Amelioration of vanadium-induced testicular toxicity and adrenocortical hyperactivity by vitamin E acetate in rats

Vanadium toxicity is a challenging problem to the health professionals and a cutting-edge medical problem. Vanadium has been recognized as industrial hazards that adversely affect human and animal reproductive health. Since testicular function is exquisitely susceptible to reactive-oxygen species, the present study elucidates the possible involvement of oxidative stress in vanadium-induced testicular toxicity and the prophylactic effects of vitamin E acetate against such adverse effects of vanadium. The study also characterizes the effects of vanadium on rat adrenal steroidogenesis and determines the underlying mechanisms of testicular and adrenal interactions in response to vanadium exposure. Significantly reduced sperm count associated with decreased serum testosterone and gonadotropins level in the vanadium-injected group of rats compared to control substantially proves the ongoing damaging effects of vanadium-induced ROS on developing germ cells. This is in turn reflected in the appreciable increase in testicular lipid peroxidation level and decline in the activities of steroidogenic and antioxidant enzymes. However, oral administration of vitamin E acetate could protect testes from the toxic effects of vanadium. Vanadium also results in adrenocortical hyperactivity, as evidenced by the elevated secretion of glucocorticoids, adrenal gland hypertrophy and increased activity of adrenal Δ⁵3β-HSD. However, reversibility of these alterations in adrenocortical activities was vividly reflected after vitamin E acetate supplementation. All these studies reveal that oxidative stress is the major mechanism of health deterioration and that vanadium can act as a stressor metal causing chronic stress effects through excitation of hypothalamo-pituitary-adrenal axis. However antioxidant support by vitamin E acetate may provide significant protection.     

Aortic coarctation induces oxidative stress in rat tissues

The purpose of this study was to evaluate the induction of oxidative stress in heart and erythrocytes from rats with abdominal aorta coarctation (Coa) compared with sham-operated normotensive controls (Sham). The group of Coa animals developed myocardial hypertrophy, showing heart homogenates markedly increased levels of reduced glutathione (48%), lipid peroxidation (148%) and activation of superoxide dismutase and glutathione peroxidase (189% and 37%, respectively), compared with controls. Other oxidative stress indicators were also altered in erythrocytes from Coa rats: increased protein carbonyl content (141%) and total glutathione level (349%) were determined. Inactivation of the antioxidant enzymes catalase (27%), superoxide dismutase (58%) and glutathione peroxidase (25%) was observed in erythrocytes from the Coa group. Taken jointly our results provide strong evidence for the production of oxidative stress in heart and erythrocytes from aortic coarcted rats.     

Beneficial effects of DL-alpha-lipoic acid on cyclophosphamide-induced oxidative stress in mitochondrial fractions of rat testis

The present study investigated the protective efficacy of dl-alpha-lipoic acid on the peroxidative damage and abnormal antioxidant levels in the mitochondrial fraction of testis in cyclophosphamide (CP) administered rats. Male Wistar rats of 140+/-20 g were categorized into four groups. Two groups were administered CP (15 mg/kg body weight once a week for 10 weeks by oral gavage) to induce testicular toxicity; one of these groups received lipoic acid treatment (35 mg/kg body weight intraperitoneally once a week for 10 weeks, 24 h prior to CP administration). A vehicle-treated control group and a lipoic acid drug control group were also included. The mitochondrial fraction of untreated CP-exposed testis showed 1.84-fold increase in lipid peroxidation, along with a significant (P<0.001) increase in hydrogen peroxide levels. In CP-exposed rats, we observed abnormal changes in the activities/levels of mitochondrial enzymic (superoxide dismutase, glutathione peroxidase and glutathione reductase) and non-enzymic (reduced glutathione, ascorbate and alpha-tocopherol) antioxidants. CP-treated rats also showed decline in the activities of mitochondrial enzymes such as succinate dehydrogenase, malate dehydrogenase and isocitrate dehydrogenase. In contrast, rats pretreated with lipoic acid showed normal lipid peroxidation and antioxidant defenses, thereby showing the protection rendered by lipoic acid.     

No evidence for oxidative stress as a mechanism of action of hyperhomocysteinemia in humans

Oxidative stress has been suggested as one of the physiopathologic conditions underlying the association of total plasma homocysteine (p-tHcy) with cardiovascular disease (CVD), but this hypothesis has not been validated in human epidemiological studies. We measured plasma and erythrocyte antioxidant enzymes glutathione peroxidase (GPx) and superoxide dismutase (SOD), along with serum lipid-soluble antioxidants alpha-tocopherol, beta-carotene, lycopene and retinol, in a sample of 123 healthy elderly subjects (54 men, 69 women). Plasma malondialdehyde (p-MDA) was determined as a marker of lipid peroxidation, and p-tHcy was quantified by HPLC. No significant differences were found for p-MDA, GPx or SOD activities or serum antioxidant concentrations, in subjects with elevated p-tHcy (≥15 μmol/l) as compared to those with lower plasma homocysteine. Hyperhomocysteinemia did not lead to increased risk of having the highest p-MDA values, in either sex. We found no evidence that p-tHcy was associated with lipid peroxidation in this elderly human sample. Our results do not support the view that hyperhomocysteinemia would induce an adaptive response of antioxidant systems, either. More epidemiologic and clinical research is needed to clarify whether homocysteine promotes atherosclerosis by means of an oxidative stress mechanism.     

Biochemical markers of oxidative stress in Perna viridis exposed to mercury and temperature

Oxidative damage and antioxidant properties have been studied in Perna viridis subjected to short-term exposure to Hg along with temperature (72h) and long-term temperature exposures (14 days) as pollution biomarkers. The elevated thiobarbituric acid reactive substances (TBA-RS) levels observed in gills and digestive gland under exposure to Hg, individually and combined with temperature, as also long-term temperature stress have been assigned to the oxidative damage resulting in lipid peroxidation (LPX). Increased activities of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-S-transferase (GST) both in gills and digestive glands under long-term exposures to temperatures are more prominent to heat rather than cold stress suggesting activation of physiological mechanism to scavenge the ROS produced during heat stress. Also decreased values of reduced glutathione (GSH) on long exposures to temperature stress indicate utilisation of this antioxidant, either to scavenge oxiradicals or act in combination with other enzymes, was more than its production capacity under heat stress. The results suggest that temperature variation does alter the active oxygen metabolism by modulating antioxidant enzyme activities, which can be used as biomarker to detect sublethal effects of pollution.     

Effects of 28-homobrassinolide on growth, lipid peroxidation and antioxidative enzyme activities in seedlings of Zea mays L. under salinity stress

The effects of 28-homobrassinolide (28-homoBL) on seedling growth, lipid peroxidation and antioxidative enzyme activities in the seedlings of Zea mays L. (var. Partap-1) under salt (NaCl) stress were studied. The surface-sterilized seeds were germinated in petriplates containing different concentrations of NaCl (25, 50, 75 and 100 mM) only, 28-homoBL (10⁻⁷, 10⁻⁹ and 10⁻¹¹ M) only and NaCl supplemented with 28-homoBL for 7 days. The activities of superoxide dismutase (SOD, EC 1.15.1.1), guaiacol peroxidase (POD, EC 1.11.1.7), catalase (CAT, EC 1.11.1.6), ascorbate peroxidase (APOX, EC 1.11.1.11) and glutathione reductase (EC 1.6.4.2) were analysed in 7 day-old seedlings. It was observed that 28-homoBL treatments reduced the toxicity of salt on seedling growth considerably. Lipid peroxidation level was significantly increased under saline stress, but lowered with 28-homoBL applications revealing less oxidative damage. Further 28-homoBL treatments to the seedlings showed an enhancement in activities of SOD, POD, CAT and APOX. The activities of all antioxidative enzymes were further increased in seedlings treated with solution containing 28-homoBL and salt together as compared to seedlings treated with different concentration of salt solution only.     

温度和紫外辐射胁迫对西藏飞蝗抗氧化系统的影响

为探讨西藏飞蝗(Locusta migratoria tibetensis Chen)对环境的适应机制,报道了温度和紫外辐射胁迫对西藏飞蝗抗氧化系统影响。以西藏飞蝗成虫为试材,研究5—20℃低温、30—45℃高温胁迫和紫外线辐射对其抗氧化酶活性和膜脂过氧化物丙二醛(MDA)含量的影响。在5—20℃低温胁迫下,成虫体壁和消化道超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性及丙二醛(MDA)含量分别随温度降低而升高;在30—35℃高温胁迫下,成虫SOD、POD和CAT活性分别随温度升高而升高,当温度超过35℃时,3种氧化酶活性均下降。长波紫外辐射(UV-A)和中波紫外辐射(UV-B)对处理后24h和72h成虫的SOD活性的影响大于可见光,在UV-A、UV-B和可见光3种光波长处理下,成虫的POD和CAT活性随光照时间的延长而增加,其中UV-B对两种酶活性影响大于UV-A和可见光,表现为UV-B处理组>UV-A处理组>可见光处理组;UV-A和UV-B处理能导致虫体体壁MDA含量明显升高,且对脂质过氧化的诱导存在时间效应;雌虫体壁、雌虫消化道、雄虫体壁和雄虫消化道的MDA含量分别在UV-B72h、UV-A72h、UV-A72h和UV-B72h达最大值0.72、0.88、0.66和0.94 nmol/g鲜重。在20—5℃低温胁迫下,西藏飞蝗成虫抗氧化酶活性升高,能较好的保护自身免遭活性氧自由基的伤害;西藏飞蝗对高温忍耐力差,在高于35℃高温胁迫下,成虫SOD、POD、CAT活性均下降;在长波和中波紫外辐射下,西藏飞蝗抗氧化酶活性显著升高,是西藏飞蝗对紫外线辐射强度大的青藏高原的一种重要适应。     

Effect of anti-estrogen and anti-progesterone on spermatogenesis,testosterone production and expression of steroidogenic enzyme genes in adult male rats

The present study was planned to investigate the anti-spermatogenic and anti-steroidogenic effects of Clomiphene Citrate (CC) an anti-estrogen and Mifepristone (MT) an anti-progesterone in the testis of male rats. Following the oral administration of 1.0 mg and 5.0 mg/kg b.w/day of each for the duration of 30 and 60 days, quantitation of spermatogenesis, RIA for serum and intra-testicular testosterone levels, western blotting and RT-PCR for expression of StAR, 3β-HSD and P450arom enzymes in the testis was done. Clomiphene Citrate at 5.0 mg/kg b.w/day for 60 days significantly reduced testosterone (T) levels however the effect was not significant with the lower doses. Reproductive parameters in animals treated by Mifepristone remained mostly unaffected, however, a significant decline in testosterone levels and altered expression of selected genes was observed in 5.0 mg for the 30d treatment group. Clomiphene Citrate at higher doses affected the weights of the testis and secondary sex organs. Seminiferous tubules revealed hypo-spermatogenesis with a significant decrease in the number of maturing germ cells and a reduction in tubular diameter. Attenuation in serum testosterone was associated with the downregulation of expression in StAR, 3β-HSD, and P450arom mRNA and protein levels in the testis even after 30 d of CC administration. The results indicate that the anti-estrogen (Clomiphene Citrate) but not anti-progesterone (Mifepristone) induces hypo-spermatogenesis in rats which are associated with a downregulation of expression of two of the steroidogenic enzymes, 3β-HSD and P450arom mRNA and StAR protein.     

Genotoxicity and oxidative stress in fish after a short-term exposure to silver nanoparticles

This study examined the effects of waterborne silver nanoparticles (AgNPs) on juvenile fish Piaractus mesopotamicus (“pacú”), and analyzed toxicological endpoints such as metal burdens, oxidative stress and genotoxicity in a short-term assay. Fish were individually exposed to 0 (control), 2.5, 10, and 25 μg AgNPs/L. After 24 h, silver accumulation was greater in the brain than the liver and gills at all silver concentrations. Fish exposed to higher AgNPs concentrations showed major alterations in oxidative stress markers. An increase in lipid peroxidation (LPO) levels was observed in the liver of fish exposed to 10 μg AgNPs/L with no changes in the antioxidant enzymes activities. In the case of the 25 μg AgNPs/L treatment, a hepatic activation of the enzymatic antioxidant defense occurred, and LPO levels resulted unaltered. On the other hand, the brain presented the highest LPO levels at both 10 and 25 μg AgNPs/L exposures. The AgNPs toxicity was also evidenced by the DNA damage in fish erythrocytes at higher concentrations. Summarizing, a short exposure to sublethal concentrations of AgNPs is enough to generate deleterious effects on fish, including DNA damage.     

Ameliorative effect of kaempferol,a flavonoid,on oxidative stress in streptozotocin-induced diabetic rats

Abstract

Objective

The aim of the present study was to evaluate the protective effect of kaempferol against oxidative stress in streptozotocin (STZ)-induced diabetic rats.

Methods

Diabetes was induced in male, adult albino rats of the Wistar strain, by intraperitoneal administration of STZ (40 mg/kg body weight (BW)). Kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) was administered orally once daily for 45 days to normal and STZ-induced diabetic rats.

Results

The STZ-induced diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes in plasma, liver, kidney, and heart whereas they showed significantly decreased level of plasma insulin. The levels of non-enzymic antioxidants (vitamin C, vitamin E, reduced glutathione) in plasma, liver, kidney, and heart and the activities of enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) in liver, kidney, and heart were significantly decreased in diabetic rats. Administration of kaempferol to diabetic rats was showed brought back in plasma glucose, insulin, lipid peroxidation products, enzymatic, and non-enzymatic antioxidants to near normal.

Conclusion

The present study indicates that kaempferol has a good antioxidant property, as evidenced by its increase of antioxidant status and decrease of lipid peroxidation markers, thus providing protection from the risks of diabetic complications.     

Arbuscular mycorrhizal fungi regulate the oxidative system,hormones and ionic equilibrium to trigger salt stress tolerance in Cucumis sativus L.

Arbuscular mycorrhizal fungi (AMF) association increases plant stress tolerance. This study aimed to determine the mitigation effect of AMF on the growth and metabolic changes of cucumbers under adverse impact of salt stress. Salinity reduced the water content and synthesis of pigments. However, AMF inoculation ameliorated negative effects by enhancing the biomass, synthesis of pigments, activity of antioxidant enzymes, including superoxide dismutase, catalase, ascorbate peroxidase and glutathione reductase, and the content of ascorbic acid, which might be the result of lower level lipid peroxidation and electrolyte leakage. An accumulation of phenols and proline in AMF-inoculated plants also mediated the elimination of superoxide radicals. In addition, jasmonic acid, salicylic acid and several important mineral elements (K, Ca, Mg, Zn, Fe, Mn and Cu) were enhanced with significant reductions in the uptake of deleterious ions like Na+. These results suggested that AMF can protect cucumber growth from salt stress.     

Chilling,oxidative stress and antioxidant responses inArabidopsis thaliana callus

Chilling ofArabidopsis thaliana (L.) Heynh. callus tissue to 4 °C led to conditions of oxidative stress, as indicated by increased levels of the products of peroxidative damage to cell membranes. Cellular H₂O₂ was also observed to increase initially upon chilling but by day 8 cellular levels had declined to below control levels. Although levels of catalase activity remained similar to those in unchilled tissue, activity of ascorbate peroxidase increased between days 4 and 8 of chilling to 4 °C. In callus held at 23 °C, levels of reduced glutathione remained static whereas they rose in callus held at 4 °C. Levels of oxidised glutathione were initially low but increased significantly by day 4 in the chilled callus. At 23 °C, however, levels of oxidised glutathione remained low. Between days 1 and 3 at 4 °C, levels of glutathione reductase activity increased but by day 8 glutathione reductase activity was similar to that in cells held at 23 °C. Exposure of callus to abscisic acid at 23 °C also led to increased activities of ascorbate peroxidase and glutathione reductase.Abbreviations ABA abscisic acid - GSH reduced glutathione - GSSG oxidised glutathione - TTC 2,35-triphenyltetrazolium chloride This work is supported by a grant from the Biotechnology and Biological Sciences Research Council.     

Dapsone induces oxidative stress and impairs antioxidant defenses in rat liver

Dapsone (DDS) is currently used in the treatment of leprosy, malaria and in infections with Pneumocystis jirovecii and Toxoplasma gondii in AIDS patients. Adverse effects of DDS involve methemoglobinemia and hemolysis and, to a lower extent, liver damage, though the mechanism is poorly characterized. We evaluated the effect of DDS administration to male and female rats (30 mg/kg body wt, twice a day, for 4 days) on liver oxidative stress through assessment of biliary output and liver content of reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and expression/activities of the main antioxidant enzymes glutathione peroxidase, superoxide dismutase, catalase and glutathione S-transferase. The influence of DDS treatment on expression/activity of the main DDS phase-II-metabolizing system, UDP-glucuronosyltransferase (UGT), was additionally evaluated. The involvement of dapsone hydroxylamine (DDS-NHOH) generation in these processes was estimated by comparing the data in male and female rats since N-hydroxylation of DDS mainly occurs in males. Our studies revealed an increase in the GSSG/GSH biliary output ratio, a sensitive indicator of oxidative stress, and in lipid peroxidation, in male but not in female rats treated with DDS. The activity of all antioxidant enzymes was significantly impaired by DDS treatment also in male rats, whereas UGT activity was not affected in any sex. Taken together, the evidence indicates that DDS induces oxidative stress in rat liver and that N-hydroxylation of DDS was the likely mediator. Impairment in the activity of enzymatic antioxidant systems, also associated with DDS-NHOH formation, constituted a key aggravating factor.     

Influence of 50 Hz electromagnetic frequency on oxidative stress and morphological characteristics in mosquito-borne filariasis Culex pipiens

The electromagnetic field (EMF) is a vital issue in research, but its use as an alternative technique for insect management is still in its beginnings. The study aimed to evaluate the effects of exposure to the electromagnetic field on the biochemical analysis and morphological characteristics in Culex pipiens. Therefore, the third instar larvae were exposed to EMF frequency (50 Hz) at different intensities (250, 500, 1000 mT) for 1 h during four successive days. After end exposure to EMF, the biochemical analysis, oxidative stress parameters, body weight, and morphological features were investigated. The results showed that larval body weight and total protein content were decreased significantly in all treated groups compared to controls. The total lipid content significantly decreased at 500 & 1000 mT exposure, while the treatment group exposed to EMF at 250 mT was not statistically different compared to control. At a high intensity of EMF 1000 mT all oxidative stress parameters; catalase (CAT) and Glutathione S-transferase (GST) activity and lipid peroxidation level (MDA) were decreased significantly compared to the control. On the other hand, at a low intensity (250 mT), CAT and GST activity was significantly increased, while MDA content was not statistically changed. Scanning electron microscopy showed that both 500 & 1000 mT caused distinct malformations to the larval body parts, mouthparts, thorax and abdomen with last abdominal structures. In conclusion, the results demonstrated that EMF exposure is a considerable stress factor that affects oxidative state and morphological features in mosquitoes and give hope that EMF will be used as an alternative method for Culex pipiens vector control.     

Ameliorating effects of troxerutin on nickel-induced oxidative stress in rats

Abstract

Objective

This study investigates the effects of troxerutin on nickel (Ni)-induced oxidative stress in rats.

Methods

Nickel as nickel sulfate (20 mg/kg body weight (b.w.)) was administered intraperitoneally for 20 days to induce toxicity in the subject rats. The levels of stress markers AST, ALT, ALP, LDH, and GGT in the hepatic tissue were significantly increased while a decrease in the levels of enzymic and non-enzymic antioxidants was observed in Ni intoxicated rats.

Results

Oral administration of troxerutin along with Ni for 20 days in a dose-dependent manner significantly reverted the stress markers in the liver tissue to near normal level. Troxerutin exhibited significant protection at 100 mg/kg b.w. Histopathological studies also supported the above findings.

Conclusions

Thus, we conclude that troxerutin preserved the histo-architecture and ameliorated stress markers in the liver tissue of Ni-intoxicated rats.     

水分胁迫对黄檗幼苗保护酶活性及脂质过氧化作用的影响

以轻度干旱、重度干旱和水涝处理黄檗幼苗,测定丙二醛(MDA)和游离脯氨酸含量及超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性的动态变化.结果表明,处理40 d以后,轻度干旱、重度干旱和水涝处理的叶片MDA含量始终显著高于对照,最高分别达对照的2.9、2.37和4.12倍,三者之间在处理80 d以后MDA含量差异不显著.水涝处理和对照的游离脯氨酸含量在处理期间没有明显变化,干旱处理的游离脯氨酸含量从处理后40 d开始增加、80 d后回落,重度干旱处理的增加幅度显著大于轻度干旱处理.SOD、POD和CAT活性的变化趋势缺乏一致性,但重度干旱处理的黄檗幼苗,叶片的SOD、POD和CAT活性在处理期间始终显著高于轻度干旱、水涝处理和对照.     

Combined effect of salicylic acid and salinity on some antioxidant activities,oxidative stress and metabolite accumulation in <Emphasis Type="Italic">Phaseolus vulgaris</Emphasis>

It has been shown that salicylic acid (SA) acts as an endogenous signal molecule responsible for inducing abiotic stress tolerance in plants. The effect of SA and sodium chloride (NaCl) on growth, metabolite accumulation, oxidative stress and enzymatic and non-enzymatic antioxidant responses on common bean plants (Phaseolus vulgaris, cv. F-15) was studied. Results revealed that either SA or NaCl decrease, shoot, root and total plant dry weights. SA treatments decreased the contents of proline, and reduced forms of ascorbate and glutathione, however, the content of soluble sugars (TSS), thiobarbituric acid-reactive substances (TBARs) and oxidized ascorbate remained unaffected. On the other hand, salinity significantly reduced the levels of endogenous SA but increased the content of proline, soluble sugars, TBARs, ascorbate and glutathione, as well as all increasing the levels of antioxidant enzyme activities assayed, except CAT. The application of SA improved the response of common bean plants to salinity by increasing plant dry weight and decreasing the content of organic solutes (proline and TSS) and damage to the membrane (TBARs). Moreover, SA application under saline conditions decreased the levels of antioxidant enzyme activities POX, APX and MDHAR which could indicate successful acclimatization of these plants to saline conditions.     

Silicon-mediated changes of some physiological and enzymatic parameters symptomatic for oxidative stress in spinach and tomato grown in sodic-B toxic soil

We investigated effect of silicon (Si) on the growth, uptake of sodium (Na), chloride (Cl), boron (B), stomatal resistance (SR), lipid peroxidation (MDA), membrane permeability (MP), lipoxygenase (LOX) activity, proline (PRO) accumulation, H₂O₂ accumulation, non-enzymatic antioxidant activity (AA) and the activities of major antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT and ascorbate peroxidase, APX) of spinach and tomato grown in sodic-B toxic soil. Si applied to the sodic-B toxic soil at 2.5 and 5.0 mM concentrations significantly increased the Si concentration in the plant species and counteracted the deleterious effects of high concentrations of Na, Cl and B on root and shoot growth by lowering the accumulation of these elements in the plants. Stomatal resistance, MP, MDA and the concentrations of H₂O₂ and PRO were higher in the plants grown in sodic-B toxic soil without Si: LOX activity of excised leaves of both species was increased by Si. Antioxidant activities of both species were significantly affected by Si, with the activities of SOD, CAT and APX decreased and AA increased by applied Si. For most of the parameters measured, it was found that 5 mM Si was more effective than the 2.5 mM Si. Based on the present work, it can be concluded that Si alleviates sodicity and B toxicity of the plants grown in sodic-B toxic soil by preventing both oxidative membrane damage and also translocation of Na, Cl and B from root to shoots and/or soil to plant, and lowering the phytotoxic effects of Na, Cl and B within plant tissues. It was concluded that tomato was more responsive to Si than spinach since it was more salt sensitive than spinach. To our knowledge, this is the first report that Si improves the combined salt and B tolerance of spinach and tomato grown in naturally sodic-B toxic soil, and which describes membrane-related parameters and antioxidant responses.     

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy

Oxidative stress has been implicated to play an important role in the pathogenesis of diabetic neuropathy, which is the most common complication of diabetes mellitus affecting more than 50% of diabetic patients. In the present study, we have investigated the effect of U83836E [(-)-2-((4-(2,6-Di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl)methyl)-3,4-dihydro-2,3,7,8-tetramethyl-2H-1-benzopyran-6-ol, 2HCl], a potent free radical scavenger in streptozotocin (STZ)-induced diabetic neuropathy in rats. STZ-induced diabetic rats showed significant deficit in motor nerve conduction velocity (MNCV), nerve blood flow (NBF) and thermal hyperalgesia after 8 weeks of diabetes induction, indicating development of diabetic neuropathy. Antioxidant enzyme (superoxide dismutase and catalase) levels were reduced and malondialdehyde (MDA) levels were significantly increased in diabetic rats as compared to the age-matched control rats, this indicates the involvement of oxidative stress in diabetic neuropathy. The 2-week treatment with U83836E (3 and 9 mg/kg, i.p.) started 6 weeks after diabetes induction significantly ameliorated the alterations in MNCV, NBF, hyperalgesia, MDA levels and antioxidant enzymes in diabetic rats. Results of the present study suggest the potential of U83836E in treatment of diabetic neuropathy.