Role of oxidative stress in pathophysiology of peripheral neuropathy and modulation by N-acetyl-L-cysteine in rats.

OBJECTIVES: The objectives of this study were to examine the role of reactive oxygen species and oxidative stress in peripheral neuropathy and behavioural pain responses in experimentally induced chronic constriction injury (CCI) of sciatic nerve of rat. Effect of N-acetyl-L-cysteine (NAC) administered intraperitoneally, was also investigated on CCI-induced neuropathic pain in rats. METHODS: Neuropathy was induced by CCI of the right sciatic nerve in ketamine anaesthetized rats. Effect of intraperitoneally administered NAC in rats was also investigated using nociceptive behavioural tests. Malondialdehyde, an index of oxidative stress and antioxidant enzymes was also estimated in ligated sciatic nerve. RESULTS: Behavioural tests, mechanical, thermal and cold stimuli confirmed the development of neuropathic pain after the CCI. The malondialdehyde levels of ligated sciatic nerves were significantly increased compared to non-ligated sciatic nerves (sham operated). The antioxidant enzyme reduced, glutathione was inhibited, while superoxide dismutase increased. However, catalase remained unaffected in the injured sciatic nerves. Intraperitoneal administration of NAC resulted in significant reduction of hyperalgesia in CCI-induced neuropathic rats. CONCLUSIONS: This study identifies antioxidants superoxide dismutase and reduced glutathione, and oxidative stress as important determinants of neuropathological and behavioural consequences of CCI-induced neuropathy, and NAC may be a potential candidate for alleviation of neuropathic pain.     

血清内脂素及氧化应激状态评价在妊娠糖尿病患者病情评估中的意义

目的探讨血清内脂素及氧化应激状态评价在妊娠糖尿病患者病情评估中的意义。方法选择妊娠糖尿病患者68例为糖尿病组,对照组选择非糖尿病孕妇60例。人选后分别检测两组对象血清内脂素、空腹血糖、胰岛素抵抗指数、丙二醛、过氧化氢酶、超氧化物歧化酶、谷胱甘肽并计算体重指数。结果糖尿病组空腹血糖、胰岛素抵抗指数,内脂素较非糖尿病组差异有统计学意义（P〈0．05）。糖尿病组的MDA、CAT较非糖尿病组有显著性增高（P〈0．05）,糖尿病组SOD水平较非糖尿病组有极显著性下降（P〈0．01）,GSH较非糖尿病组有显著性下降（P〈0．05）。空腹血糖与内脂素、MDA呈显著正相关（P〈0．05）,空腹血糖与SOD、GSH呈显著负相关（P〈0．05）;胰岛素抵抗指数与内脂素、MDA呈显著正相关（P〈0．05）,胰岛素抵抗指数与SOD、GSH呈显著负相关（P〈0．05）。结论血清内脂素及氧化应激状态评价可有效反映妊娠糖尿病患者病情严重程度,对判断病情进展具有重要意义。     

Redox status and lipid peroxidation in alcoholic hypertensive patients and alcoholic hypertensive patients with diabetes

Background: Free radical-mediated oxidative stress has been implicated in the progression of alcoholic hypertension and diabetic hypertension. Methods: The lipid peroxides and antioxidant status of plasma and erythrocytes were investigated in alcoholic hypertensive patients and alcoholic hypertensive patients with diabetes and compared with normal subjects. Results: A significant increase is observed in the levels of glucose, lipid peroxidation (P<0.05) in the alcoholic hypertensive patients with/without diabetes and the increase was significantly higher in alcoholic hypertensive patients with diabetes. The activities of erythrocyte antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione (GSH) and plasma concentrations of GSH, vitamin C, vitamin E and β-carotene decreased significantly and the level of ceruloplasmin increased in alcoholic hypertensive patients with/without diabetes when compared to normal subjects. Plasma GSH and vitamin E levels exhibited a further decrease in alcoholic hypertensive patients with diabetes. Conclusions: An enhanced lipid peroxidation is observed in alcoholic hypertensive patients with diabetes and a more pronounced decrease in the levels of plasma GSH and vitamin E among antioxidants.     

Glutathione and alpha-lipoate in diabetic rats: nerve function, blood flow and oxidative state

BACKGROUND: Increased oxidative stress is considered to be a causal factor in the development of diabetic complications, among which peripheral neuropathy. The pathophysiology of nerve dysfunction in diabetes has been explained both by reduced endoneurial microcirculation and alterations in endoneurial metabolism. It is unclear whether antioxidants primarily improve nerve blood flow or normalise systemic or endoneurial oxidative metabolism. Therefore, we evaluated the effects of the antioxidants glutathione and alpha-lipoic acid on both nerve microcirculation and the antioxidative capacity and lipid peroxidation in experimentally diabetic rats. MATERIALS AND METHODS: Streptozotocin-diabetic rats were treated with different doses of alpha-lipoic acid, reduced glutathione or placebo, and were compared with nondiabetic controls. We measured systemic and endoneurial antioxidants, malondialdehyde and whole blood hydrogen peroxide. Furthermore, we evaluated sciatic and tibial motor and sensory nerve conduction velocity, caudal nerve conduction velocity, and assessed sciatic nerve blood flow and vascular resistance by Laser-Doppler flowmetry. RESULTS: We observed a rise in erythrocyte glutathione by 27 % (P < 0.05), and a trend towards decreased plasma malondialdehyde in alpha-lipoic acid, but not in glutathione-treated animals in comparison with the placebo group. Simultaneously, sciatic nerve blood flow and vascular resistance were improved by daily alpha-lipoic acid administration by 38% (P < 0.05). Peripheral nerve conduction velocity and endoneurial glutathione were not significantly influenced by antioxidant treatment. CONCLUSIONS: Only minor beneficial effects of alpha-lipoic acid on nerve blood flow and oxidative state occur at the given doses; these effects were insufficient to improve nerve conduction deficits.     

Decrease in antioxidant status of plasma and erythrocytes from patients with ankylosing spondylitis

ObjectivesThe aim of the study was to evaluate the antioxidant status in plasma and erythrocytes from patients with ankylosing spondylitis (AS).Methods16 patients with AS and 16 healthy volunteers were involved in this study. Activities of antioxidant enzymes: superoxide dismutase (SOD) and its isoenzymes — (SOD-Mn) and (SOD-ZnCu), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione transferase (GST), as well as the total antioxidant status (TAS) and concentration of malondialdehyde (MDA) in plasma and/or erythrocytes, respectively were determined.ResultsIn patients with AS, a statistically significant decrease in plasma activity of SOD, SOD-CuZn and TAS, significant drop in activity of SOD, GPx, GST and GR in erythrocytes, as well as increased concentration of MDA in comparison with control group of healthy volunteers was observed.ConclusionDecrease in antioxidant status leading to generation of oxidative stress may play an important role in the pathogenesis of ankylosing spondylitis.     

Elevated lipid peroxidation and disturbed antioxidant enzyme activities in plasma and erythrocytes of patients with uterine cervicitis and myoma.

OBJECTIVES: We investigated whether oxidative stress is associated with human uterine cervicitis and uterine myoma. DESIGN AND METHODS: We measured lipid peroxidation and antioxidant enzymes in plasma and erythrocytes of cervicitis patients and myoma patients in comparison with matched controls. Thiobarbituric acid-reactive substances (TBARS), a measure of lipid peroxidation, were determined in plasma; glutathione peroxidase (GSHPx) and catalase in erythrocytes; and superoxide dismutase (SOD) in both plasma and erythrocytes. RESULTS: We showed that plasma TBARS were significantly higher (p < 0.05) in both cervicitis patients and myoma patients than in controls. Plasma TBARS were significantly (and negatively) correlated with plasma and erythrocyte T-SOD activities in cervicitis patients only. Plasma T-SOD activity was significantly lower in both groups of patients than in controls whereas erythrocyte T-SOD activity was only significantly lower in myoma patients. The lowered plasma T-SOD activity in the cervicitis patients was attributed to decreased Mn-SOD activity whereas the lowered plasma T-SOD activity in myoma patients was attributed to decreased activities of both Cu,Zn-SOD and Mn-SOD. Erythrocyte GSHPx activity was 14% higher (p < 0.05) in cervicitis patients and 11% lower (p > 0.05) in myoma patients than in controls; catalase activity was 10% higher (p > 0.05) in cervicitis patients and 13% lower (p > 0.05) in myoma patients than in controls. Neither erythrocyte GSHPx nor catalase activity was significantly correlated with plasma TBARS. CONCLUSIONS: The elevated lipid peroxidation and disturbed antioxidant enzyme activities demonstrate the potential of oxidative injury in patients with uterine cervicitis and myoma.     

Oxidative stress and male IGF-1, gonadotropin and related hormones in diabetic patients.

Elevation of glucose concentration in diabetes may induce generation of oxygen free radicals such as superoxide (O2*-) and hydroxyl (*OH). The aim of the present study was to investigate the effect of the oxidative stress on the activities of blood superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and aldose reductase, the levels of reduced glutathione (GSH), lipid peroxidation (thiobarbituric acid reactive substances; TBARS) and plasma levels of insulin-like growth factor-1 (IGF-1), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone in type 2 (non-insulin-dependent diabetes) patients and in healthy controls. Blood SOD, CAT, GSH-Px and GSSG-R were lower in type 2 diabetic patients compared with the the control group. Blood aldose reductase activity was elevated in patients with type 2 diabetes compared with the control group. GSH was decreased while TBARS concentration was increased in red blood cells (RBC) and leukocytes from the patients with type 2 diabetes mellitus in comparison to the control group. The mean values of plasma LH, FSH and testosterone were decreased, whereas the mean plasma IGF-1 concentration was increased in type 2 diabetes compared with controls. These findings support the hypothesis that hyperglycemia enhances the activity of the polyol pathway and impairs the antioxidant status, particularly glutathione redox cycle, resulting in poorer defense against oxidative stress. In addition, decreased circulating testosterone and gonadotropin levels may reflect the oxidative stress exerted by diabetes.     

Effect of macrocyclic binuclear oxovanadium complex on tissue defense system in streptozotocin-induced diabetic rats

BACKGROUND: Oxidative stress plays an important role in chronic complications of diabetes mellitus and hence the regulation of free radicals is essential in the treatment of diabetes. The protective effect of a new macrocyclic binuclear oxovanadium complex on antioxidant defense systems of liver and kidney was examined in streptozotocin-induced experimental diabetes in rats. METHODS: The levels of lipid peroxides, glutathione and the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase were assayed according to standard procedures in the liver and kidney of control and experimental groups of rats. RESULTS: A significant decrease (p < 0.05) was observed in both the glutathione content and in the activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase and a concomitant increase in the level of lipid peroxides in diabetic rats. The observed alterations in the antioxidant status of tissues reverted back to near normal levels after the oral administration of macrocyclic vanadium complex at a dose of 5 mg/kg body weight/rat/day for a period of 30 days. CONCLUSION: The normoglycemic efficacy of the vanadium complex alleviates oxidative stress in streptozotocin-induced diabetes in rats.     

Spinal Manipulation Therapy Improves Tactile Allodynia and Peripheral Nerve Functionality and Modulates Blood Oxidative Stress Markers in Rats Exposed to Knee-Joint Immobilization

ObjectiveThe purpose of our study was to evaluate the effect of manually assisted lumbar spinal manipulation therapy on tactile allodynia, peripheral nerve functional recovery, and oxidative markers in rats exposed to knee immobilization-inducing hypersensitivity.MethodsTactile allodynia and sciatic, tibial, and peroneal functional indices were assessed before the knee joint immobilization, 24 hours after the knee cast removal, and 24 hours after 3 weeks of lumbar therapy with the Activator Adjusting Instrument, model 4 (AAI 4). Subsequently, the blood was collected from each rat, and oxidative markers such as lipid hydroperoxide levels; nitric oxide metabolites; and superoxide dismutase, catalase, and glutathione peroxidase activities were assessed.ResultsThe AAI 4 improved the immobilization-induced allodynia and recovered the peripheral nerve functional indices impaired after knee immobilization. Immobilized rats treated with AAI 4 therapy presented a lack of significant changes in lipid hydroperoxides and nitric oxide metabolites in the plasma contrasting with rats that were kept freely in their cages, with no therapy applied, which presented elevated lipid hydroperoxides levels. Also, the antioxidant catalase enzymatic activity decreased in the blood of rats immobilized and treated with AAI 4.ConclusionThese results suggest that manually assisted lumbar spinal manipulation therapy modulates systemic oxidative stress, which possibly contributes to the analgesia and recovery of peripheral nerve functionality.     

Improved antioxidative protection in winter swimmers.

Adaptation to oxidative stress is an improved ability to resist the damaging effects of reactive oxygen species, resulting from pre-exposure to a lower dose. Changes in uric acid and glutathione levels during ice-bathing suggest that the intensive voluntary short-term cold exposure of winter swimming produces oxidative stress. We investigated whether the repeated oxidative stress in winter swimmers results in improved antioxidative adaptation. We obtained venous blood samples from winter swimmers and determined important components of the antioxidative defense system in the erythrocytes or blood plasma: reduced and oxidized glutathione (GSH and GSSG), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (Cat). The control group consisted of healthy people who had never participated in winter swimming. The baseline concentration of GSH and the activities of erythrocytic SOD and Cat, were higher in winter swimmers. We interpret this as an adaptative response to repeated oxidative stress, and postulate it as a new basic molecular mechanism of increased tolerance to environmental stress.     

Lipid peroxides in blood plasma and enzymatic antioxidative defence of erythrocytes in Down's syndrome

The level of lipid peroxides was significantly increased in the blood of patients with Down's syndrome. In erythrocytes increased activities of superoxide dismutase and glutathione peroxidase were confirmed while catalase activity was similar to that of healthy controls. The concentration of selenium in erythrocytes of Down's syndrome patients was reduced, in spite of increased glutathione peroxidase activity. These results confirm the hypothesis of an altered oxidative metabolism in Down's syndrome.     

Oxidative stress-related parameters in the liver of non-alcoholic fatty liver disease patients

Oxidative stress is implicated in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In the present study, hepatic and plasma oxidative stress-related parameters were measured and correlated with clinical and histological findings in 31 NAFLD patients showing increased body mass index. Liver protein carbonyl content was enhanced by 403% in patients with steatosis (n=15) compared with control values (n=12), whereas glutathione content, superoxide dismutase (SOD) activity and the ferric reducing ability of plasma (FRAP) were decreased by 57%, 48% and 21% (P<0.05) respectively. No changes in microsomal p-nitrophenol hydroxylation and the total content of cytochrome P450 (CYP) or CYP2E1 were observed. Patients with steatohepatitis (n=16) exhibited protein carbonyl content comparable with that of controls, whereas glutathione content, SOD and catalase activities were decreased by 27%, 64% and 48% (P<0.05). In addition, FRAP values in patients with steatohepatitis were reduced by 33% and 15% (P<0.05) when compared with controls and patients with steatosis respectively, whereas p-nitrophenol hydroxylation (52%) and CYP2E1 content (142%) were significantly increased (P<0.05) compared with controls. It is concluded that oxidative stress is developed in the liver of NAFLD patients with steatosis and is exacerbated further in patients with steatohepatitis, which is associated with CYP2E1 induction. Substantial protein oxidation is followed by proteolysis of the modified proteins, which may explain the co-existence of a diminished antioxidant capacity and protein oxidation in the liver of patients with steatohepatitis.     

Evaluation of plasma,erythrocytes, and brochoalveolar lavage fluid antioxidant defense system in sulfur mustard-injured patients

Introduction. Sulfur mustard (SM) is a strong alkylating agent that causes acute and chronic effects on different organs following exposure. Main late respiratory complications are chronic obstructive pulmonary disease, bronchiectasis, asthma, and bronchiolitis obliterans. It seems that oxidative stress plays a major role in pathogenesis of diseases. This study was undertaken to evaluate the long-term effect of SM on plasma, erythrocytes, and brochoalveolar lavage fluid antioxidant defense system in SM-injured patients. Methods. Brochoalveolar lavage fluid, plasma, and erythrocyte samples were taken from 54 patients in the case group exposed to SM and 25 controls with chronic respiratory disease without a history of exposure to SM. Results. Superoxide dismutase, catalase, and glutathione peroxidase activities in lavage fluid, plasma, and erythrocytes were significantly higher in case group. The increased glutathione S-transferase activity in lavage fluid was associated with a depletion of glutathione and an increase of malondialdehyde levels. There was no significant change observed in glutathione reductase activity. Conclusions. The data suggest that oxidative damage might have an important role for patients exposed to SM. SM may induce an oxidative stress response by depleting the antioxidant defense systems and increasing lipid peroxidation in lung cells.     

Effect of pentylenetetrazol-induced epileptic seizure on the antioxidant enzyme activities, glutathione and lipid peroxidation levels in rat erythrocytes and liver tissues

OBJECTIVES: In order to clarify whether oxidative stress accompanies epilepsy, we examined the effects of pentylenetetrazol (PTZ)-induced epilepsy on the lipid peroxidation and antioxidant enzyme activities in erythrocytes and liver tissues of adult Wistar rats. MATERIALS AND METHODS: The activities of antioxidative enzymes (glucose-6-phosphate dehydrogenase (G-6-PD)), copper, zinc-superoxide dismutase (Cu,Zn-SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px) and the levels of reduced glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) were measured in erythrocytes and liver tissues of pentylenetetrazol (PTZ)-induced epileptic adult Wistar rats. RESULTS: Single PTZ treatment in a convulsive dose of 50 mg/kg significantly reduced the erythrocyte Cu,Zn-SOD, CAT enzyme activities and GSH levels compared to controls (P < 0.001, P < 0.001, P < 0.05, respectively). Erythrocyte and liver tissue TBARS levels in the epileptic group were significantly higher than controls (P < 0.0001). There was a significant decrease in liver tissue Cu,Zn-SOD activity and GSH levels in the epileptic group (P < 0.0001), whereas significantly higher activities of G-6-PD and Se-GSH-Px were found in the epileptic group. CONCLUSIONS: Our results demonstrate a generalized diminished antioxidant activity and increased TBARS level indicating enhanced oxidative stress in the liver and erythrocytes of epileptic rats. Increased oxidative stress in the liver of epileptic rats might be due to the activation of the recently found glutamate receptors in the liver. These findings suggest that the use of antioxidants with antiepileptic drugs and new drugs such as type-5 metabotropic glutamate receptor (mGlu5) antagonist (MPEP) might protect erythrocytes and liver tissue against anoxic damage and oxidative stress.     

Antioxidant defense status of red blood cells of patients with beta-thalassemia and Ebeta-thalassemia

Anemia in beta-thalassemia is caused by a combination of ineffective erythropoiesis and premature hemolysis of RBC in the peripheral circulation. Excess of the alpha-globin chain present in beta-thalassemic RBC is mainly responsible for oxidative damage of erythrocyte membrane protein. The activities of glucose-6-phosphate dehydrogenase, glutathione reductase, glutathione peroxidase, and glutathione-S-transferase, and the catalytic activity of catalase and superoxide dismutase, and the concentrations of non-enzymic antioxidants such as reduced glutathione were measured to estimate the status of the antioxidant defense system in the erythrocytes for protection against oxidative stress. The extent of lipid peroxidation was also estimated in thalassemic erythrocytes. Significantly lower activities of reduced glutathione indicate the cell to be in a pro-oxidant state and decreased activity of catalase favors hydrogen peroxide-mediated lipid peroxidation in beta-thalassemic and Ebeta-thalassemic RBC.     

Oxidative stress and antioxidant status in non-metastatic prostate cancer and benign prostatic hyperplasia

OBJECTIVES: We undertook the present study to investigate the possible alteration of oxidant/antioxidant status in the circulation of patients with prostate cancer and benign prostatic hyperplasia. DESIGN AND METHODS: Thiobarbituric acid reactive substances (TBARS), the enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and copper (Cu) and zinc (Zn) levels were estimated in the erythrocytes of 25 non-metastatic prostate cancer patients, 36 benign prostatic hyperplasia (BPH) patients and 24 age- and sex-matched healthy subjects (controls). RESULTS: TBARS concentrations were significantly increased, while erythrocyte GPX and SOD activities were significantly decreased in the prostate cancer group versus controls (P < 0.001) and BPH group (P < 0.05). Zn levels were lowered in prostate cancer patients versus controls (P < 0.01) with no significant changes between BPH and cancer groups. Similarly, lipid peroxidation was increased (P < 0.05) with decreased SOD activity and Zn level (P < 0.05) in BPH versus controls. CONCLUSION: These results reveal an alteration in the lipid peroxidation index, with concomitant changes in the antioxidant defense system in prostate cancer patients compared to BPH patients. We hypothesize that an altered prooxidant-antioxidant balance may lead to an increase in oxidative damage and consequently may play an important role in prostate carcinogenesis.     

Inactivation of antioxidant enzymes by peroxynitrite

Exposure of hemolysates and whole erythrocytes to peroxynitrite (bolus of 50 micromol dm(-3)-2 mmol dm(-3)) was found to inactivate erythrocyte antioxidant enzymes: glutathione peroxidase > superoxide dismutase > catalase. Inactivation of antioxidant enzymes by peroxynitrite may be one reason for the secondary oxidative stress in peroxynitrite-treated cells. When hemoglobin was not converted into the cyanmet form, an apparent activation of glutathione peroxidase activity by peroxynitrite was observed in hemolysates; this effect was artifactual and due to the pseudoenzymatic glutathione peroxidase activity of hemoglobin.     

不同类型胰岛素对老年糖尿病患者氧化应激的影响

目的探讨不同类型胰岛素联合阿卡波糖对老年2型糖尿病患者体内氧自由基代谢的影响。方法随机选取80例老年2型糖尿病患者分为2组:A组(甘精胰岛素联合阿卡波糖治疗组)、B组(诺和灵30R联合阿卡波糖治疗组);并选取40例体检健康者作为健康对照组。每组40例老年2型糖尿病患者,均接受为期4周的降糖治疗。并分别测定治疗前后患者空腹血糖(FPG)、餐后2 h血糖(2 h PG)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-PX)、8-异前列腺素(8-iso-PGF2a)、一氧化氮(NO)等。结果老年2型糖尿病患者的FPG、2 h PG、血清MDA、8-iso-PGF2a均较健康对照组增高,而血清GSH-PX、SOD、NO低于健康对照组,差异具有统计学意义(P<0.05),甘精胰岛素联合阿卡波糖治疗组较诺和灵30R联合阿卡波糖治疗组能明显地改善糖尿病患者体内的氧化应激状态,差异具有统计学意义(P<0.05)。结论联合应用甘精胰岛素和阿卡波糖治疗可以显著降低糖尿病患者体内氧化应激水平,提示该方案可有效降低氧自由基对靶器官的损伤,延缓糖尿病并发症的发生与发展。     

The nitroxide tempol has similar antioxidant effects as physiological levels of 17β‐oestradiol in reversing ovariectomy‐induced oxidative stress in mice liver and kidney

Objective: Oestrogen defciency increases oxidative stress postmenopause, while tempol is an intracellular radical scavenger that interferes with the formation or effects of many radicals. We aimed to investigate the effects of oestrogen and tempol on oxidative stress parameters in the kidney and liver of ovariectomized mice. Material and methods: Forty 8‐week‐old female Bald/c mice were divided into five groups: sham‐operated, ovariectomized mice without treatment, ovariectomized mice treated with tempol, ovariectomized mice treated with 17β‐oestradiol and ovariectomized mice treated with 17β‐oestradiol and tempol. Oxidative stress in liver and kidney tissues was investigated by measuring 2‐thiobarbituric acid reactive substances (TBA‐RS), reduced glutathione, myeloperoxidase, superoxide dismutase and catalase levels. Results: TBA‐RS levels were increased and reduced glutathione, myeloperoxidase, superoxide dismutase levels were decreased in the tissues of ovariectomized mice. This effect of ovariectomy on oxidative stress parameters was opposed significantly by the administration of tempol and 17β‐oestradiol either alone or in combination. Ovariectomy reduced the kidney catalase levels, but the effect was not statistically significant (p>0.05). On the other hand, catalase levels were elevated significantly in all treatment groups compared to those of the ovariectomized group (p<0.05). Conclusion: These study findings demonstrate that tempol significantly opposes the oxidative stress generated by ovariectomy. This effect, which is evident in remote tissues such as liver and kidney, is comparable to that of physiological levels of oestradiol.     

Sesame oil protects against lipopolysaccharide-stimulated oxidative stress in rats

OBJECTIVE: The aim of this study was to determine the effects and the defense mechanisms of sesame oil on lipopolysaccharide-induced oxidative stress in rats. DESIGN: Laboratory in vivo study of the effect of sesame oil on lipid peroxide, superoxide anion, superoxide dismutase, catalase, glutathione, and nitrite concentrations. To assess the effect of sesame oil on hepatic function, we determined serum aspartate aminotransferase, total bilirubin, and liver histology. SETTING: University laboratory. SUBJECTS: Male SPF Wistar rats. INTERVENTIONS: Blood testing, administration of oils, and liver biopsies. MEASUREMENTS AND MAIN RESULTS: Oxidative stress induced by lipopolysaccharide (5 mg/kg, intraperitoneally) was assessed by determination of lipid peroxidation. Sesame oil was given orally immediately after lipopolysaccharide administration, and lipid peroxidation concentrations were determined. The reactive oxygen species superoxide anion was measured by chemiluminescence analyzer. The enzyme activities of superoxide dismutase and catalase and the concentrations of glutathione and nitrite also were determined. Hepatic injury was evaluated by determining the concentrations of serum aspartate aminotransferase and total bilirubin and by liver histologic examination. Sesame oil significantly reduced lipid peroxidation but failed to affect nitrite concentrations in lipopolysaccharide-treated rats. Superoxide anion counts were decreased, and glutathione, but not superoxide dismutase or catalase, was increased in sesame oil-treated groups with lipopolysaccharide-induced oxidative stress. Only sesame oil-treated groups, but not corn oil- or mineral oil-treated groups, showed attenuated hepatic disorder induced by lipopolysaccharide. In addition, sesame oil given 6 hrs after lipopolysaccharide also attenuated lipid peroxidation and hepatic disorder. Furthermore, sesame oil given immediately or 6 hrs after lipopolysaccharide administration significantly reduced morphologic changes induced by lipopolysaccharide. CONCLUSION: A single dose of sesame oil may attenuate oxidative stress and subsequently relieve hepatic disorder in endotoxemic rats.