Male Reproductive Organs Of Rats Research Articles

Echis ocellatus venom-induced sperm functional deficits, pro-apoptotic and inflammatory activities in male reproductive organs in rats: antagonistic role of kaempferol

BackgroundEchis ocellatus envenoming is potentially toxic initiating clinical damages on male reproductive system. Kaempferol is a therapeutic agent with neutralizing potentials on snake venom toxins. This study investigated the antagonistic effect of kaempferol on E. ocellatus venom (EoV)-induced reproductive toxicities.MethodsFifty adult male rats were sorted at random into five groups of ten rats for this study. The control rats were allotted to group 1, while rats in groups 2–5 were injected with 0.22 mg/kg bw (LD50) of EoV intraperitoneally. Rats in group 2 were not treated while groups 3–5 rats were treated with serum antivenom (0.2 ml), and 4 and 8 mg/kg bw of kaempferol post envenoming, respectively.ResultsEoV actuated reproductive toxicity, significantly decreased sperm parameters, and enhanced inflammatory, oxidative stress, and apoptotic biomarkers in reproductive organs of untreated envenomed rats. However, treatment with kaempferol alleviated the venom-induced reproductive disorders with a dose dependent effect. Kaempferol significantly increased the testicular weight, organo-somatic index, sperm parameters, and normalized the levels of serum luteinizing hormone, testosterone, and follicle stimulating hormone. Kaempferol ameliorated testicular and epididymal oxidative stress as evidenced by significant decrease in malondialdehyde (MDA) levels, enhancement of reduced glutathione (GSH) levels, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. The inflammatory biomarkers; nitric oxide (NO) levels and myeloperoxidase activity (MPO), and apoptotic biomarkers; caspase 3 and caspase 9 activities were substantially suppressed in the testis and epididymis of envenomed rats treated with kaempferol.ConclusionResults revealed kaempferol as a potential remedial agent against reproductive toxicity that could manifest post-viper envenoming.

Testicular histopathology in rats co-exposed to heat and psychological stressors

ObjectivesThe present study aimed to investigate the effect of co-exposure to heat and psychological stressors on testicular tissue as one of the major male reproductive organs in rats. MethodsForty adult male Wistar rats were divided into four groups of 10 animals each. The first group was exposed to heat stress (Temperature Humidity Index: 57.75 ± 3), the second group was exposed to three psychological stressors including strobe light ultrasonic sound, and tilting cage, and the third group was co-exposed to both heat and psychological stress daily. The order of exposure to various psychological stressors was randomized. Following the last day of the 40 -day exposure, the rats were euthanized and their testicular tissues were fixed in Bouin's solution. Moreover, a tissue processor, a microtome as well as hematoxylin, and eosin staining were used for tissue preparation. ResultsThe co-exposure to psychological and heat stress can cause negative testis histopathological changes including spermatid retention, degeneration of round spermatids and spermatocytes, degeneration and depletion of elongated Spermatid, Sertoli cell status, tubular degeneration/atrophy, Leydig cell atrophy, tubular dilatation, re-tubular dilation, and sclerosis status in a number of rats. Moreover, the histopathological changes were higher in the group exposed to heat stress compared with those exposed to psychological stress. ConclusionsAlthough exposure to either stressor alone can affect testicular tissue as part of the reproductive system, co-exposure to both stressors may result in an increased risk of adverse effects on testicular tissue.

Alpha-Lipoic Acid Protects Co-Exposure to Lead and Zinc Oxide Nanoparticles Induced Neuro, Immuno and Male Reproductive Toxicity in Rats.

We evaluated the neuro-, immuno-, and male reproductive toxicity of zinc oxide nanoparticles (ZnO NPs) alone and in combination with lead acetate. We also studied the therapeutic role of α-lipoic acid postexposure. Lead (10 mg/kg, body weight), ZnO NPs (100 mg/kg, bwt) alone, and their combination were administered orally in Wistar rats for 28 days, followed by the administration of α-lipoic acid (15 mg/kg, bwt) for the next 15 days. Our results demonstrated protective effects of α-lipoic acid on lead and ZnO NP–induced biochemical alterations in neurological, immunological, and male reproductive organs in rats. The altered levels of blood δ-aminolevulinic acid dehydratase (ALAD), immunoglobulins (IgA, IgG, IgM, and IgE), interleukins (IL-1β, IL-4, and IL-6), caspase-3, and tumor necrosis factor (TNF-α) were attenuated by lipoic acid treatment. Lead and ZnO NP–induced oxidative stress was decreased by lipoic acid treatment, while a moderate recovery in the normal histoarchitecture of the brain section (cortex and hippocampus) and testes further confirmed the neuro- and male reproductive toxicity of lead and ZnO NPs. We also observed a significant decrease in the blood metal content in the animals treated with lipoic acid compared to the lead-administered group, indicating the moderate chelating property of lipoic acid. It may thus be concluded that lipoic acid might be a promising protective agent against lead and ZnO NP–induced alterations in the neurological, immunological, and reproductive parameters.

Toxic pathological effect of mitomycin-c on male reproductive organs in rat

Toxic pathological effect of mitomycin-c on male reproductive organs in rat

Regucalcin is widely distributed in the male reproductive tract and exerts a suppressive effect on in vitro sperm capacitation in the water buffalo (Bubalus bubalis).

Regucalcin is a multi-functional, calcium-binding protein with roles in calcium homeostasis, apoptosis, cell proliferation, and free radical neutralization. Regucalcin is broadly expressed in the male reproductive organs of rat and bovine; here, we report its expression in the reproductive tract of male buffalo-especially in testis, epididymis, seminal vesicle, prostate, and bulbourethral gland of buffalo-as analyzed by real-time PCR, Western blot, and immunolocalization. Regucalcin degradation in seminal plasma, despite its high abundance in vesicular fluid, was demonstrated using recombinant regucalcin co-incubated with buffalo seminal plasma. This depletion of regucalcin appears to be related to its suppressive effect on in vitro sperm capacitation, observed using the chlortetracycline assay after treating buffalo spermatozoa with recombinant protein. Indeed, addition of recombinant regucalcin to capacitating media significantly reduced (P < 0.05) the percentage of capacitated spermatozoa to 6.1 ± 0.6 from 36.4 ± 1.8 in the untreated group. Taken together, the wide distribution of regucalcin in male buffaloes, versus its degradation in the seminal plasma and suppressive effects on in vitro capacitation of spermatozoa, indicate its possible anti-capacitation role in the reproductive tract. Mol. Reprod. Dev. 84: 212-221, 2017. © 2016 Wiley Periodicals, Inc.

Organophosphorus insecticide dichlorvos inhibits fatty acid amide hydrolase in the male reproductive organs of rats

Organophosphorus insecticide dichlorvos inhibits fatty acid amide hydrolase in the male reproductive organs of rats

The effects of long-lasting hypoglycemia on male reproductive organs in rats.

Glucose has an important role in spermatogenesis. Nevertheless there are few reports in which the effects of long-lasting hypoglycemia on male reproductive organs have been evaluated. Therefore, insulin was administered subcutaneously at 100, 200, and 400 IU/kg to male rats twice a day for one month. This treatment regimen produced plasma glucose levels that rapidly decreased after treatment, with decreased glucose levels lasting for several hours after each administration on the first and final treatment days. During the treatment period, no abnormalities in clinical signs or body weight were observed. No statistically significant differences were noted in the weights of testes, epididymides, prostates and seminal vesicles, or pituitary glands. Histopathological examination revealed that the insulin-treated animals exhibited degeneration of seminiferous tubules in the testes and exfoliation of germ cells in the lumens of epididymides as a secondary change related to the testicular lesions. The incidences of the histopathological findings were found to be proportional to insulin dose. Sperm analysis of the group receiving the highest dosage indicated that the sperm concentration tended to decrease and the incidences of sperm malformations tended to increase. Our results suggest that long-lasting hypoglycemia affects male reproductive organs in rats.

Effect of Melatonin Intake on Oxidative Stress Biomarkers in Male Reproductive Organs of Rats under Experimental Diabetes.

This study investigated the antioxidant system response of male reproductive organs during early and late phases of diabetes and the influence of melatonin treatment. Melatonin was administered to five-week-old Wistar rats throughout the experiment, in drinking water (10 μg/kg b.w). Diabetes was induced at 13 weeks of age by streptozotocin (4.5 mg/100 g b.w., i.p.) and animals were euthanized with 14 or 21 weeks old. Activities of catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), and lipid peroxidation were evaluated in prostate, testis, and epididymis. The enzymes activities and lipid peroxidation were not affected in testis and epididymis after one or eight weeks of diabetes. Prostate exhibited a 3-fold increase in GPx activity at short-term diabetes and at long-term diabetes there were 2- and 3-fold increase in CAT and GST, respectively (p ≤ 0.01). Melatonin treatment to healthy rats caused a 47% increase in epididymal GPx activity in 14-week-old rats. In prostate, melatonin administration normalized GST activity at both ages and mitigated GPx at short-term and CAT at long-term diabetes. The testis and epididymis were less affected by diabetes than prostate. Furthermore, melatonin normalized the enzymatic disorders in prostate demonstrating its effective antioxidant role, even at low dosages.

Harmful effects of ascorbic acid and α-tocopherol on male reproductive organs of rats chronically exposed to sodium nitrate

Background: Humans and animals are exposed to sodium nitrate through the air, food and drinking water. Because nitrates induce oxidative stress, the effects of antioxidant vitamins ascorbic acid and α-tocopherol on oxidative damage induced by sodium nitrate on reproductive organs of male Wistar rats were studied. Methodology: Five rats each in four groups were treated for 60 days. They received distilled water (Group I), 3 mg/100 g body weight NaNO 3 (Group II), 3 mg/100 g body weight NaNO 3 + 50 mg/100 g body weight ascorbic acid (Group III) and 3 mg/100 g body weight NaNO 3 + 30 mg/100 g body weight α-tocopherol (Group IV). Live weights of the animals were obtained at the beginning of the experiment and every 2 weeks subsequently. At the end of the study, the left testis, epididymis and seminal vesicle of each rat was carefully removed and weighed. These organs were also examined for histopathological lesions. Results: Testis:body weight ratio and seminal vesicle:body weight ratio of Group II animals were less than (P < 0.05) those of the control. Epididymis:body weight and seminal vesicle:body weight ratios of Group III animals were significantly lower than those of Group II. Testis:body weight ratio of Group IV animals was significantly less than that of Group II. There was testicular degeneration with absence of spermatids and spermatogenic cells in the semeniferous tubules and absence of epididymal sperm reserve in Group IV animals. Conclusions: The results indicate that intake of ascorbic acid and α-tocopherol may enhance oxidative damage in the testis, epididymis and seminal vesicle during chronic sodium nitrate exposure.

Triclosan exhibits a tendency to accumulate in the epididymis and shows sperm toxicity in male sprague-dawley rats

Triclosan (TCS) is considered a potent endocrine disruptor that causes reproductive toxicity in non-mammals, but it is still unclear exactly whether TCS has adverse effects on the sperm or reproductive organs in mammals. In this study, we aimed to evaluate the distribution status of TCS in male reproductive organs of rats, and seek the correlation with the TCS-induced sperm toxicity or reproductive organ damage. Male rats were intragastrically administered with TCS at a dose of 50 mg/kg, the kinetics of TCS in the plasma and reproductive organs were investigated. TCS in testes and prostates both showed a lower-level distribution compared to that in the plasma, which indicates it has no tendency to accumulate in those organs. However, TCS in the epididymides showed a longer elimination half-life (t1/2 z), a longer the mean retention time (MRT), and a lower clearance (CLZ /F) compared with those in the plasma. Besides, the ratios of mean area under the concentration-time curve (AUC)(0-96 h(epididymides/plasma)) and AUC(0-∞(epididymides/plasma)) were 1.13 and 1.51, respectively. These kinetic parameters suggest TCS has an accumulation tendency in the epididymides. Based on this, we investigated the TCS-induced sperm toxicity and histopathological changes of reproductive organs in rats. TCS was given intragastrically at doses of 10, 50, and 200 mg/kg for 8 weeks. Rats treated with the high dose (200 mg/kg) of TCS showed a significant decrease in daily sperm production (DSP), changes in sperm morphology and epididymal histopathology. Considering the histopathological change in the epididymides, TCS may induce the epididymal damage due to the epididymal accumulation of that.

Histochemical study of the effect of heat on the function of male reproductive organs of rats

The literatures mentional that the male reproductive organs are under the effect of androgens which secreted from the testes ( Greenspan and Baxter 1994) . To know the role of scrotum in decreasing of testicular temperature we used twenty mature male rate . The animals were randomly divided into two groups , ten animals each ( Control and treated ) . Both testes of the treated animals sutured to the abdominal wall while the control animals were shamly operated .After one month all animal were killed and the testes , prostate and seminal vesicle were removed and put in liquid nitrogen ( - 196c ) . frozen section made and stained according to the stander histochemical methods . The results showed an increase in acid phosphatase activity in the treated tissues compared with the control . Alkaline phosphatase enzyme activity were unstable , while the succinate dehydrogenase enzyme activity decreased markedly in the treated tissues compared with the control tissues . The present observation confirmed the role of androgen in regulation of male organs function .

Effects of sulfasalazine on sperm acrosome reaction and gene expression in the male reproductive organs of rats

Effects of sulfasalazine on sperm acrosome reaction and gene expression in the male reproductive organs of rats

Effects of Sulfasalazine on Sperm Acrosome Reaction and Gene Expression in the Male Reproductive Organs of Rats

Sulfasalazine (SASP) has been reported to depress the fertility in men and experimental male animals, but the fundamental mechanisms of infertility caused by SASP are still unknown. This study was designed to investigate the mechanisms of infertility in rats treated with SASP at a dose of 600 mg/kg for 28 days, including monitoring of sperm motility using computer associated sperm analysis system and acrosome reaction by FITC-concanavalin A lectin staining. The sperm motility and acrosome reaction, which are important for fertilization, were significantly reduced by SASP. Furthermore, to investigate the molecular mechanisms of infertility induced by SASP, mRNA expression analysis in the testes was performed using cDNA microarray as a first screening. It was revealed that CD59, which is located on the acrosomal membrane and is known to be important for the reproductive function of sperm, was affected in the testes; this was also confirmed by real-time PCR analysis, but the spermatogenesis-related genes examined in this study were not affected. Therefore, we focused on CD59 and two other acrosome membrane related-genes: MCP and DAF. CD59, MCP, and DAF in the epididymides of SASP-treated rats were significantly decreased as assessed by real-time RT-PCR analysis and additionally, the expression of CD59 protein was found to be decreased by Western blotting. These results allowed us to hypothesize that the suppression of epididymal acrosomal membrane proteins synthesis with their consequent reduced incorporation to the sperm membrane leads to a depressed sperm motility and acrosome reaction, and thereby leads to infertility in SASP treated male rats.

Effects of 17beta-estradiol and tamoxifen on the selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) mRNA expression in male reproductive organs of rats.

The selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) is highly expressed in testes under gonadotropin control. The expression patterns of PHGPx mRNA by 17beta-estradiol (E2) as an estrogen and tamoxifen (Tam) as an estrogen antagonist were investigated in the reproductive organs of male rats. Twelve-week-old male Sprague-Dawley rats were subcutaneously injected with E2 (7.5 microg/kg/day) or Tam (5 mg/kg/day) for 1 week. The E2 treatment significantly increased the levels of PHGPx mRNA in both testes and prostates, whereas the Tam treatment significantly decreased the levels of PHGPx mRNA, compared to the vehicle control (p<0.01). The treatment with E2 or Tam slightly decreased the levels of PHGPx mRNA in epididymides. In histopathological examination, severe vacuolization and depletion of germ cells in the seminiferous tubules, cell debris in the tubular lumen, and mild proliferative changes in interstitial tissues were observed in the testes of Tam-treated rats, whereas only mild spermatogonial proliferation was observed in the seminiferous tubules of E2-treated rats. There were no typical histopathological changes in the epididymides of any of the laboratory rats but mild epithelial proliferation in the prostates of E2- and Tam-treated rats. These results suggest that PHGPx mRNA expression may be influenced by estrogen in the male reproductive organs.

Morphometric and Histopathological Studies on the Effects of Some Chromatographic Fractions of Phyllanthus amarus and Euphorbia hirta on the Male Reproductive Organs of Rats

The aqueous crude extracts of P. amarus and E. hirta were administered to thirty eight-week old sexually mature male albino to determine the effects of these extracts on the male reproductive organs of these animals. The results from this study revealed that the aqueous crude extracts of P. amarus and E. hirta caused varying degrees of testicular degeneration as well as reduction in the mean seminiferous tubular diameter (STD) in the treated rats. It thus shows that the aqueous crude extracts of P. amarus and E. hirta have potentially deleterious effects on the testes and accessory organs of rats. Great caution should therefore be exercised in the use of these plants for medicinal purpose.

The Antagonistic Effect of Chlorpromazine on Cadmium Toxicity

Adult male rats were injected sc with cadmium chloride (CdCl2) in a single dose of 7 mg/kg body wt. Twenty-four hours postinjection, exposure to CdCl2 increased the hemoglobin absorbance of the testes from 0.36 ± 0.01 to 2.46 ± 0.02. Pretreatment of rats with chlorpromazine (CPZ) 3 mg/kg ip either for 1 or 2 days before exposure to CdCl2 significantly (p < 0.05) reduced the testicular damage and the hemoglobin absorbance decreased to 1.03 ± 0.02 and 0.92 ± 0.04, respectively. After CdCl2 injection there was a progressive increase in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. CdCl2 injection induced hemorrhage and a diffuse area of coagulative necrosis in liver. Pretreatment with CPZ partially protected liver from the effect of CdCl2. Two months postinjection, exposure to CdCl2 significantly decreased the weights of testes, epididymis, and accessory sex organs. Furthermore, CdCl2 induced a highly significant (p < 0.01) decrease in sperm cell concentration and the percentage of mobile cells. Moreover CdCl2 induced degenerative changes in testes, epididymis, and seminal vesicles. Pretreatment with CPZ partially protected these organs from the toxic effects of CdCl2. It could be concluded that chlorpromazine partially antagonized the toxic effects of cadmium on liver, testes, and other male reproductive organs of rats.

Regulation by testosterone of the glucosamine-6-phosphate synthase activity in the male reproductive organs of rat

Accessory reproductive organs of male rat were found to contain high activities of glucosamine-6-phosphate synthase (glucosaminephosphate isomerase (glutamine-forming), EC 5.3.1.19). Castration caused drastic reduction (75%) in the enzyme activity of ventral prostate. Testosterone propionate administration restored the enzyme activity while cortisol and estradiol-17 β did not cause any effect. Cycloheximide blocked the stimulation caused by testosterone.

Effect of androgen administration on the cholesterol content of male reproductive organs in rats

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