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.     

大鼠隐睾、隐睾下降固定对生殖细胞发育、凋亡影响的实验研究

目的　探讨大鼠隐睾、隐睾下降固定对生殖细胞发育、凋亡的影响。方法　 6 8支SD雄性大鼠 ,分为三组 :隐睾组 (5 2 ) ;隐睾下降固定组 (8)及对照组 (8)。于日龄 2 2d时复制单侧隐睾模型 ,一部分于单侧隐睾模型术后 14d复制隐睾下降固定模型。采用生物素 dUTP/酶标亲和素测定法检测睾丸生殖细胞凋亡。结果　 1.单侧隐睾模型术后第 13d内隐睾侧睾丸生殖细胞凋亡指数随时间的延长而增加 ;从术后第 4天起 ,与自身对侧正常睾丸 (4.8± 0 .9) %相比 ,隐睾侧睾丸 (11.2±3.6 ) %发生凋亡的生殖细胞数显著增加 (P <0 .0 1)。 2 .与隐睾组 (47.5± 8.6 ) %相比 ,隐睾下降固定组 (6 .2± 1.8) %发生凋亡的生殖细胞数显著降低 (P <0 .0 1)。结论　 1.大鼠隐睾模型建立术后13d内隐睾侧睾丸生殖细胞凋亡指数随时间的延长而增加 ;2 .在日龄 36d时隐睾下降固定能使大鼠隐睾恢复正常的生精功能 ;3.隐睾患儿应及早施行睾丸下降固定术 ,可以恢复其生育能力。     

人绒毛膜促性腺激素对单侧隐睾大鼠睾丸生殖细胞凋亡的影响

目的探讨人绒毛膜促性腺激素（HCG）对单侧隐睾大鼠睾丸生殖细胞凋亡的影响。方法将sD雄性大鼠40只随机分为单侧隐睾组和假手术组，各20只，于日龄21d制备单侧隐睾模型。单侧隐睾组和假手术组各又分为HCG治疗组和未治疗组。日龄22d时HCG治疗组开始肌肉注射HCG20U，隔日1次，共7次。日龄35、60d时处死大鼠，取其睾丸，采用生物素-dUTP／酶标亲和素法（TUNEL法）检测其生殖细胞凋亡水平。结果单侧隐睾组隐睾睾丸生殖细胞凋亡指数（AI）高于假手术组，但无统计学差异（P〈0．05）；单侧隐睾各组对侧睾丸生殖细胞AI高于假手术未治疗组（P〉0．05）。假手术和单侧隐睾模型HCG治疗组阴囊内睾丸生殖细胞AI高于相应未治疗组，且35d假手术组治疗组与未治疗组间差异有统计学意义（P〈0．05）。60d单侧隐睾HCG治疗组大鼠隐睾侧睾丸生殖细胞AI高于相应未治疗组，但无统计学差异（P〉0．05）。结论单侧隐睾时不仅患侧睾丸生殖细胞凋亡增加，而且隐睾对侧阴囊内睾丸生殖细胞凋亡也增加；HCG的应用可加重睾丸生殖细胞凋亡，且停用后仍存在着一些不可逆的病理损害，故临床应用HCG要慎再，应尽早手术治疗。     

单侧隐睾大鼠对侧睾丸组织中SCF/c-kit基因表达变化及意义

目的 研究单侧隐睾大鼠对侧睾丸病理变化及SCF/c-kit基因表达,探讨单侧隐睾致对侧睾丸损害的机制.方法 30只SD大鼠随机分为对照组和实验组,实验组复制单侧(左侧)腹腔隐睾模型.3个月后分别取两组右侧睾丸组织进行real-time RT-PCR、Western blot及免疫组化检测干细胞生长因子(SCF)和其受体c-kit基因及其蛋白表达变化,TUNEL法检测细胞凋亡.结果 所有动物均存活,与对照组相比实验组对侧睾丸明显缩小,光镜下观察其曲细精管发生退化,生精上皮变薄,管腔较空,生殖细胞明显减少,细胞凋亡增加.两组凋亡指数分别为14.4±0.63和4.45±0.37,差异有统计学意义(P＜0.05).荧光实时定量PT-PCR检测SCF、c-kit基因mRNA含量,实验组对侧睾丸明显降低,两组相比差异有统计学意义(P＜0.05).Western blot检测SCF及c-kit蛋白表达含量,实验组对侧睾丸同样明显降低,两组相比差异有统计学意义(P＜0.05).免疫组化染色显示各级生精细胞膜均有c-kit表达,SCF主要表达于支持细胞膜表面,但实验组两者的表达均较对照组减弱.相关性检验SCF与AI相关系数r=-0.941,P＜0.01;c-kit与AI相关系数r=-0.908,P＜0.01;SCF与c-kit相关系数r=0.956,P＜0.01,均有统计学意义.结论 单侧隐睾可致对侧睾丸SCF/c-kit基因表达减弱,生精细胞凋亡增加引起不育.     

人绒毛膜促性腺激素对内分泌型双侧隐睾大鼠生精细胞凋亡的影响

目的探讨人绒毛膜促性腺激素(HCG)对内分泌型双侧隐睾大鼠生精细胞凋亡的影响。方法取60只SD大鼠,随机抽取20只作为正常对照组,余40只采用皮下注射17-β雌二醇方法制成双侧隐睾模型,随机分为隐睾+HCG组、隐睾+9 g.L-1盐水组(隐睾+NS组)。隐睾+HCG组自日龄26 d起隔日肌注HCG 20 U,共10次;隐睾+NS组自日龄26 d起隔日肌注9 g.L-1盐水1 mL,共10次。于日龄45 d、60 d每组各抽10只采集血清,取其睾丸组织后处死。采用ELISA间接法测定其血清抗精子抗体(AsAb)水平,放射免疫方法测其血清雌二醇(E2)、睾酮(T)水平,生物素-脱氧尿嘧啶核苷三磷酸(dUTP)/酶标亲和素(TUNEL)法检测其生殖细胞凋亡指数(AI)。结果日龄45 d和60 d时,隐睾+HCG组双侧睾丸生殖细胞AI均明显高于同日龄其他各组(Pa<0.01);隐睾+HCG组血清E2水平较同日龄其余各组均显著增高(Pa<0.01),而血清T水平均降低(Pa<0.01);隐睾+HCG组AsAb水平均高于同日龄其他组(Pa<0.01)。结论 HCG注射治疗双侧隐睾大鼠不仅能增加AsAb产生,且能加重睾丸生殖细胞的凋亡。     

绒毛膜促性腺激素对双侧隐睾大鼠睾丸生殖细胞凋亡的影响

目的探讨绒毛膜促性腺激素(HCG)对双侧隐睾生殖细胞凋亡的影响。方法SD雄性幼鼠于日龄22d制备双侧隐睾模型(模型组)后开始隔日肌注HCG20U,共7次。假手术组作为对照。日龄35、60d时处死取睾丸,采用生物素-dUTP/酶标亲和素(TUNEL)法检测生殖细胞凋亡情况。结果模型组双侧隐睾睾丸凋亡指数(AI)高于假手术组。35d假手术HCG治疗组AI高于假手术HCG未治疗组(P<0.05)。60d各HCG治疗组睾丸的AI高于相应HCG未治疗组,组间比较无显著差异(P>0.05)。结论隐睾时睾丸生殖细胞凋亡增加;HCG可增加生殖细胞的凋亡。     

冷诱导RNA结合蛋白在小鼠隐睾中的表达及与生精细胞损害的关系

目的 探讨冷诱导RNA结合蛋白(cold inducible RNA-binding protein,CIRP)在小鼠隐睾睾丸中的表达,及其与隐睾生精细胞损害的关系.方法 雄性BALB/c小鼠20只用手术的方法建立左侧隐睾模型,分别于术后第7天和第10天取双侧睾丸称重,光镜下观察睾丸组织学变化,RTPCR法检测睾丸CIRP mRNA的表达水平,Western-blot检测睾丸CIRP蛋白的表达水平,并用Annexin V-FITC/PI双染流式细胞仪检测生精细胞凋亡.结果 CIRP强表达于正常小鼠睾丸中,隐睾模型建立后,隐睾睾丸CIRP mRNA和蛋白的表达水平均明显降低(P<0.05),术后第10天隐睾睾丸CIRP表达水平明显低于第7天(P<0.05).同时隐睾侧睾丸重量较对侧睾丸明显减轻(P<0.05),术后第10天对侧睾丸重量明显重于第7天(0.102±0.006)g比(0.080±0.005)g(P<0.05);而术后第7天和第10天隐睾睾丸重量相比,(0.072±0.007)g比(0.062±0.004)g(P>0.05),差异无统计学意义.另外生精细胞的凋亡明显增加(P<0.05),术后第10天隐睾侧睾丸的生精细胞凋亡率明显高于第7天(29.2%±1.3%)比(20.2%±1.6%)(P<0.05);而对侧睾丸生精细胞凋亡率无明显差异(5.8%±1.5%)比(5.6%±1.8%)(P>0.05).组织切片显示隐睾侧睾丸生精上皮变薄,生精细胞排列紊乱.结论 小鼠隐睾中CIRP的表达明显降低,CIRP表达的降低可能在隐睾生精细胞损害中起着重要的作用.     

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.     

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.     

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.     

Division of the genitofemoral nerve in normal scrotal testicular rats

The role of the genitofemoral nerve (GFN) on testicular descent has been clearly shown. It has also been suggested that in unilateral cryptorchid rats, after division of the ipsilateral GFN fertility rates are higher, i.e., transection of the GFN prevents contralateral testicular damage, but the mechanism is unclear. The purpose of this study was to investigate the effect of dividing the GFN on the normal scrotal testes. Thirty male Wistar albino rats were divided into three groups: group A, transection of right GFN; group B, bilateral transection of the GFN; and group C, sham operations, all at the age of 30 days. The animals were killed at 90 days of age and the testes were removed. Each excised testis was weighed and fixed for histological studies. Mean seminiferous tubular diameter was measured and germinal epithelium maturity was determined using the modified Johnsen testicular-biopsy score. In all groups, all three parameters were similar, suggesting that division of the GFN had no effect on normal testes. Accepted: 12 January 2000     

Effect of diclofenac on germ cell apoptosis following testicular ischemia-reperfusion injury in a rat

Recent evidence suggests that enhanced cell apoptosis is responsible for germ cell loss following testicular ischemia-reperfusion (IR) injury. A nonsteroidal anti-inflammatory drug diclofenac sodium (Voltaren) is a prostaglandin-synthesis inhibitor, which is widely used in many testicular disorders. The purpose of the present study was to examine the effect of diclofenac (DIC) on germ cell apoptosis in the ischemic and contralateral testes following testicular IR in a rat. Forty rats were divided randomly into four experimental groups of ten rats each: group A (Sham)—Sham operated animals; group B (Sham-DIC)—Sham operated rats that were treated with DIC given subcutaneously at a dose of 10 mg/kg, once daily, 24, 48 and 72 h following operation; group C (IR) underwent 90 min of unilateral testicular IR; group D (IR-DIC)—rats underwent 90 min of unilateral testicular IR and were treated with DIC similarly to group B. Ninety-six hours following operation, the rats were sacrificed and testes were harvested. Johnsen’s criteria and the number of germinal cell layers were used to categorize the spermatogenesis. TUNEL assay was used to determine germ cell apoptosis in both the ischemic and contralateral testes. Statistical analysis was performed using the non-parametric Kruskal–Wallis ANOVA test, with P less than 0.05 considered statistically significant. Testicular ischemia in rats led to histological damage in the ipsilateral testis. In the contralateral testis, minimal damage was observed. Germ cell apoptosis in both the ischemic and the contralateral testes increased significantly after IR. Treatment with DIC did not change histologic parameters of spermatogenesis in both the ischemic and contralateral testes, but decreased germ cell apoptosis in both testes following testicular IR. We conclude that testicular ischemia causes an increase in germ cell apoptosis in the contralateral testis. Diclofenac may be beneficial for spermatogenesis following testicular IR by decreasing germ cell apoptosis.     

Division of the genitofemoral nerve and late orchiectomy: effects on the contralateral testis in ipsilateral testicular torsion

Unilateral torsion of the spermatic cord has been demonstrated to damage the contralateral testis; however, the pathogenesis has not yet been examined in detail. The purpose of this study was to evaluate the influence of unilateral torsion on the contralateral testis in rats by performing ipsilateral division of the genitofemoral nerve (GFN) and/or late orchiectomy. Male 25-day-old, prepubertal Wistar albino rats were divided into five groups: (1) sham operation; (2) unilateral testicular torsion; (3) simultaneous unilateral testicular torsion and ipsilateral GFN division; (4) unilateral testicular torsion and orchiectomy on the 4th day after torsion; and (5) simultaneous unilateral testicular torsion and GFN ipsilateral division, and orchiectomy on the 4th day after torsion. Torsions performed were 720°, all on the right testes. On day 55 after torsion, which represents the early postpubertal period of the rat, the contralateral testes were removed. Tubular biopsy score (TBS) was calculated, and seminiferous tubular diameters (STD) were measured. Student's t-test was used for statistical analysis. There was no contralateral testicular damage in the control group, but in all of the study groups destructive changes were found in the left gonad after torsion of the right testicle. The mean TBS of the study groups was higher than that of the control group. STD values were lower in the study groups, but the differences were not statistically significant between groups. In prepubertal rats, unilateral torsion causes histologically measurable changes in the contralateral testis. Ipsilateral division of the GFN and late orchiectomy did not cause any significant alterations in terms of contralateral damage. Further investigations are needed to determine the role of the GFN in testicular torsion.     

Effect of testicular ischemia-reperfusion on recruitment of neutrophils,E-selectin expression and germ cell apoptosis in the contralateral testis in a rat

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.     

Effect of allopurinol on germ cell apoptosis following testicular ischemia–reperfusion injury in a rat

Recent evidence suggests that apoptosis is involved in germ cell loss following testicular ischemia-reperfusion (IR) injury. Allopurinol (Allo) is as a free radical scavenger which prevents tissue damage caused by reperfusion and oxygenation after ischemia; however, its effect on apoptosis in this type of injury has not been studied. To examine the effect of allopurinol on germ cell apoptosis following testicular IR in a rat. Forty rats were divided randomly into 4 experimental groups of 10 rats each: group A (Sham)-Sham operated animals; group B (Sham-Allo)-Sham operated rats treated with allopurinol given PO (by gavage) at a dose of 200 mg/kg, once daily, immediately before and 24 h following operation; group C (IR)-rats underwent 90 min of unilateral testicular ischemia and 48 h of reperfusion; group D (IR-Allo)-rats underwent IR and were treated with allopurinol similar to group B. The ipsilateral and contralateral testes were harvested 48 h following operation. Johnsen's criteria and the number of germinal cell layers were used to categorize spermatogenesis. TUNEL assay was used to determine germ cell apoptosis. Statistical analysis was performed using one-way ANOVA test, with P < 0.05 considered statistically significant. Testicular ischemia in rats led to histological damage in the ipsilateral testis. In the contralateral testis minimal damage was observed. Treatment with allopurinol increased significantly Johnsen's score in both the ischemic (7.3 +/- 0.5 vs 5.6 +/- 0.5, P < 0.05) and contralateral (8.9 +/- 0.1 vs 8.3 +/- 0.2, P < 0.05) testis, compared to IR-animals. Germ cell apoptosis in both the ischemic and the contralateral testis increased significantly after IR. Treatment with allopurinol resulted in a significant decrease in germ cell apoptosis in the ipsilateral testis, expressed as the number of positive tubules per 100 tubules (AI-1, (apoptotic index) threefold decrease, P < 0.005) and the number of apoptotic cells per 100 tubules (AI-2, fivefold decrease, P < 0.005) as well as a significant decrease in germ cell apoptosis in the contralateral testis (AI-1, 3.5-fold decrease, P < 0.05, AI-2- sixfold decrease, P < 0.005) compared to IR animals. In a rat model of testicular IR, treatment with allopurinol decreases germ cell apoptosis in both ischemic and contralateral testes and improves spermatogenesis.     

The effect of the genitofemoral nerve division on the contralateral descended testis in the unilateral cryptorchidism model

It is widely accepted that there are degenerative changes and decreased spermatogenesis in the contralateral descended testis (CDT) in unilateral undescended testis (UUDT). While some investigators have postulated that the mechanism may be related to primary (congenital) or secondary (autoimmune, vascular, and neural) events, the exact mechanism of the damage to the CDT is still unknown. The present study was planned to investigate the role of the genitofemoral nerve (GFN) on the changes in the CDT. Forty male Wistar albino rats were divided into four groups of 10 each. During the newborn period a UUDT model was created and at the age of 30 days ipsilateral GFN division was done (group A). In addition, UUDT with intact GFN (group B), divided right GFN with bilateral scrotal testes (group C), and control (group D) groups were formed. When the animals reached early adulthood, they were killed and the testes were removed. Mean seminiferous-tubular diameter (STD) and germinal-ephitelium maturity was determined using modified Johnson testicular biopsy scores (TBS). The mean STD and TBS of the study groups did not show any differences suggesting that ipsilateral division of the GFN has no effect on the CDT in the UUDT model. Accepted: 11 August 2000     

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.     

Resveratrol may reduce apoptosis of rat testicular germ cells after experimental testicular torsion.

The aim of the study is to evaluate the effects of resveratrol on apoptosis of testicular germ cells after experimental testicular torsion. Thirty Wistar albino rats were divided into 3 groups. Torsions were created by rotating the right testis 720 degrees in a clockwise direction for 4 h in all groups except the control group (group 1). They were then repaired by counter-rotation and replaced into the scrotum. In group 2, saline was infused 30 min before detorsion. In group 3, 30 mg/kg resveratrol was infused 30 min before detorsion. In groups 2 and 3, the bilateral testes were removed to determine germ cell apoptosis after 20 h of detorsion. The number of apoptotic cells was evaluated using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) technique and caspase 3. Mean apoptotic score of ipsilateral testes in group 3 was lower than that of group 2 (p < 0.05). Mean apoptotic score of the contralateral testes in group 3 was not different from that of group 2 (p > 0.05). The present study demonstrates that intraperitoneal administration of resveratrol in rats may decrease germ cell apoptosis in the ipsilateral testes.     

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.