular tissue in the I-R/untreated group. However, an ICAM-1 expression was mild in the I-R/BN-52021 group. BN-52021 may play an important role in the immunohistochemical expression of adhesion molecule ICAM-1 and may reduce oxidative stress in rats with reperfusion damage due to unilateral testicular torsion.     

Effect of unilateral testicular torsion on contralateral testis in a rat model

The aim of this study was to investigate the function of the contralateral testis after unilateral testicular torsion (UTT) and its possible mechanism. 56 rats were randomly divided into four groups: Group A: Sham operation, Group B: Testicular torsion (TT)+normal saline (NS), Group C: Testicular torsion (TT)+cyclosporine, Group D: Testicular torsion (TT)+NG-Monomethyl-l-arginine (l-NMMA). The right testes were removed 1 week and 8 weeks after surgery, respectively. Biochemistry and histopathologic evaluations were used to evaluate the germ cell damage. Compared with Group A, the levels of malondialchehyche (MDA) and nitric oxide (NO)/nitricoxide synthase (NOS) were increased remarkably in Group B. Significant differences were shown between histopathological damages and density and motility of sperm in two groups. Compared with Group B, the levels of MDA and NO/NOS in Group D decreased significantly while mean seminiferous tubule diameter (MSTD) and mean testicular biopsy scoring (MTBS) maintained in a better condition. The levels of major histocompatibility complex (MHC) peptide-tetramer complex in Group C and Group D decreased significantly than Group B, while sperm density and motility were significantly higher than Group B. It was also known that the histopathological damages in Group C and Group D were less than those in Group B in the 8 weeks after operation. UTT can cause impairment of contralateral testicular function and decrease of spermatogenic function. The mechanism may be related to ischemia–reperfusion (IR) in early stage and autoimmune response in late stage.     

Investigation of tyrphostin AG 556 for testicular torsion-induced ischemia reperfusion injury in rat

ObjectiveTo investigate the effects of tyrphostin AG 556, a tyrosine kinase inhibitor (TKI) in an experimental model of testicular ischemia–reperfusion (I/R) injury.Material and methodsTwenty-four adult male rats were randomly divided into four groups (n = 6): sham, torsion/detorsion (T/D), T/D + dimethylsulfoxide (DMSO) (vehicle group), and T/D + DMSO + tyrphostin AG 556. Testicular torsion was achieved by rotating the left testis 720° clockwise for 4 h. Thirty minutes before detorsion, 3 mg/kg tyrphostin AG 556 was injected transperitoneally in the AG 556 group and DMSO was injected transperitoneally in the DMSO group. After 2 h of reperfusion arterial blood samples were collected for biochemical analysis for malondialdehyde (MDA), ischemia modified albumin (IMA), SCUBE1 (signal peptide-CUB [complement C1r/C1s, Uegf, and Bmp1] and EGF [epidermal growth factor] like domain-containing protein 1), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) parameters, and ipsilateral orchiectomies were performed for histopathological examination based on the semi-quantitative Johnsen's mean testicular biopsy score (MTBS) in all groups.ResultsTyrphostin AG 556 exhibited a protective effect against I/R injury in testicular torsion. Of the biochemical parameters evaluated as a result of testicular I/R, IMA, MDA, and TOS levels were significantly elevated. There was no significant difference in terms of these biochemical parameters between the sham and AG 556 groups. Significant histopathological injury was determined by comparing the T/D and sham groups. According to histopathological injury scores, significant differences were determined between T/D and AG 556 groups and between AG 556 and sham groups. AG 556 had a superior improving effect on Johnsen's scores than DMSO.ConclusionsOur results suggest that the use of tyrphostin AG 556 prior to testicular reperfusion has a protective effect against testicular I/R injury.     

Beneficial effects of taurine and carnosine in experimental ischemia/reperfusion injury in testis

Purpose

Testicular torsion can be thought of as an ischemia/reperfusion (I/R) injury to the testis. This study aimed to investigate the effects of taurine (TAU) and carnosine (CAR), which are strong antioxidants, on experimental testicular I/R injury model.

Methods

Male Wistar albino rats were divided into four groups with eight animals in each. A sham operation was performed in group 1. To create testicular I/R, the left testis was torsioned 720° for 2?h followed by 2?h of detorsion. Groups 2 (I/R), 3 (I/R?+?TAU) and 4 (I/R?+?CAR) received intraperitoneal saline, TAU (250?mg/kg) and CAR (250?mg/kg), respectively, 1?h before detorsion. Thiobarbituric acid reactive substances (TBARS), diene conjugate (DC), protein carbonyls (PC), nonprotein sulfhydryl (NPSH), and vitamin C levels were measured in testis tissues as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Histopathological evaluation was also performed.

Results

TBARS, DC, and PC levels were significantly increased in I/R group. TAU and CAR did not alter TBARS levels, but decreased the elevated DC and PC levels. There were no changes in testicular NPSH levels, SOD, and GPx activities in all groups; however, vitamin C significantly decreased in I/R group. CAR treatment was found to increase vitamin C levels as compared to I/R group. Histopathologically, both I/R?+?TAU and I/R?+?CAR groups showed significant increase in testicular spermatogenesis in comparison to I/R group.

Conclusion

Our results indicate that TAU and CAR reduces oxidative stress and may have a protective role in testicular I/R injury.     

Dexpanthenol attenuates lipid peroxidation and testicular damage at experimental ischemia and reperfusion injury

Prevention of tissue damage after testicular torsion caused by I/R injury is still a clinical and experimental problem. There are many experimental studies made with several chemicals in the literature for decreasing the effect of reactive oxygen species after ischemia and reperfusion. Dexpanthenol (Dxp) is the biologically active alcohol of pantothenic acid. Pantothenic acid increases the content of reduced glutathione, Coenzyme A and ATP in cell. We studied the effect of Dxp on lipid peroxidation and testicular damage. Forty adult rats were separated randomly into five groups: group Sh, Sham-operation; group TD, torsion–detorsion; group NS, torsion–normal saline-detorsion; group D, torsion–Dxp 250 mg/kg detorsion; group D2, torsion–Dxp 500 mg/kg detorsion group. Serum MDA levels were taken before detorsion, after torsion at the first and fifth minute and at the first hour. Tissue sample was taken at the first hour. The alterations of I/R injury on testis were histological graded. Serum MDA levels were significantly lower in group D2 compared to all groups. The histopathology score of group D2 was significantly lower than groups TD, NS and D. Histopathological score and serum MDA levels are strikingly compatible. Dxp attenuated lipid peroxidation and tissue damage at I/R injury. This effect depends on its antioxidant effect with increasingly reduced glutathione, Coenzyme A and ATP. The effect of Dxp on I/R injury has been shown for the first time in the experimental testicular torsion.     

Ischemia-reperfusion injury of rabbit ovary and protective effect of trapidil: an experimental study

We aimed to detect the protective effect of trapidil in ischemia–reperfusion (IR) injury due to ovarian torsion and detorsion. Thirty-two pubertal New Zealand albino rabbits were used. Adnexal torsion was created by rotating the left adnexa including the tubal and ovarian vessels in a 360° clockwise direction. Adnexal detorsion was done by untwisting the adnexa. In the IR group, left oopherectomy was performed after 3 h of adnexal torsion and 3 h of adnexal detorsion. In the study group, a 3-h adnexal torsion was performed and trapidil was administered intraperitoneally as a single dose of 40 mg/kg, 1 h before detorsion. The left oopherectomy was performed after a 3-h adnexal detorsion. In the sham group, sham operation was performed followed by left oopherectomy. In the control group, normal ovarian tissue was evaluated. Catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels of ovarian tissue were determined for each group. The values of SOD and GSH-Px activities in the IR group were significantly decreased (P < 0.05). In addition, the MDA level was significantly higher in the IR group (P < 0.01). The trapidil-administered group showed significant increase in the levels of GSH-Px (P < 0.05), catalase (P < 0.05), SOD (P < 0.05), and decreased MDA levels (P < 0.05) compared to those in the IR group. The study has shown that trapidil treatment prevents ischemia induced oxidative damage in the ovarian tissues of rabbits.