Testes Of Diabetic Rats Research Articles

The antioxidant role of agomelatine and gallic acid on oxidative stress in STZ induced type I diabetic rat testes.

Diabetes is a multisystem disorder and its effects are observed on the reproductive system. One of the main causes of testicular tissue damage is diabetes-induced overproduction of reactive oxygen species and glycated end products. The main objectives of this study were to investigate the possible effects of agomelatine (AG) and gallic acid (GA) in suppressing oxidative stress in Type I diabetes induced testicular damage. A total of 28 adult male rats were included in the study. Diabetes was induced by intraperitoneal injection of streptozocin (STZ, 55mg/kg) to 21 rats, which were then randomly assigned to 3 groups; 1mL saline solution was given to the diabetes+saline group by oral gavage, 20mg/kg/day oral AG was given to the diabetes+AG group, and 20mg/kg/day oral GA was given to the diabetes+GA group for 4 weeks. Tumor necrosis factor α (TNFα), nitric oxide synthase 2 (NOS2), fibronectin and vascular endothelial growth factor (VEGF) were used for the investigation of inflammation, fibrosis and vascular structures. The terminal-deoxynucleoitidyl-transferase mediated nick end-labeling assay (TUNEL) was used to detect apoptosis. Testicular tissue total antioxidant capacity values were tested by biochemical analysis. AG treatment showed an improvement on biochemical parameters and histopathological appearance on the rat testes. GA showed dose-related regenerative effects on biochemical parameters. Histologically, a minimal healing effect was determined on the testes damage. In conclusion, it was observed that AG is a potentially beneficial agent for reducing testicular damage by decreasing oxidative stress level. However, GA was seen to have a poor therapeutic effect.

Furan toxicity on testes and protective role of lycopene in diabetic rats.

Furan (C4H4O) is a heat-induced food contaminant that is utilized as an industrial chemical agent. Lycopene is a natural substance that is produced by plants and tomatoes. We aimed to evaluate the toxicity of furan on testes and the protective effect of lycopene in diabetic rats. Male Wistar albino rats were divided into five groups: Group 1 (control group) received 1 mL/kg corn oil. Group 2 (diabetic control group) received 55 mg/kg STZ and 1 mL/kg corn oil. Group 3 (diabetic lycopene group) received 55 mg/kg STZ and 4 mg/kg lycopene. Group 4 (diabetic furan group) received 55 mg/kg STZ and 40 mg/kg furan. Group 5 (diabetic furan + lycopene group) received 55 mg/kg STZ, 40 mg/kg furan, and 4 mg/kg lycopene. After 28 days, the testes were extirpated in all groups. In the testicular tissue samples, the level of malondialdehyde (MDA) and the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and reducted glutathione (GST) were studied. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured. Histopathologic examination was performed by light microscope. The MDA level and the activities of CAT, GPx, SOD, and GST were found to be higher in the furan group than in the control and diabetic control groups (p<0.05). The MDA level and the activities of CAT, GPx, SOD, and GST were significantly lower in the furan + lycopene group than in the furan group (p<0.05). The low blood testosterone level in the rats who received furan suggested the presence of endocrinological defects and cellular degenerative changes. Lycopene may be effective to reverse furan toxicity in diabetic rat testes.

Gum arabic improves semen quality and oxidative stress capacity in alloxan induced diabetes rats

ObjectiveTo explore effect of gum arabic (GA) on semen quality and oxidative stress capacity of alloxan induced diabetes rats. MethodsIn this study, male Sprague–Dawley rats were divided into 3 groups (n = 20 of each): control group, diabetic group which were injected with alloxan, and diabetic group which was given 10% GA in the form of drinking water for 10 weeks. The effect of GA on testicular oxidative stress and sperm quality were investigated. Testicular antioxidant was detected by the measurement of antioxidant enzymes, malondialdehyde in testis tissue. Moreover, plasma lipids, testis histopathological changes and oxidative stress related genes mRNA were evaluated. ResultsThe treatment of GA significantly (P < 0.05) increased semen quality compared the diabetic and control groups. Similarly, the treatment of GA significantly (P < 0.05) increased the activities of catalase, superoxide dismutase and glutathione peroxidase compared to diabetic and control groups. The treatment of GA significantly (P < 0.05) decreased testis malondialdehyde, plasma total cholesterol, low-density lipoprotein cholesterol and triglyceride concentrations, whereas increased high-density lipoprotein cholesterol concentrations compared to the diabetic groups. Glutathione peroxidase and superoxide dismutase mRNA expression were significantly (P < 0.05) increased in GA treated group compared to diabetic and control groups. All testes of diabetic rats displayed obvious degeneration; whereas slight degeneration was seen in GA treated rats when compared to diabetic control group. ConclusionOur findings imply that GA may protect testis via enhancement of antioxidant capacity, it may be useful to meliorate the diabetic fertility complications.

Antioxidant and protective effects of Royal jelly on histopathological changes in testis of diabetic rats

Diabetes is the most common endocrine disease. It has adverse effects on male reproductive function. Royal Jelly (RJ) has antioxidant and anti-diabetic effects and show protective effects against diabetes. This study was conducted to evaluate the effect of RJ on histopathological alterations of the testicular tissue in streptozotocin (STZ)-induced diabetic rats. In this experimental study, 28 adult Wistar rats were randomly divided into control (C), royal jelly (R), diabetic (D) and RJ-treated diabetic (D+R) groups. Diabetes was induced by a single intraperitoneal injection of STZ at 50 mg/kg body weight (BW). The rats from the R and D+R groups received daily RJ (100 mg/kg BW) for 6 wks orally. Hematoxylin-Eosin staining was used to analyze histopathological changes including: tunica albuginea thickness (TAT), seminiferous tubules diameter (STsD), Johnsen's score, tubular differentiation index (TDI), spermiogenesis index (SPI), Sertoli cell index (SCI), meiotic index (MI), and mononuclear immune cells (MICs) in testes. The antioxidant status was examined by evaluating testicular levels of ferric reducing antioxidant power (FRAP) and catalase (CAT) activity. Histological results of the testis from diabetic rats showed significant decrease in STsD, Johnsen's score, TDI, SPI, SCI and MI, and significant increase in TAT and MICs, while administration of RJ significantly reverted these changes (p<0.05). RJ treatment markedly increased activity of CAT and FRAP. There were significant differences in FRAP levels among C (13.0±0.5), RJ (13.4±0.3), D (7.8±0.6) and D+R (12.4±0.7) groups (p<0.05). RJ improved diabetes-induced impairment in testis, probably through its antioxidant property.

Effect of Root Kudzu on Caspease-3 Activity by Immunohistochemy Method in the Testis in Streptozotocin-Induced Diabetic Rats

Effect of Root Kudzu on Caspease-3 Activity by Immunohistochemy Method in the Testis in Streptozotocin-Induced Diabetic Rats

Evaluation of the Fas/FasL signaling pathway in diabetic rat testis

We investigated the role of the Fas/Fas ligand (FasL) signaling pathway in diabetic male infertility. Male rats were divided into two groups: a control group and a streptozotocin induced diabetic group. Thirty days after induction of diabetes, samples of testes were harvested and fixed in 10% formalin for light microscopy. Germ cell apoptosis was determined using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate in situ nick end-labeling (TUNEL) and immunostaining of caspase 8 and active caspase 3. We also investigated the expressions of Fas and FasL using immunohistochemistry. Streptozotocin-induced diabetes caused severe histopathological damage and increased apoptotic tubule and apoptotic cell indices, caspase 8 and caspase 3 expressions, and Fas and FasL-immunopositive cells in the rat testes. We suggest that the Fas/FasL signaling pathway may play a role in male infertility caused by diabetes.

Effect of Telmisartan or Insulin on the Expression of Adiponectin and its Receptors in the Testis of Streptozotocin-Induced Diabetic Rats

This study investigated the effect of insulin and telmisartan on the expression of adiponectin and its receptors, oxidative stress, and inflammatory cytokines in the testis of streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into control (C, n=8), diabetic (D, n=8), diabetic treated with insulin (DI, n=8), and diabetic treated with telmisartan (DT, n=8). Diabetic was induced by the peritoneal injection of a single dose of streptozotocin. Eight weeks later, bilateral testes were immediately removed after the rat was sacrificed. Epididymis was harvested to prepare sperm suspension. Plasma adiponectin, testicular interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α) were detected by enzyme linked immunosorbent assay (ELISA). The mRNA or protein expression of testicular adiponectin receptor 1 (adipoR1) and 2 (adipoR2), p22phox, transcription factor NF-E2 associated factor 2 (Nrf2), NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), AMPK-α, Akt, and eNOS was assayed by real-time fluorescence quantitative PCR or Western blot. There were significant pathological changes in the testes of diabetic rats. The levels of testicular weight, sperm number and motility, serum and testicular testosterone, plasma insulin and adiponectin, testicular adiponectin and its receptor 1, Nrf2, NQO1, HO-1, and phosphorylated-AMPK were significantly decreased in diabetic rats. The levels of blood glucose and lipids, and the levels of testicular p22phox, IL-6, TNF-α, phosphorylated-AKT, e-NOS, and nitric oxide (NO) were significantly increased in diabetic rats. These changes could be significantly reversed by insulin treatment. Similar results were observed with telmisartan treatment except for NQO1 mRNA and phosphorylated-AMPK. There was no significant difference in the expression of testicular adiponectin receptor 2 among 4 groups. The decreased adiponectin and its receptors, and the increased oxidative stress and inflammatory cytokines may play an important role in the testopathy of type 1 diabetic rats. Insulin and telmisartan may produce the protective effect on the testes of diabetic rats by upregulating the expression of adiponectin and its receptors and downregulating the level of oxidative stress and inflammatory cytokines.

Taurine and pioglitazone attenuate diabetes-induced testicular damage by abrogation of oxidative stress and up-regulation of the pituitary-gonadal axis.

Chronic hyperglycemia is associated with impairment of testicular function. The current study aimed to investigate the protective effects and the possible mechanisms of taurine and pioglitazone against diabetes-induced testicular dysfunction in rats. Diabetes was induced by streptozotocin injection. Both normal and diabetic rats received taurine (100 mg/kg) or pioglitazone (10 mg/kg) orally and daily for 6 weeks. Diabetic rats showed a significant (P < 0.001) increase in glycosylated hemoglobin, glucose, homeostasis model of insulin resistance, and pro-inflammatory cytokines. Serum insulin, testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were significantly (P < 0.001) decreased in diabetic rats. Taurine and pioglitazone alleviated hyperglycemia, decreased pro-inflammatory cytokines, and increased circulating levels of insulin, testosterone, LH, and FSH. Gene and protein expression of LH and FSH receptors and cytochrome P450 17α-hydroxylase (CYP17) was significantly (P < 0.001) down-regulated in testes of diabetic rats, an effect which was significantly increased after administration of taurine and pioglitazone. In addition, taurine and pioglitazone significantly decreased lipid peroxidation and DNA damage, and enhanced activity of the antioxidant enzymes in testes of diabetic rats. In conclusion, taurine and pioglitazone exerted protective effects against diabetes-induced testicular damage through attenuation of hyperglycemia, inflammation, oxidative stress and DNA damage, and up-regulation of the pituitary/gonadal axis.

The effect of 2-month bromocriptine treatment on the activity of the adenylyl cyclase signaling system in the myocardium and testes of rats with type 2 diabetes

Cardiovascular diseases and dysfunctions of the reproductive system are common complications of type 2 diabetes (T2D), and, therefore, development of new approaches for the alleviation of these pathologies is highly important. Bromocriptine (BC), an agonist of type 2 dopamine receptors, recently became widely used for the treatment of type 2 diabetes; this drug both restores energy metabolism and prevents the development of cardiovascular disease. However, the targets of BC and mechanisms underlying its action are still poorly characterized. The aim of the present work was to investigate the effect of BC treatment on the functional activity of the adenylyl cyclase signaling system (ACSS) in the myocardium and testes of male rats suffering from type 2 diabetes induced by high-fat diet and administration of streptozotocin (25 mg/kg). Oral BC administration (0.6 mg/kg every other day for 60 days) started 90 days after the commencement of highfat diet. Body weight and triglyceride levels were elevated in diabetic rats. Glucose tolerance of the animals was impaired, and they developed insulin resistance. BC treatment enabled the recovery of glucose metabolism parameters and increased the sensitivity of tissues to insulin. Adenylyl cyclase (AC) stimulation by guanylyl imidodiphosphate (GppNHp), relaxin, and the β-adrenergic receptor (β-AR) agonists isoproterenol and norepinephrine in the myocardium of diabetic rats was impaired, while the stimulatory effects of the β3-agonists BRL-37344 and CL-316243 persisted. The inhibitory effect of somatostatin on forskolin-stimulated AC activity was attenuated, while the inhibitory effect of norepinephrine mediated by α2-AR was enhanced. BC treatment normalized adrenergic signaling in the myocardium and partially restored the effects of relaxin and somatostatin on AC. AC activity, both basal and stimulated by GppNHp, forskolin, human chorionic gonadotropin, and pituitary AC-activating polypeptide, decreased in the testis of diabetic rats, and the inhibitory effect of somatostatin was attenuated. BC treatment induced only slight changes in the testicular ACSS. Thus, prolonged BC treatment restored the functional activity of ACSS in the myocardium and testes of diabetic rats; this accounts for the therapeutic effect of BC on the impaired functioning of the cardiovascular and reproductive systems in T2D and should be taken into account upon the selection of treatment strategies for T2D and its complications.

The effects of streptozotocin-induced diabetes on ghrelin expression in rat testis: biochemical and immunohistochemical study.

Ghrelin is a hormone which has effects on the secretion of growth hormone, gastrointestinal system, cardiovascular system, cell proliferation and reproductive system. The present study we focused on the relation between ghrelin and GHS-R1a gene expression and the regulation of their expression in the testes of diabetic rats. 40 male Wistar albino rats were divided into four groups: control, and sampled 4, 8 and 12 weeks after induction of diabetes by streptozotocin (STZ) intraperitoneal injection (40 mg/kg). The rats were decapitated under ketamine anesthesia and their testes were removed. Blood was obtained from heart and serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured by ELISA. Tissue ghrelin and GHS-R mRNA levels were determined by qRT-PCR, while ghrelin protein expression was studied by immunohistochemistry. Histopathological damage scores were also assessed. Eight weeks after diabetes induction serum FSH level was increased, whereas LH and testosterone concentrations decreased. The ghrelin and GHS-R1a gene expression and ghrelin immunohistochemistry score first tended to increase after first four weeks of diabetes, and then tended to decrease. Ghrelin-immunopositive cells were detected in Leydig cells in all groups of rats, however, not in the germinal epithelium. Congestion of vessels and hemorrhage, formation of the vacuoles in spermatogonia and spermatocytes, desquamation of spermatids in the lumen and disorganization of seminiferous tubule germinal epithelium were observed in testis of all the diabetic rats. In addition, mean testicular biopsy score and mean seminiferous tubule diameter were getting lower in diabetic animals. Our results suggest that diabetes affects ghrelin expression in rat testis.

Ameliorative Effect of Zinc Oxide Nanoparticles on Antioxidants and Sperm Characteristics in Streptozotocin-Induced Diabetic Rat Testes.

The present study investigated the impact of zinc oxide nanoparticles (ZnONPs) on the oxidative status and sperm characteristics in diabetic rat testicular tissue. Forty male albino rats were used in this study; 10 of them served as a control and 30 rats were injected with a single dose (100 mg/kg) of streptozotocin intraperitoneally. They were subdivided into diabetic, diabetic + ZnONPs (10 mg/kg B.W.), and diabetic and cotreated with ZnONPs + insulin groups. The sperm count and motility were assessed. The activity and mRNA expression of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GRD), and Glutathion-S-Transferase (GST) were determined in the testicular tissue. Malondialdehyde (MDA) and reduced glutathione (GSH) levels were estimated in the testicular tissue. Sperm count and motility increased in ZnONPs treated diabetic rats. A significant increase in the activity and mRNA expression of SOD, CAT, GPx, GRD, and GST was shown in ZnONPs treated diabetic rats. MDA significantly decreased, while GSH increased in testicular tissue of ZnONPs treated diabetic rats. It was concluded that ZnONPs either alone or in combination with insulin have the ability to increase the sperm count and motility and protect the testicular tissue against the oxidative stress induced by diabetes in rats.

Effects of pentoxifylline administration on histomorphological parameters of streptozotocin-induced diabetic rat testes.

The effect of pentoxifylline (PTX) administration on histomorphological parameters of streptozotocin (STZ)-induced type 1 diabetes mellitus (DM) in male rat testes were evaluated. We randomly divided 40 male rats into the following four groups: group 1: control or normal glycemic (NG) rats; group 2 or NG rats that received only normal saline (NS), (NG+NS); group 3 or diabetic rats which were not treated by PTX (DM+vehicle solution (NS)); and group 4 which comprised diabetic rats treated with 50 mg/kg of PTX (DM+PTX). Type 1 DM was induced by intraperitoneal injection of STZ (55 mg/kg). Rats were held for 30 days after which the experimental group received PTX twice daily (25 mg/kg) or NS. After 14 days of treatment by PTX or NS, the left testes from all rats were extracted and prpared for histological study. Apoptotic cells, blood vessel density, and spermatogenesis were evaluated. Data were analyzed by ANOVA test. PTX-treated-diabetic rats showed a significant decrease in number of apoptotic cells and decrease in blood vessel density compared to the DM+NS rats. A significant increase in spermatogenesis was observed in the PTX-treated diabetic group, compared to the DM+NS groups. It was concluded that PTX administration to STZ-induced type 1 DM rats affected apoptotic cell number positively. Moreover, blood vessel density significantly decreased and improvements were observed in spermatogenesis.

Extracts of Gongronema latifolium and Vernonia amygdalina improve glycaemia and histomorphology of testes of diabetic Wistar rats

This study aimed to assess the histomorphological and glycaemic effects of the ethanolic leaf extracts of Vernonia amygdalina (VA) and Gongronema latifolium (GL) on the testis of alloxan-induced diabetic Wistar rats. Forty male Wistar rats were divided into two groups A and C; the former served as negative control group received normal saline, while the later was the diabetic group. This group was further divided into seven (C1 to C7) groups and treated as follows: C1 was diabetic positive control, C2 (150 mg/kg of GL), C3 (300 mg/kg of GL), C4 (150 mg/kg of VA), C5 (300 mg/kg of VA), C6 (100 mg/kg each of GL and VA) and C7 (Insulin 1 IU/kg), respectively. Alloxan (150 mg/kg) was used to induce diabetes and animals were anesthetized with chloroform and sacrificed. Blood glucose was recorded at the start, during and at the end of treatment. Testes were processed for histopathological examination. The groups treated with GL and VA extracts showed better cellular architecture upon histopathological examination than the diabetic control group that revealed marked necrosis and cellular hypoplasia. Blood glucose levels of the treated rats were reduced by GL and VA extracts with good leverage in organ and body weight indices. In conclusion, GL and VA have a protective effect on the histology of the testes and hypoglycemic activity in diabetic rats. Key words: Vernonia amygdalina, Gongronema latifolium, testis, histomorphology, diabetic rats.

The effect of exogenous oxytocin on streptozotocin (STZ)-induced diabetic adult rat testes

Oxytocin (OXY) plays a crucial role in reproduction. The aim of this study is to investigate the therapeutic and protective effects of oxytocin treatment on streptozotocin (STZ) induced diabetes in testicular tissue. The rats were randomly divided into four experimental groups: (I) Control Group, (II) STZ induced Diabetic Group (STZ Group), (III) STZ induced Diabetic Group with Pre-Oxytocin treatment (Pre-OXY Group) and (IV) STZ induced Diabetic Group with Post-Oxytocin treatment (Post-OXY Group); each group contains six animals. The rats whose blood glucose levels were more than 200mg/dl were included to the experiment. At the end of the 4th week, testes tissue samples were taken to be processed for light microscopy and transmission electron microscopy. Malondialdehyde (MDA), Glutathione (GSH) and Advanced Oxidation Protein Products (AOPP) levels were determined biochemically in blood samples. Testicular tissue samples stained with Hematoxylin and Eosin (H&E) and Periodic acid-Schiff (PAS) reaction were evaluated under light microscope. The histopathological damage score of testicular tissue, which was significantly increased in STZ group, was decreased by oxytocin treatment. According to biochemical data, MDA and AOPP levels have been increased in the blood of STZ Group compared to the Control Group whereas they decreased significantly in Oxytocin-treated Groups compared to STZ Group. GSH levels were significantly decreased in the blood of STZ Group and increased in the blood of Oxytocin-treated Groups compared to STZ Group. In conclusion, oxytocin has a potential protective effect on the testes tissue of STZ-induced diabetic rats.

Expression of visfatin in alloxan-induced diabetic rat testis

Diabetes mellitus is a potential epidemic all over the world and causes dysfunction of reproductive activity. Visfatin, one of the adipokines, is present in various tissues including the testis. Our hypothesis was the level of testicular visfatin is affected in diabetic condition. The aim of the present study was to investigate the expression and localization of visfatin in the diabetic rat testis. No similar studies have been performed in diabetic rat testis with reference to visfatin. Overnight fasted adult male Wistar rats were made diabetic by the administration of alloxan (150mg/kg i.p., in 0.9% saline). Blood glucose levels were tested on five days after alloxan treatment, rats with high blood glucose levels (>250mg/dL) were considered as diabetic. Immunolocalization and Western blotting analysis of visfatin were performed. Correlation of visfatin expression was made in relation to body weight, testis weight, glucose concentration and serum testosterone level. Expression of visfatin was observed in Leydig cells, spermatocytes and sperm in control as well as in the diabetic group. Mild immunostaining of visfatin was observed in affected seminiferous tubules of alloxan-induced diabetic rat testis. Western blot analysis showed decreased expression of testicular visfatin in diabetic rats. The expression of visfatin showed a positive correlation with serum testosterone levels, body and testis weight, while a negative correlation was observed with blood glucose levels. This study showed involvement of visfatin in diabetic associated impairment of testicular activity.

Diabetes-induced DNA damage and apoptosis are associated with poly (ADP ribose) polymerase 1 inhibition in the rat testis

Molecular mechanisms responsible for diabetes-induced testicular dysfunction are not well understood. This study investigated oxidative stress, stage-dependent DNA base modification and expression of poly (ADP ribose) polymerase 1 (PARP1) in the testes of streptozotocin-induced diabetic rats. Hyperglycemia led to testicular dysfunction characterized by impaired sperm parameters and testicular structure at the end of first (DM1) and third (DM3) month after the induction of diabetes. In the testis, total oxidant levels increased and total antioxidant levels decreased, which led to the induction of oxidative stress status. The oxidative stress up-regulated the levels of 8-oxo-7, 8-dihydro-2′-deoxyguanosine – an oxidized form of the DNA base, deoxyguanosine – in a stage-dependent manner. In DM1, stage VII–IX tubules showed more cytoplasmic expression of 8-oxo-7, 8-dihydro-2′-deoxyguanosine in all germ cell types and the Sertoli cells than did the other stage tubules, which suggested mitochondrial DNA damage. In DM3, mainly a stage-dependent nuclear expression of 8-oxo-7, 8-dihydro-2′-deoxyguanosine was observed in germ cells, but not in the Sertoli cells. Diabetes increased the cytoplasmic expression of 4-hydroxynonenal and concurrently inhibited the expression of both full length and 89kDa large cleaved-fragment of PARP1 in DM1 and DM3. The germ and Sertoli cells showed the nuclear expression of the protein in a stage-dependent manner, which decreased from DM1 to DM3. The increase in oxidative DNA damage and a decrease in PARP1 led to a stage-dependent induction of apoptosis of testicular cells. In conclusion, diabetes-induced oxidative stress, oxidative DNA damage and apoptosis occur in parallel with PARP1 inhibition in the testis.

Oral supplementation of standardized extract of Withania somnifera protects against diabetes-induced testicular oxidative impairments in prepubertal rats

Male reproductive dysfunctions and infertility are the common consequences of overt diabetes. Available evidence support oxidative stress to be the underlying mechanism for the manifestation of testicular complications during diabetes. In the present study, we assessed the attenuating effects of Withania somnifera root extract (WS) on diabetes-induced testicular oxidative disturbances in prepubertal rats. Four-week-old prepubertal rats were assigned into nondiabetic control, streptozotocin (STZ)-treated and STZ+WS supplemented (500 mg/kg b.w./d, oral, 15 days) groups. Experimental diabetes was induced by a single intraperitoneal injection of STZ (90 mg/kg b.w). Terminally, all animals were killed, and markers of oxidative stress were determined in the testis cytosol and mitochondrial fraction. Severe hyperglycemia and regression in testis size were apparent in diabetic rats. A decline in antioxidant defenses with subsequent elevation in the generation of reactive oxygen species and lipid peroxidation was discernible in testis cytosol and mitochondria of diabetic prepubertal rats, which was significantly reversed by WS. However, there was partial restoration of glucose-6-phosphate dehydrogenase, lactate dehydrogenase, and 3-beta hydroxysteroid dehydrogenase activities in testis of diabetic prepubertal rats administered with WS. Taken together, data accrued suggest the potential of WS to improve diabetes-induced testicular dysfunctions in prepubertal rats.

Protective effect of Vitamin E (a-tocopherol) on nickel-induced alteration of testicular pathophysiology in alloxan-treated diabetic rats

Background and Aim: Diabetes mellitus is a global problem associated with increased formation of free radicals and decrease in antioxidant potential. Nickel generates free radicals and induces oxidative and nitrosative stress with depletion of antioxidants. Vitamin E is the most effective chain-breaking antioxidant against lipid peroxidation. Therefore, the present study was intended to evaluate the possible protective effect of Vitamin E (α-tocopherol) on oxidative stress in the testis of diabetic rats exposed to nickel. Methods: Diabetes was induced by alloxan monohydrate (15 mg/100 g b.wt, i.p.) in adult male Wistar albino rats. Diabetic rats in respective groups were exposed to nickel sulfate (2.0 mg/100 g b.wt, i.p) and α-tocopherol (10 mg/100 g b.wt, i.m.) alone as well as in combination on alternate days until the tenth doses. Testicular cholesterol and protein, aspartate aminotransferase (AST), alanine aminotransferase (ALT), nitric oxide, and lipid peroxide were evaluated by ultraviolet-visible spectrophotometer. Testicular histopathology was also evaluated. Results: Exposure of diabetes and nickel showed significantly decreased body weight, testicular-somatic index, testicular cholesterol and protein, AST, ALT, nitric oxide, and lipid peroxide levels. Simultaneous α-tocopherol supplementation showed remarkable improvement in all these alterations. We observed damage in testicular architecture with, tortuous seminiferous tubules, foci of congestion, necrosis, loss of spermatogenesis > 75% and loss of germ cell layer in diabetic and nickel-exposed diabetic rats. Testis of simultaneous α-tocopherol supplemented diabetic rats showed many normal seminiferous tubules and normal spermatogenesis (≥50%). Conclusion: Vitamin E (α-tocopherol) supplementation could exert a protective effect on the testis of diabetic rats exposed to nickel by suppressing the increased oxidative stress.

Gibberellic acid acts as an agonist of steroidogenesis in male rats

Testicular steroidogenesis has significant implication in male reproductive function. Although the effects of various signalling molecules on testicular functions have been studied earlier, the influence of the plant hormone gibberellic acid (GA3 ) on steroidogenesis has not been investigated. Acute (4 h) and subacute (15 days) studies using this compound through oral administration (150 μg day(-1) ) to groups of normal and diabetic Wistar male rats were therefore carried out. Results indicate that (i) enhanced activity of steroidogenic markers 3β-hydroxysteroid dehydrogenase (3β-HSD), 17β-hydroxysteroid dehydrogenase (17β-HSD), elevated tissue testosterone (T) content, increased steroidogenic acute regulatory protein (StAR) and androgen binding protein (ABP) levels with reduced lipid peroxidation and improved antioxidant defence in this treatment group of normal and diabetic rat testis, and (ii) elevated lipid peroxidation and diminished antioxidant defence, with insignificant change in 3β-HSD and 17β-HSD activity and testosterone level in acute treatment group of normal and diabetic rats testis, were noted. The observed increase in the activity of testicular 3β-HSD and 17β-HSD along with elevated testosterone content established GA3 as an inducer of steroidogenesis in rat.

Experimental diabetes‐induced testicular damage in prepubertal rats (在青春期前大鼠中实验性糖尿病导致的睾丸损伤)

There has been a marked increase in the prevalence of childhood and/or adolescent diabetes worldwide. Testicular dysfunction in adult-onset diabetes is well established, whereas the impact of early onset diabetes on the functional development of the testis remains elusive. In the present study we investigated early oxidative impairments and progressive histological changes in streptozotocin (STZ)-induced diabetic prepubertal rat testis. Testes were sampled from prepubertal rats injected with a single bolus of STZ (90 mg/kg, i.p.) on Days 1, 3, 5, 7 and 14 after STZ injection for quantitation of testicular oxidative stress parameters in isolated subcellular fractions and mitochondrial and microsomal functional efficiency, as well as at weekly intervals over a period of 8 weeks for histological and flow cytometry analyses. Prepubertal diabetic rats were severely hyperglycemic with reduced testes size. At the subcellular level, a progressive increase in oxidative stress parameters was discernible in the cytosolic and microsomal compartments from Day 1 after STZ, together with decreased antioxidant defenses. Surprisingly, tissue ascorbate and free catalytic iron levels were notably increased in diabetic rat testis. Mitochondrial dysfunction was manifested from Day 5, as evidenced by a reduction in electron transport activity. Histologically, tissue sections showed distorted seminiferous tubules and extensive cell vacuolization with progressive disappearance of spermatids in the lumen by Week 7 after STZ injection, observations that were consistent with flow cytometry data. Herein we provide evidence that the onset of diabetes brings about oxidative changes at the subcellular level that cumulatively affect the functional growth of testes.