Oxidative Stress In Testicular Tissue Research Articles

Effects of boric acid feeding on the oxidative stress parameters in testes, sperm parameters and DNA damage in mice

This study was aimed to determine the effects of boric acid on oxidative stress, testicular tissue and spermatozoon DNA. Experiments were performed with Swiss Albino mice divided equally into two groups based on the tratment period: one for 4 and the other for 6-week duration. These groups were further divided into subgroups as Control and those administered daily at oral doses of 115 mg/kg, 250 mg/kg and 450 mg/kg of boric acid. Then, testicular tissue were examined postmortem and analyzed using ex-vivo biochemical tools for oxidative stress, spermatozoon membrane integrity, sperm motility and live cell rate (%). In both 4 and 6-week groups, v. seminalis weight, membrane integrity, motility, live cells and GSH levels exhibited a decreasing trent compared to the controls. In addition, 6-week group had a decrease in SOD level. MDA level was higher in controls in both 4 and 6-week groups. Spermatozoon DNA was intact in the 4-week group, but damaged in the 6-week group, and the degree of the damage dependent on the administered dose. Boric acid induces oxidative stress in testicular tissue, and its long-term application (only 6 weeks) caused damage in spermatozoon DNA.

The Possible Role of Curcumin against Changes Caused by Paracetamol in Testis of Adult Albino Rat ( Histological, Immunohistochemical and Biochemical Study)

Background: Paracetamol is widely used analgesic which was wrongly thought to be entirely harmless by lots of people. Curcumin has many pharmacological uses such as antibacterial, antiviral, antifungal and anticancer.The aim of the Work: This study aimed to evaluate the histopathological effects of paracetamol on testicular tissue and how far curcumin can protect testicular tissue from these changes.Material and Methods: Twenty eight adult rats were used in this work. Rats were equally divided into four groups. Group I: the control group was divided into(subgroup a,b given distilled water ,corn oil respectively ),Group II: was given curcumin 50mgkg body weight, Group III: was given single daily dose of paracetamol 500mg kg for five days ,Group IV: pretreated with curcumin 50mgkgbody weight for 10 days then received single daily dose of paracetamol 500mgkg in association with curcumin for five days. In the present work, the sperm count, histological and immunohistochemical,biochemical and morphometric studies were evaluated.Results: Paracetamol caused loss of normal architecture of testicular tissue, wide interstitial spaces , loss of stratal arrangement of germinal epithelium with intercellular spacing. Also,reduction in number of +ve vimentin staining Sertoli cells and marked decrease in number and intensity of PCNA positive cells with increased oxidative stress in testicular tissue. Curcumin protected testis against these alterations.Conclusion: Curcumin, is effective in reducing paracetamol testicular toxicity in albino rat, by ameliorating oxidative stress, histopathological and immunhistochemical changes and restoring the normal testicular tissue architecture and function and this can be considered for humans.

Ameliorative effects of rutin against cisplatin-induced reproductive toxicity in male rats

BackgroundCisplatin (CP) or cis-diammine dichloroplatinum (II) is a platinum based standard antineoplastic drug which is used against variety of solid tumors and neoplasms. The present study aimed to evaluate the shielding effects of rutin against CP induced testicular toxicity in rats.Methods28 male rats were divided into four groups. First group was given saline orally while second group received intra-peritoneal (i.p) injection of cisplatin (7 mg/kg) on day first and received saline for next 13 days. Third group received i.p injection of cisplatin at day one and treated with rutin (75 mg/kg) orally for next 13 days. Fourth group was treated with rutin orally for 13 days. Animals were sacrificed on 14th day and reproductive organs were analyzed for various parameters.ResultsCisplatin treatment resulted in a significant decrease in daily sperm production, decrease in head length and % DNA in head, reduction of epithelial cell height, tubular diameter, reduction of the number of spermatogonia, spermatocytes and spermatids, increase in the thiobarbituric acid reactive substances (TBARS) and oxidative stress in testicular tissues, and change of the intra-testicular testosterone concentrations. Rutin co-treatment resulted in reversing cisplatin effect on DNA damage, sperm count, histological and biochemical parameters.ConclusionThese results indicated that rutin co-treatment could ameliorate cisplatin-induced reproductive toxicity in male rats.

Di-(2-Ethylhexyl) Phthalate Increases Obesity-Induced Damage to the Male Reproductive System in Mice.

Objective This study evaluated the effects of di-(2-ethylhexyl) phthalate (DEHP) and obesity on male reproductive organ function in male mice and the potential mechanism of male secondary hypogonadism (SH) in such mice. Methods 140 mice were assigned to six groups for 12 weeks: normal, DEHP, DIO, DIO + DEHP low, DIO + DEHP middle, and DIO + DEHP high. The effects of DEHP and obesity upon the reproductive organs were determined by measuring sperm count and motility, relative testis and epididymis weight, hormone level, and pathological changes. Oxidative stress was evaluated by determining malondialdehyde, T-AOC, SOD, GSH, H2O2, CAT, and GSH-PX in testicular tissues. Nrf2 and Keap1 protein were measured by Western blotting. Results DEHP and obesity reduced sperm count and motility, relative testis and epididymis weight, and testosterone level but increased the levels of MDA, H2O2, leptin, and estradiol. Pathological injury was observed in the testicular Leydig cells. Moreover, the activity of CAT, SOD, and GSH-Px enzymes was inhibited. Nrf2 protein expression was reduced but that of Keap1 was increased. Conclusions DEHP and obesity jointly caused damage to male productive function. Oxidative stress in testicular tissue, and a high level of leptin, may provide some evidence to clarify the mechanisms of male SH with DEHP and obesity.

THE PROTECTIVE ROLE OF SESAME SEED OIL AGAINST PENCONAZOLE-INDUCED OXIDATIVE STRESS IN THE TESTES OF MALE RATS

the present study was carried out to elucidate the potential protective effect of sesame seed oil (Ses) against testicular oxidative stress induced by penconazole fungicide in adult male albino rats. Sixty male rats were divided into six groups, a control group, Ses-supplemented rats, rats treated with penconazole at two doses 30 & 60 mg/kg body weight, which represent 1/20 and 1/10 LD50 respectively, rats co-administered Ses along with penconazole treatment. Testicular redox status was evaluated, including lipid peroxidation (LPO) level, reduced glutathione (GSH) level, catalase (CAT) and superoxide dismutase (SOD) activities and the residues of penconazole in testicular tissue was determined. Penconazole induced oxidative stress in testicular tissue as demonstrated by the significant increase in the lipid peroxidation level as well as the significant reduction in antioxidant activity. In contrast, co-administration of Ses along with penconazole treatment counteracted the induced oxidative stress by lowering lipid peroxidation level and enhancing testicular antioxidant enzymes activities. In addition, residues of penconazole in the testes of treated rats were below the determination limit. In conclusion, supplementation of male rats with sesame seed oil protects the testes against penconazole-induced oxidative stress which could be attributed to the antioxidant property of the sesame seed oil.

Beneficial effects of quercetin on titanium dioxide nanoparticles induced spermatogenesis defects in mice.

Many recent studies have demonstrated that most nanoparticles (NPs) have an adverse or toxic action on male germ cells. In present study, protective effect of quercetin (Que) on titanium dioxide nanoparticle (NTiO2)-induced spermatogenesis defects in mice was investigated. Thirty-two Naval Medical Research Institute (NMRI) mice were randomly divided into four groups. Que group received 75mg/kg of Que for 42days. NTiO2 group received 300mg/kg NTiO2 for 35days. NTiO2 + Que group initially received 75mg/kg Que for 7days and was followed by concomitant administration of 300mg/kg NTiO2 for 35days. Control group received only normal saline for 42days. Sperm parameters, testosterone concentration, histological criteria, and apoptotic index were assessed. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were also evaluated for oxidative stress in testicular tissue. Administration of NTiO2 significantly induced histological changes in testicular tissue; increased apoptotic index; and decreased testicular weight, testosterone concentration, and sperm quality (p<0.01). In the testis, NTiO2 increased oxidative stress through an increase in lipid peroxidation and a decrease in SOD and CAT activities (p<0.05). Que pretreatment could significantly attenuate testicular weight; apoptotic index; and histological criteria including vacuolization, detachment, and sloughing of germ cells in seminiferous tubules. Serum and tissue testosterone levels were significantly increased in Que-pretreated mice (p<0.01). Sperm parameters including sperm number, motility, and percentage of abnormality were also effectively improved by Que pretreatment (p<0.01). Pretreatment of Que significantly ameliorated oxidative stress and increased the activities of SOD and CAT in testicular tissue. These results indicate that sperm production can be increased by Que pretreatment in NTiO2-intoxicated mice. The improved sperm quality and reverse testis histology by Que pretreatment may be a consequence of elevation testosterone concentration, reduction in germ cell apoptosis, and suppression of oxidative stress in testicular tissue.

Effects of strontium fructose 1,6‐diphosphate on expression of apoptosis‐related genes and oxidative stress in testes of diabetic rats

To investigate the effects of strontium fructose 1,6-diphosphate (FDP-Sr) on testicular dysfunction induced by diabetes. Diabetes was induced by a single injection of streptozotocin (65 mg/kg, i.p.). After 28 days, therapy with three doses (50, 100, and 200 mg/kg per day, p.o.) of FDP-Sr was carried out for another 4 weeks. The rats exhibited morphological lesions of testes and significant decreases in serum testosterone levels after 2 months of diabetes. Testicular tissues of diabetic rats showed significantly increased malondialdehyde levels and declined glutathione peroxidase activity. Meanwhile, augmented DNA fragmentation was observed, along with downregulated Bcl-2 and upregulated Bax expressions at both mRNA and protein levels. FDP-Sr showed significant antioxidant effects in both in vitro and in vivo experiments, and significantly relieved apoptosis and the decline of serum testosterone caused by diabetes. Testicular injury and apoptosis induced by diabetes are partially attributed to the augmented oxidative stress in testicular tissue. FDP-Sr indirectly alleviates these pathologic alterations by suppressing the generation of reactive oxygen species.

Levels of oxidative stress parameters and the protective effects of melatonin in psychosis model rat testis

To evaluate the effects of melatonin on antioxidant enzyme levels and histopathologic changes in dizocilpine (MK-801)-induced psychosis model rat testis. A total of 24 adult male Wistar-Albino rats were divided into three groups with 8 in each. Group I was used as control. Rats in Group II were injected with MK-801 (0.5 mg/kg body weight i.p. for 5 days). In addition to MK-801, melatonin (50 mg/kg body weight i.p. once a day for 5 days) was injected into the rats in Group III. The testes were harvested bilaterally for biochemical and histopathological examinations. Antioxidant enzyme activities, malondialdehyde, protein carbonyl and nitric oxide (NO) levels in testicular tissues were analyzed using spectrophotometric analysis methods. Histopathological examinations of the testes were also performed. MK-801 induced testicular damage, which resulted in significant oxidative stress (OS) by increasing the levels of antioxidant enzymes. The malondialdehyde, protein carbonyl and NO levels were increased in testicular tissues of rats. Treatment with melatonin led to significant decrease in oxidative injury. Administration of melatonin also reduced the detrimental histopathologic effects caused by MK-801. The results of the present study showed that MK-801 cause OS in testicular tissues of rats and treatment with melatonin can reduce the harmful effects of MK-801.

Oxidative stress in testicular tissues of rats exposed to cigarette smoke and protective effects of caffeic acid phenethyl ester

To show the oxidative stress after cigarette smoke exposure in rat testis and to evaluate the effects of caffeic acid phenethyl ester (CAPE). Twenty-one rats were divided into three groups of seven. Animals in Group I were used as control. Rats in Group II were exposed to cigarette smoke only (4 x 30 min/d) and rats in Group III were exposed to cigarette smoke and received daily intraperitoneal injections of CAPE (10 micromol/kg x d). After 60 days all the rats were killed and the levels of nitric oxide (NO) and anti-oxidant enzymes such as superoxide-dismutase, catalase and glutathione peroxidase (GSH-Px) and the level of malondialdehyde were studied in the testicular tissues of rats with spectrophotometric analysis. There was a significant increase in catalase and superoxide-dismutase activities in Group II when compared to the controls, but the levels of both decreased after CAPE administration in Group III. GSH-Px activity was decreased in Group II but CAPE caused an elevation in GSH-Px activity in Group III. The difference between the levels of GSH-Px in Group I and Group II was significant, but the difference between groups II and III was not significant. Elevation of malondialdehyde after smoke exposure was significant and CAPE caused a decrease to a level which was not statistically different to the control group. A significantly increased level of NO after exposure to smoke was reversed by CAPE administration and the difference between NO levels in groups I and III was statistically insignificant. Exposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects.