Effects of melatonin on lipid peroxidation and antioxidant enzymes in streptozotocin-induced diabetic rat testis (original) (raw)
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Kafkas Universitesi Veteriner Fakultesi Dergisi, 2015
The aim of this study was to examine the protective effect of melatonin (MLT) on the alloxan-induced post-diabetic testicular damage in rats. Forty-eight Sprague Dawley male rats were divided into four groups (n=12). Group C received 0.9% saline for 45 days, as control. Group DM (Diabetes Mellitus) was injected by 120 mg/kg single dose alloxan intraperitoneally (IP). Group MLT was treated by 10 mg/ kg/d MLT IP for 45 d. Group DM+MLT was treated by 10 mg/kg/d MLT IP for 45 days following alloxan injection. Six animals on days 15 and the remaining 6 on days 45 were sacrificed in each group after the initiation of the study. Testis tissues and blood samples were collected to investigate blood glucose, oxidant and antioxidant statues, sperm parameters, and histopathological and 8-hydroxy-2′-deoxyguanosine (8-OHdG)-immunopositive cell examinations. MLT treatment of diabetic rats prevented the increases in malondialdehyde (MDA) levels and 8-OHdG concentrations, and the decreases in the GSH and SOD levels observed in DM groups. Alloxan administration depressed the sperm concentration, the number of progressively motile spermatozoa, premature acrosome reaction (AR) and calcium ionophore A23187-induced AR rates, without any change in dead and/or abnormal sperm rates in DM group. Histopathological and immunohistochemical observations also revealed that MLT-treated diabetic rats had an enhanced histological architecture and DNA damage in testis. These findings suggest that MLT treatment prevents the testicular damage by declining the oxidative stress, but it did not recover the depressed sperm parameters in diabetic rats.
Melatonin inhibits lipid peroxidation and stimulates the antioxidant status of diabetic rats
Journal of Pineal Research, 2001
Although melatonin has been established as a free radical scavenger and antioxidant, its effects in diabetes have not been thoroughly investigated. The purpose of this study, therefore, was to investigate the effects of melatonin administration on lipid peroxidation and antioxidant status in streptozotocin (STZ)-induced diabetes in rats. Concentrations of malondialdehyde (MDA) and reduced glutathione (GSH) in erythrocytes and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were compared in 3 groups of 10 rats each [control non-diabetic rats (group I), untreated diabetic rats (group II) and diabetic rats treated with melatonin (group III)]. In the study groups, diabetes developed 3 days after intraperitoneal (i.p.) administration of a single 60-mg/kg dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10-mg/kg i.p. dose of melatonin per day. After 6 wk, the rats in groups II and III had significantly lower body weights and significantly higher blood glucose levels than the rats of group I (PB 0.001 and P B 0.001, respectively). There were no significant differences in body weight or blood glucose levels between groups II and III. MDA levels in untreated diabetic rats were higher than those in control group rats and in diabetic rats treated with melatonin (PB 0.01 and PB 0.05, respectively). However, MDA levels in diabetic rats treated with melatonin were not different from those of the control group. The GSH, GSH-Px and SOD levels of untreated diabetic rats were significantly lower than those of the control group (P B 0.02, P B0.002 and P B 0.05, respectively). In group III, however, melatonin prevented decreases in the thiol antioxidant and the associated enzymes, and so these levels were not significantly different from those in the control group. These results confirm the presence of oxidative stress in STZ-induced experimental diabetes and indicate the beneficial free radical-scavenging and antioxidant properties of melatonin.
Effect of melatonin on testicular damage in streptozotocin-induced diabetes rats
European Surgical Research
It is well known that diabetes mellitus is associated with impairment of testicular function. In the present study, we aimed to demonstrate the effect of melatonin on testicular damage in male rats with streptozotocin (STZ)-induced diabetes. Male Wistar rats were divided into 4 groups: (1) control group, (2) melatonin-treated nondiabetic group, (3) diabetic group and (4) melatonin-treated diabetic group. Diabetes was induced by STZ injection. Melatonin was administered intraperitoneally at the dose of 10 mg/kg for 5 days. Testicular damage was examined by using hematoxylin and eosin staining and periodic acid-Schiff staining, and apoptosis was determined by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). Potential disorders associated with seminiferous tubular sperm formation were evaluated using the Johnsen score. Diabetic rats showed a reduction in seminiferous tubule diameter, increased thickening of the basement membrane in seminiferous tubules and...
2017
This study was aimed to evaluate the altered histoarchitecture and biochemical changes in Testis, Epididymis and Seminal vesicle of male albino rats treated with streptozotocin. Also, another objective was to evaluate the possible protective role of using exogenous melatonin in combination with streptozotocin. After histological and biochemical analysis, it was concluded that the exogenous melatonin may be used with other antioxidants to enhance and modulate the functions of antioxidative system and also to overcome cellular damages during diabetes
Oxidative stress in diabetic rats induced by streptozotocin: Protective effects of melatonin
Journal of Pineal Research, 1998
We have studied the effect of the administration of two doses of melatonin (melatonin 100 and melatonin 200 pgkg bw) on diabetes and oxidative stress experimentally induced by the injection of streptozotocin (STZ) in female Wistar rats. STZ was injected as a single dose (60 mg/kg i.p. in buffered citrate solution, pH 4.0) and melatonin (melatonin 100, 100 pg/kgJday i.p.; melatonin 200, 200 pg/kg/day i.p.) beginning 3 days before diabetes induction and continuing until the end of the study (8 weeks). The parameters analysed to evaluate oxidative stress and the diabetic state were a) for oxidative stress, changes of lipoperoxides (i.e., malondialdehyde, MDA) in plasma and erythrocytes and the changes in reduced glutathione (GSH) in erythrocytes and b) for diabetes, changes in glycemia, lipids (triglycerides: TG; total cholesterol: TC; HDL-cholesterol, HDL-c), percentage of glycosylated hemoglobin (Hb%), and plasma fructosamine. The injection of STZ caused significant increases in the levels of glycemia, percentage of glycosylated hemoglobin, fructosamine, cholesterol, triglycerides, and lipoperoxides in plasma and erythrocytes, whereas it decreased the levels of HDL-c and the GSH content in erythrocytes. The melatonin 100 dose reduced significantly all these increases, except the percentage of glycosylated hemoglobin. With regard to the decreases of plasma HDL-c and GSH content in erythrocytes, this melatonin dose returned them to normal levels. The melatonin 200 dose produced similar changes, though the effects were especially noticeable in the decrease of glycemia (55% vs. diabetes), percentage of hemoglobin (P < 0.001 vs diabetes), and fructosamine (3 1 % vs. diabetes). This dose also reversed the decreases of HDL-c and GSH in erythrocytes. Both doses of melatonin caused significant reduction of the percentage of glycosylated hemoglobin in those groups that were non-diabetic. These illustrate the protective effect of melatonin against oxidative stress and the severity of diabetes induced by STZ. In particular, this study confirms two facts: 1) the powerful antioxidant action of this pineal indole and 2) the importance of the severity of oxidative stress to maintain hyperglycemia and protein glycosylation, two pathogenetic Cornerstones indicative of diabetic complications. Melatonin reduces remarkably the degree of lipoperoxidation, hyperglycemia, and protein glycosylation, which gives hope to a promising perspective of this product, together with other biological antioxidants, in the treatment of diabetic complications where oxidative stress, either in a high or in a low degree, is present.
Journal of Clinical Research & Bioethics, 2016
Objective: To evaluate the therapeutic efficacy of exogenous melatonin (MEL) on hepato-renal tissue in a diabetic rat model. Methodology: Streptozotocin (STZ) was used to establish diabetic rat model. Diabetes was confirmed by monitoring the blood glucose level, animals having glucose level above 250 mg/dl were considered as diabetic and were divided into six different groups. Model control group, diabetic group, melatonin treatment to diabetic rats, melatonin per se group, glibenclamide (a standard hypoglycemic drug) treatment to diabetic rats and glibenclamide (standard control) alone respectively. The model control was given 0.5 ml (0.1 M) citrate buffer, experiment was conducted for one month. After the completion of experiment, rats were sacrificed. Blood was collected and centrifuged at 3000 rpm for 10 minutes to obtain the serum. Serum was kept at-800c for further analysis of liver and renal function tests and lipid profile. Liver and kidney tissues were weighed, fixed in Bouin's fixative for histopathological studies. Further tissues were processed for Lipid peroxidation (LPO), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). Major findings: Administration of MEL to STZ induced diabetic rat showed a significant decrease of lipid peroxidation (TBARS) in kidney and liver tissue comparable to the control and GLIBEN group of rats. In addition MEL prevented the decrease in antioxidative enzyme parameters viz. superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) of hepato-renal tissues. Parameters of liver functions (alanine amino transaminase (ALT), aspartate amino transaminase (AST) and alkaline phosphatase (ALP) and renal function (urea, uric acid and creatinine) were noted restored following MEL treatment. MEL administration further maintained the normal levels of lipid profiles i.e., triglyceride, cholesterol, low and high density lipoprotein (LDL, HDL) to that of the control group of rats. Histological architecture of liver and kidney tissues were noted repaired and rescued as judged by cellularity of hepatocytes and renal cells. Conclusion: The present finding strongly indicates the protective effect of exogenous melatonin for hepato-renal tissues form the damages and impairment observed and noted in the experimentally induced STZ male rat model.
Bratislavské lekárske listy, 2012
The present study aimed to explore the effect of melatonin administration on lipid peroxidation in various tissues of rats with streptozocin induced diabetes and subjected to an acute swimming exercise. The study used 80 adult male rats, which were equally allocated to 8 groups: Group 1, general control; Group 2, melatonin-administered control; Group 3, melatonin-administered diabetic control; Group 4, swimming control; Group 5, melatonin-administered swimming; Group 6, melatonin-administered diabetic swimming; Group 7, diabetic swimming; Group 8, diabetic control. Diabetic rats were administered 3 mg/kg/day ip melatonin for 4 weeks. At the end of the study, the animals were decapitated to collect samples from liver, lung and spleen tissues, which were then analyzed to determine levels of liver MDA (nmol/gram/protein) and GSH (mg/g/protein). The highest MDA values in liver, lung and spleen tissues were obtained in the Group 7. The values in the Group 8 were lower than those in the G...
The present study was designated to assess oxidative damage and its effect on germ cell apoptosis in testes of streptozotocin (STZ)-induced diabetic rats. The role of antioxidant supplementation with a mixture of vitamins E and C and alpha lipoic acid for protection against such damage was also evaluated. Forty-five adult male rats were randomly divided into three groups: group I, control, non-diabetic rats; group II, STZ-induced, untreated diabetic rats; group III, STZ-induced diabetic rats supplemented with a mixture of vitamins E and C and alpha lipoic acid. Glycated hemoglobin (HbA 1C), glucose, and insulin levels were estimated in blood samples. Malondialdehyde (MDA), the activities of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and caspase-3 in addition to testosterone (T) level were all determined in testicular tissues. Histo-pathological studies using H&E stain, as well as, immunohistochemical detection of apoptosis using (TUNEL) method were also performed. Blood glucose and HbA 1c were significantly increased while insulin was significantly decreased in STZ-induced diabetic rats as compared with controls. In rat testicular tissues, MDA, and caspase-3 activity were significantly elevated while SOD and GPx enzymatic activities as well as T level were significantly decreased in diabetic rats as compared with control group. Antioxidant supple-mentation to diabetic rats restored the testicular enzymatic activities of SOD and GPx to almost control levels, in addition, MDA and caspase-3 activity decrease while T increase significantly as compared with untreated diabetic group. Prominent reduction of germ cell apoptosis was found in diabetic rats supplemented with antioxidants. An important role of testicular oxidative damage and germ cell apoptosis in diabetes-induced infertility could be suggested, treatment with antioxidants has a protective effect by restoring SOD and GPx antioxidant enzymatic activity.
Protective effect of melatonin on β-cell damage in streptozotocin-induced diabetes in rats
Acta Histochemica, 2003
The aim of the present study was the evaluation of possible protective effects of melatonin against β-cell damage in streptozotocin-induced diabetes in rats. Malondialdehyde levels and glutathione peroxidase activity were measured in pancreatic homogenates. Pancreatic β-cells were examined by immunohistochemical methods. Streptozotocin was injected intraperitoneally at a single dose of 60 mg/kg for induction of diabetes. Melatonin (200 µg/kg/day, ip) was injected for 3 days prior to administration of streptozotocin; these injections were continued until the end of the study (4 weeks). Streptozotocin induced a significant increase in malondialdehyde levels (p < 0.01) and a significant decrease in glutathione peroxidase activity (p < 0.05) in pancreatic tissue. Degeneration of islet cells and weak immunohistochemical staining of insulin was observed in diabetic rats. Treatment of diabetic rats with melatonin markedly reduced malondialdehyde production (p < 0.05) and increased glutathione peroxidase activity (p < 0.01) without affecting hyperglycemia. Increased staining of insulin and preservation of islet cells were apparent in the melatonin-treated diabetic rats. These data suggest that melatonin treatment has a therapeutic effect in diabetes by reduction of oxidative stress and preservation of pancreatic β-cell integrity.
Protective effect of melatonin on beta-cell damage in streptozotocin-induced diabetes in rats
Acta histochemica, 2003
The aim of the present study was the evaluation of possible protective effects of melatonin against β-cell damage in streptozotocin-induced diabetes in rats. Malondialdehyde levels and glutathione peroxidase activity were measured in pancreatic homogenates. Pancreatic β-cells were examined by immunohistochemical methods. Streptozotocin was injected intraperitoneally at a single dose of 60 mg/kg for induction of diabetes. Melatonin (200 µg/kg/day, ip) was injected for 3 days prior to administration of streptozotocin; these injections were continued until the end of the study (4 weeks). Streptozotocin induced a significant increase in malondialdehyde levels (p < 0.01) and a significant decrease in glutathione peroxidase activity (p < 0.05) in pancreatic tissue. Degeneration of islet cells and weak immunohistochemical staining of insulin was observed in diabetic rats. Treatment of diabetic rats with melatonin markedly reduced malondialdehyde production (p < 0.05) and increased glutathione peroxidase activity (p < 0.01) without affecting hyperglycemia. Increased staining of insulin and preservation of islet cells were apparent in the melatonin-treated diabetic rats. These data suggest that melatonin treatment has a therapeutic effect in diabetes by reduction of oxidative stress and preservation of pancreatic β-cell integrity.