Antioxidant role of coumarin on streptozotocin-nicotinamide-induced type 2 diabetic rats

The purpose of this study was to investigate the antioxidant role of coumarin on streptozotocin-nicotinamide-induced Type 2 diabetic rats. In experimental rats, the levels of plasma glucose, insulin, and the levels of thiobarbituric acid reactive substances, lipid hydroperoxides, conjugated dienes, and the activities of superoxide dismutase, catalase, glutathione-S-transferase, and glutathione peroxidase were assayed in liver and kidney. Diabetic rats showed elevated levels of plasma glucose and lipid peroxidation markers and reduced plasma insulin and antioxidant enzymes. Oral administration of coumarin resulted in a significant reduction in the plasma glucose and lipid peroxides and a significant increase in the plasma insulin and antioxidant enzymes. Chronic treatment of coumarin remarkably restored the normal status of the histopathological changes observed in the selected tissues. It can be concluded that coumarin has antioxidant effect in Type 2 diabetic rats.     

Gastroprotective,hepatoprotective, and nephroprotective effects of thymol against the adverse effects of acetylsalicylic acid in rats: Biochemical and histopathological studies

Acetylsalicylic acid (Aspirin) has been used for a long time as an antipyretic and analgesic. Nevertheless, aspirin use is associated with severe morbidity and death because of its detrimental impacts on several organs, including the liver, kidneys, and stomach. The current investigation sought to ascertain the influence of thymol in mitigating aspirin-mediated gastric and hepato-renal injury. This was done by 1) evaluating gastric juice volume and pH as well as pepsin and prostaglandin E2 level; 2) measuring serum biochemical parameters and proinflammatory cytokines; 3) determining tissue oxidant/antioxidant status, and 4) identifying a link with gastric, hepatic and renal histopathological changes. Forty-eight rats were segregated to six groups: normal control, Th100, Th200, ASA, Th100 + ASA, Th200 + ASA. Daily administration of aspirin (ASA, 150 mg/kg body weight) for 3 successive days induced a significant increase in gastric juice volume, pepsin activity, serum transaminases, alkaline phosphatase, urea, creatinine, tumor necrosis factor-α, myeloperoxidase, and tissue malondialdehyde levels. In contrast, a significant reduction in gastric pH, prostaglandin E2, tissue non-enzymatic antioxidant (glutathione), and enzymatic antioxidant (superoxide dismutase, glutathione peroxidase, and catalase) levels. These biochemical changes were accompanied by histological modifications that included changes to the normal gastric, hepatic, and renal architectures. Pretreatment and simultaneous oral treatment with thymol (100 or 200 mg/kg body weight) plus ASA significantly improved all biochemical and histological changes in a dose-dependent way. Thymol's antiinflammatory and antioxidative properties may contribute to its protective action. As a result, thymol may represent a promising medication for preventing aspirin-induced gastric, liver, and renal damage.     

The effects of a low vitamin E diet on dichloroacetate- and trichloroacetate-induced oxidative stress in the livers of mice

Groups of mice were fed either a standard (Std) diet or a diet not supplemented with vitamin E (Low-E) and were divided into three subgroups that were treated subchronically by gavage, with water (control), dichloroacetate (DCA), or trichloroacetate (TCA). The livers of the animals were assayed for various biomarkers of oxidative stress (OS), antioxidant enzyme activities, and total glutathione (GSH). In general, livers from the low-E diet group expressed lower levels of biomarkers of OS associated with greater increases in various antioxidant enzymes activities and GSH when compared with the corresponding treatments in the Std diet group. These results suggest that vitamin E supplementation to the diet, while essential to maintain certain body functions, can compromise the effectiveness of the hepatic antioxidant enzymes and GSH resulting in an increase in DCA- and TCA-induced OS and a possible increase in the compounds-induced hepatotoxic/hepatocarcinogenic effects in mice.     

Mechanisms involved in reproductive damage caused by gossypol in rats and protective effects of vitamin E

Background

Gossypol is a chemical present in the seeds of cotton plants (Gossypium sp.) that reduces fertility in farm animals. Vitamin E is an antioxidant and may help to protect cells and tissues against the deleterious effects of free radicals. The aim of this study was to evaluate the mechanisms of reproductive toxicity of gossypol in rats and the protective effects of vitamin E. Forty Wistar rats were used, divided into four experimental groups (n = 10): DMSO/saline + corn oil; DMSO/saline + vitamin E; gossypol + corn oil; and gossypol + vitamin E.

Results

Fertility was significantly reduced in male rats treated with gossypol in that a significant decrease in epididymal sperm count was observed (P < 0.05) and the number of offspring was significantly reduced in females mated with them (P < 0.05). This dysfunction was prevented by vitamin E. Gossypol caused a significant increase in the activity of the enzymes glutathione peroxidase (P < 0.01) and glutathione reductase (P < 0.01), but vitamin E did not reduce the enzyme activities (P > 0.05). The levels of reduced glutathione and pyridine nucleotides in testis homogenate were significantly reduced by gossypol (P < 0.05 and P < 0.01, respectively) and this reduction was accompanied by increased levels of oxidized glutathione (P < 0.05). Vitamin E showed a preventive effect on the changes in the levels of these substances. Gossypol significantly increased the levels of malondialdehyde (P < 0.01), a lipid peroxidation indicator, whereas treatment with vitamin E inhibited the action of the gossypol. Vitamin E prevented a decrease in mitochondrial ATP induced by gossypol (P < 0.05).

Conclusions

This study suggests that the reproductive dysfunction caused by gossypol may be related to oxidative stress and mitochondrial bioenergetic damage and that treatment with vitamin E can prevent the infertility caused by the toxin.     

Hypoglycaemic, antioxidative and nephroprotective effects of taurine in alloxan diabetic rabbits

The therapeutic potential of taurine was investigated under diabetic conditions. Alloxan diabetic rabbits were treated daily for three weeks with 1% taurine in drinking water. The following parameters were measured: 1) serum glucose, urea, creatinine and hydroxyl free radical (HFR) levels; 2) blood glutathione redox state; 3) urine albumin concentration; 4) hepatic and renal HFR levels, GSH/GSSG ratios and the activities of catalase, superoxide dismutase and the enzymes of glutathione metabolism; 5) renal NADPH oxidase activity; 6) the rates of renal and hepatic gluconeogenesis. Histological studies of kidneys were also performed. Taurine administration to diabetic rabbits resulted in 30% decrease in serum glucose level and the normalisation of diabetes-elevated rate of renal gluconeogenesis. It also decreased serum urea and creatinine concentrations, attenuated diabetes-evoked decline in GSH/GSSG ratio and abolished hydroxyl free radicals accumulation in serum, liver and kidney cortex. Animals treated with taurine exhibited elevated activities of hepatic gamma-glutamylcysteine syntetase and renal glutathione reductase and catalase. Moreover, taurine treatment evoked the normalisation of diabetes-stimulated activity of renal NADPH oxidase and attenuated both albuminuria and glomerulopathy characteristic of diabetes. In view of these data, it is concluded that: 1) diminished rate of renal gluconeogenesis seems to contribute to hypoglycaemic effect of taurine; 2) taurine-induced increase in the activities of catalase and the enzymes of glutathione metabolism is of importance for antioxidative action of this amino acid and 3) taurine nephroprotective properties might result from diminished renal NADPH oxidase activity. Thus, taurine seems to be beneficial for the therapy of both diabetes and diabetic nephropathy.     

The antidiabetic effects of cysteinyl metformin, a newly synthesized agent, in alloxan- and streptozocin-induced diabetic rats

In this paper, the antidiabetic effects of cysteinyl metformin (CM), a newly synthesized agent, were investigated to evaluate the hypoglycemic/hypolipidemic effects by measuring blood glucose, triglyceride and insulin levels in CM- and metformin-treated diabetic rats. Two diabetic models were used: (1) an alloxan-induced model in which diabetes was produced by alloxan (200 mg/kg, i.p.), then rats were treated with CM (300, 100 and 33 mg/kg) for 14 days; (2) a streptozocin-induced model in which diabetes was produced by streptozocin (30 mg/kg, i.p.) and a sustained high lipid diet, then rats were treated with CM for 8 weeks. The hypoglycemic effect of CM exceeded that of metformin while the hypolipidemic effect was similar. In addition, CM increased the blood insulin level of the alloxan-induced experimental animals (which had an insulin deficiency), but reduced the insulin level of the streptozocin-induced animals (which had an insulin excess), suggesting that CM improves pancreatic beta-cell function. The effects of CM, metformin and cysteine on the antioxidant defense system in alloxan-induced rats were also studied. The serum malondialdehyde (MDA) level was determined to provide evidence for lipid peroxidation, All the groups of animals given CM, metformin and cysteine exhibited less severe oxidative stress than the diabetic group. Then, several key antioxidants such as superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT) and the pancreatic exocrine enzyme amylase (AMS) were measured. CM restored the activity of all these agents to nearly normal values while metformin and cysteine merely restored the activity of SOD. At the end of our study, the animals were sacrificed by decapitation and the liver, kidney and pancreas were weighed to allow investigation of organ edema. The results obtained showed that CM corrected the organ edema of the diabetic rats. All these findings suggested that CM has a protective effect on the antioxidant defense system and beta-cell dysfunction in alloxan-induced diabetic rats. All these results suggest that CM is a potential candidate for the future treatment of both type 1 and type 2 diabetes.     

Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats

Several recent studies have demonstrated that organophosphorus insecticides (OPI) possess the potential to disrupt glucose homeostasis leading to hyperglycemia in experimental animals. The propensity of OPI to induce hyperglycemia along with oxidative stress may have far-reaching consequences on diabetic outcomes and associated complications. The primary objective of this study was to assess the potential of monocrotophos (MCP), an extensively used OPI, on hepatic and renal oxidative stress markers and dysregulation of hepatic glucose homeostasis in experimentally induced diabetic rats. Rats rendered diabetic by a single dose of streptozotocin (60 mg/kg b.w) were orally administered MCP (0.9 mg/kg b.w/d for 5 d). Monocrotophos per se caused only a marginal increase in blood glucose levels but significantly elevated the blood glucose levels and also disrupted glucose homeostasis by depleting liver glycogen content and increasing the gluconeogenetic enzyme activities in diabetic rats. Experimentally induced diabetes was also associated with alterations in antioxidant enzymes in liver and kidney. MCP markedly enhanced lipid peroxidation in kidney and altered the enzymatic antioxidant defense mechanisms in both liver and kidney of diabetic rats. Collectively our data provides evidence that MCP has the propensity to augment the oxidative stress and further disrupt glucose homeostasis in diabetic rats.     

Antidiabetic activity of levan polysaccharide in alloxan-induced diabetic rats

This study aims to examine the effects of polysaccharide levan on oxidative stress and hyperglycemia in alloxan-induced diabetic rats. Levan, used in this study, was a microbial levan synthetisized by a non pathogenic bacteria recently isolated and identified as Bacillus licheniformis. Animals were allocated into four groups of six rats each: a control group (Control), diabetic group (Diab.), normal rats received levan (L) and diabetic rats fed with levan (DL). Treated diabetic rats were administrated with levan in drinking water through oral gavage for 60 days. The administration of polysaccharide levan in diabetic rats caused a significant increase in glycogen level by 52% and a decrease in glucose level in plasma by 52%. Similarly, the administration of polysaccharide levan in diabetic rats caused a decrease in the thiobarbituric acid-reactive substances (TBARS) by 31%, 41%, 39% and 25%, an increase in superoxide dismutase (SOD) by 40%, 50%, 44% and 34%, and in catalase (CAT) by 18%, 20%, 12% and 18% in liver, kidney, pancreas and heart, respectively. Furthermore, a significant decrease in hepatic and renal indices toxicity was observed, i.e. alkalines phosphatases (ALP), aspartate and lactate transaminases (AST and ALT) activities, total bilirubin, creatinine and urea levels by 19%, 31%, 32%, 36%, 37% and 23%, respectively. The results show that administration of polysaccharide levan can restore abnormal oxidative indice near normal levels. This study demonstrates, for the first time, that polysaccharide levan is efficient in inhibiting hyperglycemia and oxidative stress induced by diabetes and suggests that levan supplemented to diet may be helpful in preventing diabetic complications in adult rats.     

Tenoxicam Modulates Antioxidant Redox System and Lipid Peroxidation in Rat Brain

We investigated effects of two doses of Tenoxicam, a type 2 cyclooxygenase inhibitor, administration on lipid peroxidation and antioxidant redox system in cortex of the brain in rats. Twenty-two male Wistar rats were randomly divided into three groups. First group was used as control. 10 and 20 mg/kg body weight Tenoxicam were intramuscularly administrated to rats constituting the second and third groups for 10 days, respectively. Both dose of Tenoxicam administration resulted in significant increase in the glutathione peroxidase activity, reduced glutathione and vitamins C and E of cortex of the brain. The lipid peroxidation levels in the cortex of the brain were significantly decreased by the administration. Vitamin A and β-carotene concentration was not affected by the administration. There was no statistical difference in all values between 10 and 20 mg Tenoxicam administrated groups. In conclusion, treatment of brain with 10 and 20 mg Tenoxicam has protective effects on the oxidative stress by inhibiting free radical and supporting antioxidant redox system.     

Assessment of genomic instability in normal and diabetic rats treated with metformin

To examine if a single or multiple oral administration of metformin, a member of the biguanide class of anti-diabetic agents, has any genotoxic and cytotoxic potential in normal and diabetic rats, a mammalian model, cytogenetic assays through several endpoints such as induction of micronuclei, chromosome aberrations, mitotic activity of bone marrow cells, sperm-head anomaly and assays of some oxidative stress markers have been conducted by the use of standard techniques. Diabetes was induced by streptozotocin injection. Metformin was administrated to both diabetic and non-diabetic rats in single doses of 100, 500 or 2500 mg/kg along with vehicle control groups for diabetic and non-diabetic rats. The animals were killed by cervical dislocation at 24 h after treatment, and then bone marrow cells were sampled. Also, a multiple dose study has done in which diabetic and non-diabetic animals were treated with 100 or 500 mg/kg of metformin daily for 4 or 8 weeks after which the animals were killed by cervical dislocation, and then bone marrow and sperm cells were collected. Concurrent control groups were also included in each experiment. The obtained results revealed that metformin was neither genotoxic nor cytotoxic for the rats in all groups at all tested doses. Moreover, metformin significantly reduced the diabetes-induced genomic instability and cell proliferation changes in somatic and germinal cells in a dose-dependent manner (2500, 500, >100 mg/kg). In addition, diabetes induced marked biochemical alterations characteristic of oxidative stress including, enhanced lipid peroxidation and reduction in the reduced glutathione level. Treatment with metformin ameliorated these biochemical markers. In conclusion, metformin is a non-genotoxic or cytotoxic compound and may protect from genomic instability induced by hyperglycemia. Apart from its well-known anti-diabetic effect, the antigenotoxic effect of metformin could be possibly ascribed to its radical scavenger effect that modulated the genomic instability responses and cell proliferation changes induced by hyperglycemia.     

Ameliorative effects of resveratrol on liver injury in streptozotocin‐induced diabetic rats

The objective of this study was to investigate the ameliorative property and potential mechanism of resveratrol (RVT) in a dose of 10 mg/kg for 15 consecutive days against liver injury in streptozotocin‐induced diabetic rats. Diabetic rats significantly (P < 0.05) exhibited liver injury manifested by increased aspartylaminotransferase, alanine aminotransferase, and bilirubin; disturbed liver weight to body weight; and confirmed by hematoxylin and eosin staining. Liver from diabetic rats exhibited significant increase in malondialdehyde level and significant decrease in reduced glutathione, glutathione‐S‐transferase, quinone reductase, catalase, and superoxide dismutase. Diabetic rats showed significant disturbance in serum lipid profile. Treatment with RVT significantly (P < 0.05) abrogated diabetes‐induced perturbation in these parameters and liver histology. These data suggest that RVT treatment is associated with promising hepatoprotective effect against diabetes‐induced liver damage via reduction of serum glucose level and oxidative damage and improving serum lipid profile. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:384–392, 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21432     

Evaluation of the andrographolides role and its indoleamine 2,3-dioxygenase inhibitory potential and attendant molecular mechanism against STZ-induced diabetic rats

The study is to scrutinize andrographolides with Indoleamine 2,3-dioxygenase (IDO) inhibitory potential, its molecular mechanism against streptozotocin (STZ) diabetic retinopathy (DR) in Wistar rats. Oxidative stress markers such as Kynurenine metabolites, retinal histopathological changes have been studied. Further, IDO gene expression and docking studies have been performed. Andrographolide treated rats have been reducing the level of thiobarbituric acid reactive substances and protein carbonyls Kynurenine metabolites with an improvement in the level of GSH and expression of IDO as revealed by morphological changes in inner and outer nuclear layer of the retina. The current results of this study have been generated information about an activity of the andrographolide in the essential pocket of IDO. Our results explain, involving IDO and andrographolide would constitute an attempt to identify natural products with therapeutic value and further studies in this direction would be of immense significance in the administration of diabetes and its related problems.     

The effect of α-tocopherol transfer protein gene disruption on Trypanosoma congolense infection in mice

At present 15 to 20 million people are estimated to be infected with pathogenic trypanosome parasites worldwide, mainly in developing countries. There are a number of factors that affect the severity of trypanosomiasis, including the nutritional status of the host. However, the relationship between micronutrient levels and trypanosomiasis outcome has yet to be reported in detail. Here, we demonstrate that the inhibition of α-tocopherol transfer protein, a determinant of the vitamin E concentration in host circulation, confers resistance to Trypanosoma congolense infection, evidently owing to oxidative damage to parasite DNA. These results suggest that transient inhibition of α-tocopherol transfer gene activity could possibly be exploited as a strategy for both the prevention and the treatment of trypanosomiasis.     

Induction of heme oxygenase 1 in liver of spontaneously diabetic rats

It has been suggested that diabetes induces an increase in oxidative stress; the increased expression of heme-oxygenase 1 (HO-1) in liver is believed to be a sensitive marker of the stress response. The aim of this study was to examine whether diabetes is able to induce HO-1 expression in liver. The specific mRNA was amplified by RT/PCR and calibrated with amplified β-actin mRNA.

The mRNA HO-1 levels in the liver of spontaneously diabetic rats were increased by 1.8 fold compared with non diabetics; this supports the hypothesis of weak but significant oxidative damage due to chronic hyperglycaemia. This work represents the first in vivo study exploring the semi-quantitative expression of HO-1 in the liver of spontaneously diabetic rats.     

In vivo imaging of oxidative stress in the kidney of diabetic mice and its normalization by angiotensin II type 1 receptor blocker

This study was undertaken to evaluate oxidative stress in the kidney of diabetic mice by electron spin resonance (ESR) imaging technique. Oxidative stress in the kidney was evaluated as organ-specific reducing activity with the signal decay rates of carbamoyl-PROXYL probe using ESR imaging. The signal decay rates were significantly faster in corresponding image pixels of the kidneys of streptozotocin-induced diabetic mice than in those of controls. This technique further demonstrated that administration of angiotensin II type 1 receptor blocker (ARB), olmesartan (5 mg/kg), completely restored the signal decay rates in the diabetic kidneys to control values. In conclusion, this study provided for the first time the in vivo evidence for increased oxidative stress in the kidneys of diabetic mice and its normalization by ARB as evaluated by ESR imaging. This technique would be useful as a means of further elucidating the role of oxidative stress in diabetic nephropathy.     

Action of pelargonidin on hyperglycemia and oxidative damage in diabetic rats: implication for glycation-induced hemoglobin modification

Glycation-modified hemoglobin in diabetes mellitus has been suggested to be a source of enhanced catalytic iron and free radicals causing pathological complications. The present study aims to verify this idea in experimental diabetes. Pelargonidin, an anthocyanidin, has been tested for its antidiabetic potential with emphasis on its role against pathological oxidative stress including hemoglobin-mediated free radical reactions. Male wistar rats were grouped as normal control, streptozotocin-induced diabetic control, normal treated with pelargonidin and diabetic treated with pelargonidin. Pelargonidin-treated rats received one time i.p injection of the flavonoid (3 mg/kg bodyweight). Biochemical parameters were assayed in blood samples of different groups of rats. Liver was used for histological examinations. Pelargonidin treatment normalized elevated blood glucose levels and improved serum insulin levels in diabetic rats. Glucose tolerance test appeared normal after treatment. Decreased serum levels of SOD and catalase, and increased levels of malondialdehyde and fructosamine in diabetic rats were reverted to their respective normal values after pelargonidin administration. Extents of hemoglobin glycation, hemoglobin-mediated iron release, iron-mediated free radical reactions and carbonyl formation in hemoglobin were pronounced in diabetic rats, indicating association between hemoglobin glycation and oxidative stress in diabetes. Pelargonidin counteracts hemoglobin glycation, iron release from the heme protein and iron-mediated oxidative damages, confirming glycated hemoglobin-associated oxidative stress in diabetes.     

Effects of safranal,a constituent of saffron,and vitamin E on nerve functions and histopathology following crush injury of sciatic nerve in rats

Safranal is one of the major components of saffron and has many biological effects such as antioxidant property. The present study investigated the effects of safranal on sciatic nerve function after induction of crush injury. We also used of vitamin E as a reference potent antioxidant agent.In anesthetized rats, right sciatic nerve was crushed using a small haemostatic forceps. Functional recovery was assessed using sciatic functional index (SFI). Acetone spray and von Frey filament tests were used for neuropathic pain assay. Histopathological changes including severities of Wallerian degeneration of sciatic nerve and gastrocnemius muscle atrophy were investigated by light microscopy. Blood levels of malodialdehyde (MDA) were also measured.The SFI values were accelerated, cold and mechanical allodynia were suppressed, the severities of Wallerian degeneration and muscular atrophy were improved, and the increased MDA level was reversed with 10 consecutive days intraperitoneal injections of 0.2 and 0.8 mg/kg of safranal and 100 mg/kg of vitamin E.It is concluded that safranal and vitamin E produced same improving effects on crushed-injured sciatic nerve functions. Inhibition of oxidative stress pathway may be involved in improving effects of safranal and vitamin E on functions and histopathology of an injured peripheral nerve.     

Zinc deficient diet exacerbates the testicular and epididymal damage in type 2 diabetic rat: Studies on oxidative stress-related mechanisms

Zinc (Zn) is one of the most important trace elements in the body and is required for insulin secretion and release. Zn is also required for the growth and development of the reproductive system. Alteration in the Zn levels can cause moderate to severe damage to various organs, including the reproductive system. Most of type 2 diabetic patients have altered Zn levels/signaling. So, here we investigated the role of Zn-deficient diet (ZDD) in type 2 diabetes. Type 2 diabetes in the rat was induced by the combination of high-fat diet (HFD) and a single low dose of streptozotocin (STZ, 35 mg/kg, i.p.). Control animals were fed normal pellet diet throughout the study, while ZDD was given for four consecutive weeks to the diabetic rats, which were earlier kept on HFD for 16 weeks. The present findings showed that ZDD further decreased the serum Zn, plasma insulin and serum testosterone levels, whereas it increased cholesterol, triglycerides, BUN, %HbA1c in diabetic rats. Oxidative stress in testes was increased by ZDD as evidenced by decreased glutathione, catalase and SOD1 levels. ZDD-induced several abnormalities in sperm head morphology, altered sperm decondensation, sperm chromatin and protamine content, along with significant histopathological alterations in testes and epididymis. Further, ZDD altered protein levels of MT, MTF-1, Keap1, Nrf2, Nf-κB, GPX4 and GPX5 levels in the testes and epididymis of diabetic rat. The present results demonstrated that dietary Zn deficiency could exacerbate type 2 diabetes-induced germ cell damage.     

Effects of resveratrol on biomarkers of oxidative stress and on the activity of delta aminolevulinic acid dehydratase in liver and kidney of streptozotocin-induced diabetic rats

The present study investigated the effects of resveratrol (RV), a polyphenol with potent antioxidant properties, on oxidative stress parameters in liver and kidney, as well as on serum biochemical parameters of streptozotocin (STZ)-induced diabetic rats. Animals were divided into six groups (n = 8): control/saline; control/RV 10 mg/kg; control/RV 20 mg/kg; diabetic/saline; diabetic/RV10 mg/kg; diabetic/RV 20 mg/kg. After 30 days of treatment with resveratrol the animals were sacrificed and the liver, kidney and serum were used for experimental determinations. Results showed that TBARS levels were significantly increased in the diabetic/saline group and the administration of resveratrol prevented this increase in the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). The activities of catalase (CAT), superoxide dismutase (SOD) and aminolevulinic acid dehydratase (δ-ALA-D) and the levels of non protein thiols (NPSH) and vitamin C presented a significant decrease in the diabetic/saline group when compared with the control/saline group (P < 0.05). The treatment with resveratrol was able to prevent these decrease improving the antioxidant defense of the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). In addition, the elevation in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamiltransferase (γ-GT) activities as well as in levels of urea, creatinine, cholesterol and triglycerides observed in the diabetic/saline group were reverted to levels close to normal by the administration of resveratrol in the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). These findings suggest that resveratrol could have a protector effect against hepatic and renal damage induced by oxidative stress in the diabetic state, which was evidenced by the capacity of this polyphenol to modulate the antioxidant defense and to decrease the lipid peroxidation in these tissues.     

Protective action of vitamins on the spermatogenesis in lead-treated Swiss mice

The protective action of vitamins C and E against lead acetate-induced reduced sperm count and sperm abnormalities in Swiss mice has been studied. Intraperitoneal injection of lead acetate (10mg/kg body weight) in the present study stimulates lipid peroxidation in the testicular tissue, indicated by a significant increase in malondialdehyde content in the experimental mice group. This is associated with an increased generation of noxious reactive oxygen species (ROS). Significantly reduced sperm count associated with increased sperm abnormality percentage in the lead-injected mice group compared to controls substantially proves the ongoing damaging effects of lead-induced ROS on developing germ cells. However, intraperitoneal administration of vitamin C (Vit C) at a concentration equivalent to the human therapeutic dose (10 mg/kg body weight) was able to minimize significantly the testicular malondialdehyde content with a concomitant increase in sperm count and significant decrease in the percentage of abnormal sperm population. Vitamin E (Vit E) (100 mg/kg body weight) treatment of a batch of lead-injected mice had a similar effect as Vit C but with a comparatively lower efficacy. On the other hand, coadministration of both vitamins (Vit C + Vit E) at the above mentioned doses to lead-treated mice led to the most significant decline in malondialdehyde content along with elevated sperm count and reduction in the percentage of abnormal sperm population. The protective action and the synergistic action of both vitamins (C and E) against lead-induced genotoxicity are discussed.