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Testicular Damage (testicular + damage)
Selected AbstractsDisruption effects of monophthalate exposures on inter-Sertoli tight junction in a two-compartment culture modelENVIRONMENTAL TOXICOLOGY, Issue 3 2008Yun-Hui Zhang Abstract Phthalates are suspect environmental endocrine disruptors that may affect male reproduction and development by disturbing androgen synthesis and cell,cell interactions in the seminiferous epithelium. The in vivo metabolites, monophthalates, are thought to be the active agents, and toxicant effects including testicular damage and decreased sperm motility have been described previously. In this study, the aim was to investigate the effect of monophthalates on Sertoli cells using a two-compartment cell culture model, asking whether tight junction protein structures are affected, compromising the blood-testis barrier and contributing to male-mediated toxicity. Sertoli cells were isolated from Sprague Dawley rat testes and seeded onto the filters of two-compartment wells. A Sertoli cell monolayer was allowed to form, whereupon the cultures were treated with 0, 10, 30, 150, and 600 ,mol/L monobutyl phthalate (MBP) or mono-2-ethylhexyl phthalate (MEHP) for 24 h. Effects on the tight junctions between adjacent Sertoli cells were studied by light and transmission electron microscopy, the transepithelial electrical resistance (TEER) assay, and immunofluorescence localization. Results showed that exposures to monophthalates destroyed tight junctional structure in Sertoli cell monolayers in a dose-depended manner, as evidenced by a loss of single-cell layer organization in the cultures, decline of TEER value, and decreased expression of proteins associated with tight junctions such as zonula occludens-1 (ZO-1), F-actin, and Occludin. The changes were observed at doses of 150 and 600 ,mol/L, which is 10,100 times higher relative to estimated human exposures from the environment. These results are consistent with monophthalate-induced damage to tight junctions between adjacent Sertoli cells, suggesting that damage to Sertoli cell tight junctions induced by monophthalates may be an underlying mechanism of their male-mediated reproductive toxicity. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008. [source] Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in ratsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005Mukaddes E Abstract Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury. [source] Testosterone administration promotes regeneration of chemically impaired spermatogenesis in ratsINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2006KOICHI UDAGAWA Aim: It has been proposed that gonadotropin-releasing hormone (GnRH) analog administered after testicular damage stimulates the recovery of spermatogenesis. However, GnRH analogs suppress the function of sex accessory organs. In this study, we investigated whether testosterone also stimulates the regeneration of rat spermatogenesis after exposure to busulfan. Methods: Male Fisher rats were divided into three groups of five each and all rats were treated with busulfan, 25 mg/kg, intraperitoneally at week 0. Group A served as the control. The other two groups received testosterone enanthate, 8 mg/kg, subcutaneous injections at 3 week intervals two times before (group B) or three times after (group C) busulfan. States of spermatogenesis were evaluated by histology and by the number of spermatid nuclei per testis at week 25. Results: The mean percentage of ,recovered' seminiferous tubules plus or minus standard deviation was 10.3 ± 7.8% in group A and 2.1 ± 1.2% in group B. In both groups, more than 80% of the tubules remained degenerated. However, testes of group C rats showed an improvement of up to 37.1 ± 20.5% (P < 0.05). The significant recovery of spermatogenesis was also demonstrated in group C by counting the number of spermatid nuclei per testis ([78.8 ± 57.5] ×106). However, the count was only (7.6 ± 13.5) ×106 and (0.52 ± 1.0) ×106 in group A and B, respectively. Conclusions: Testosterone administration after severe testicular damage enhanced the regeneration of spermatogenesis in rats. We assumed that supplementary doses of testosterone would be more practical for clinical application than GnRH analogs, because exogenous testosterone maintains androgenicity. [source] Effects of primary testicular damage on sperm DNA oxidative status and embryonic and foetal developmentANDROLOGIA, Issue 5 2009F. Dimitriadis Summary We evaluated the development of embryos generated from the fertilisation of oocytes with spermatozoa isolated from animals with primary testicular damage (PTD). Embryos derived in vivo or in vitro from oocytes fertilised with spermatozoa produced by PTD rats that had undergone surgical treatment for the PTD (group A1), or PTD rats (group A2), or control rats (group B) were cultured and transferred to recipients. At the end of the experimental period, the fertilisation potential of each rat was assessed in vitro (IVF trials). Sperm 8-oxodG/dG ratio (a marker of DNA oxidative status) was significantly larger in group A2 than in groups A1 and B. Blastocysts of the group A2 transferred to recipients demonstrated a significantly larger loss before implantation than transferred blastocysts of groups A1 or B. In addition, the proportion of implanted blastocysts that could not complete the intrauterine development was significantly larger in group A2 than in groups A1 and B. This study reveals a post-fertilisation detrimental effect in animals with PTD on the capacity of oocytes (fertilised either in vitro or in vivo) to develop in vitro and implant after transferring them to recipients probably attributable to sperm DNA oxidative damage. [source] Protective effect of L -carnitine on testicular ischaemia,reperfusion injury in rats,CELL BIOCHEMISTRY AND FUNCTION, Issue 6 2007Dikmen Dokmeci Abstract Testicular torsion is a urological emergency referred to as ,acute scrotum', because inappropriate treatment can lead to male subfertility and infertility. A possible cause of testicular damage is the ischaemia,reperfusion (I/R) injury attributed to oxygen free radicals. L -carnitine, a vitamin-like antioxidant, plays a pivotal role in the maturation of spermatozoa within the reproductive tract. The aim of the present paper was to determine the protective effect of L -carnitine on testicular I/R-induced injury. Thirty-two male rats were divided into 4 groups (n,=,8). Testicular torsion was created by rotating the right testis 720° in a clockwise direction. Group 1: sham-operated control; group 2: ischaemia; group 3: I/R; group 4: ischaemia,L -carnitine treatment,reperfusion group. L -carnitine (500,mg,kg,1, intraperitoneally) was administered before 30 min of detorsion in Group 4. After torsion (5,h) and detorsion (5,h), bilateral orchidectomy was performed. The malondialdehyde (MDA) level was evaluated in testes. Histopathologically, Johnsen's spermatogenesis criteria and mean seminiferous tubule diameter (MSTD) measurements were used. Testicular MDA levels were higher in the torsion group compared to the sham-control group (p,<,0.05). Detorsion (reperfusion) caused a further increase in MDA levels (p,<,0.05). Pretreatment with L -carnitine prevented a further increase in MDA levels (p,<,0.05). Histologically, torsion caused some separation among germinal cells in the seminiferous tubules, which became much more prominent in the I/R group but was attenuated with L -carnitine pretreatment. In conclusion, L -carnitine pretreatment may have a protective effect in experimental testicular torsion,detorsion model in rats by its well-known antioxidant potential. Copyright © 2006 John Wiley & Sons, Ltd. [source] ROSIGLITAZONE, AN AGONIST OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-GAMMA, PREVENTS CONTRALATERAL TESTICULAR ISCHAEMIA,REPERFUSION INJURY IN PREPUBERTAL RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2007Mustafa Inan SUMMARY 1Rosiglitazone plays a positive role in the reparation of ischaemia,reperfusion (I/R) injury in different tissues. Thus, we examined its biochemical and histological effects on the contralateral testes to determine whether exogenous rosiglitazone affords any protection against testicular damage. 2Forty-eight prepubertal male Wistar-Albino rats were divided into six groups. Testicular torsion was created by rotating the right testis 720° in a clockwise direction for 5 h in all groups except group I, which was the sham-control group. In group II, bilateral orchiectomy was performed following the torsion period. After detorsion both testes were removed in the fifth hour in group III and on the seventh day in group IV. In group V, one-shot rosiglitazone (4 mg/kg) was administered 40 min before detorsion and both testes were removed following the torsion period. In group VI, rosiglitazone was administered (4 mg/kg) 40 min before detorsion and for 7 days, and then both testes were harvested. The tissue levels of malondialdehyde (MDA) were measured and mean testicular biopsy score (MTBS) and mean seminiferous tubule diameter (MSTD) were examined. Immunoexpression of endothelial nitric oxide synthase (eNOS) in testes tissues was investigated by immunohistochemical studies. 3In the contralateral testis, the MTBS and MSTD values of group VI were significantly higher than those in group IV. Immunohistochemically, mild eNOS immunostaining was present in the germ cells of the contralateral testes in group IV after I/R. In group VI, intense eNOS immunoreactivity was seen in the contralateral testes. 4Rosiglitazone reduces contralateral testicular damage formed after unilateral testicular torsion and alleviates the oxidative events. [source] | ||||||||||