Erythrocyte glutathione, glutathione peroxidase, superoxide dismutase and serum lipid peroxidation in epileptic children with valproate and carbamazepine monotherapy

This prospective study was carried out to determine changes in the antioxidant system in epileptic children receiving long term antiepileptic drugs (AEDs). Levels of erythrocyte glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and serum lipid peroxidation were determined in 25 healthy children and 30 epileptic children who had not yet received AEDs. Sixteen patients were treated with valproic acid (VPA) and 14 with carbamazepine (CBZ); 13 months later these parameters were retested. The results showed that SOD and lipid peroxidation levels were increased but the GSH-Px levels were decreased in epileptic children on VPA therapy compared with the control group and the results before treatment. No significant differences of these parameters were found in epileptic children on CBZ therapy compared with the control group and the results before treatment, except that lipid peroxidation level was slightly higher in epileptic patients before treatment. We conclude that antioxidant systems in epileptic children on CBZ therapy are better regulated in comparison with epileptic children on VPA therapy.     

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with pregnancy--induced hypertension

The exact pro-oxidant and antioxidant status in pregnancy--induced hypertension patients is still not clear. To add a new insight to the question, changes in the erythrocyte lipid peroxidation products (malondialdehyde; MDA), levels of glutathione (GSH), ascorbic acid and plasma vitamin E (non enzymatic antioxidant parameters) and activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase in erythrocytes were studied in thirty five patients with pregnancy--induced hypertension and thirty five healthy pregnant normotensive cases. It was observed that there was a significant increase in erythrocyte MDA levels, activities of SOD, GPx and a significant decrease in erythrocyte GSH, ascorbic acid, plasma vitamin E levels and catalase activity in patients with pregnancy--induced hypertension when compared to controls. The results of our study have shown higher oxygen free radical production, evidenced by increased levels of MDA and decreased levels of GSH, ascorbic acid, vitamin E and Catalase activity supports the oxidative stress in pregnancy--induced hypertension. The increased activities of antioxidant enzymes may be a compensatory regulation in response to increased oxidative stress. The decreased concentrations of glutathione and antioxidant vitamin status supports the hypothesis that lipid peroxidation is an important causative factor in the pathogenesis of preeclampsia.     

Increased erythrocyte antioxidant status protects against smoking induced hemolysis in moderate smokers

Cigarette smoking is common in societies worldwide and has been identified as injurious to human health. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. In the present study, the possible role of antioxidant status on smoking-induced erythrocyte hemolysis of smokers was studied. Erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, reduced glutathione (GSH) level, erythrocyte membrane lipid peroxidation, total cholesterol and phospholipids were determined. Further, nitrite/nitrate levels (NO(2)/NO(3)) in both plasma and erythrocyte lysate were measured. Results showed increased plasma and erythrocyte membrane lipid peroxidation and nitrite/nitrate levels in smokers. The activities of SOD, CAT and GPx were also increased with reduced glutathione (GSH) level in smokers. No significant change was observed in smokers red cell hemolysis and cholesterol/phospholipid (C/P) ratio compared to controls. Erythrocyte membrane lipid peroxidation was positively correlated with SOD (r = 0.482, p < 0.01) and GPx (r = 0.368, p < 0.018) in smokers. Increased levels of nitrite/nitrate and antioxidant status of erythrocytes might be playing a crucial role in protecting red cell from free radical damage induced by cigarette smoke.     

LIPID PEROXIDATION AND ANTIOXIDANT STATUS IN THE LIVER,ERYTHROCYTES, AND SERUM OF RATS AFTER METHANOL INTOXICATION

Lipid peroxidation products measured as a malondialdehyde and activities of superoxide dism utase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), and concentrations of ascorbic acid,-tocopherol, and glutathione (GSH) were measured in the liver, erythrocytes, and serum of rats 6, 14, and 24 h and 2, 5, and 7 d after treatment with 3 g methanol/ kg. GSH-Px and GSSG-R activities, GSH level, and ascorbate concentration in the liver, erythrocytes, and blood serum were significantly decreased. In addition, SOD and-tocopherol in erythrocytes were diminished, while malondialdehyde (MDA) in liver, erythrocytes, and serum were elevated. Further, erythrocyte counts, hemoglobin levels, hematocrit, and mean corpuscular volume (MCV) were reduced. These results indicate that methanol intoxication in rats leads to an increase in the lipid peroxidation and impairment in the antioxidant mechanisms in liver, erythrocytes, and blood serum.     

Effects of trichlorfon on malondialdehyde and antioxidant system in human erythrocytes

Organophosphorus insecticides may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system. The aim of this study was to examine the potency of trichlorfon, an organophosphate insecticide, to induce oxidative stress response in human erythrocytes in vitro. For this purpose trichlorfon solutions in different concentrations and erythrocyte solutions were incubated at 37 °C for 60 min. At the end of the incubation time, malondialdehyde (MDA), an end product of lipid peroxidation, total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes were determined by spectrophotometric methods. Trichlorfon increased MDA formation depended on the concentration. On the other hand, decreases in the GSH-Px activity, GSH levels and increases in the total glutathione levels, SOD and CAT activities were seen in the studied concentrations. The present findings indicate that the in vitro toxicity of trichlorfon may be associated with oxidative stress.     

Brain Lipid Peroxidation and Antioxidant Status After Acute Methacrylonitrile Intoxication

The status of brain antioxidant enzymes and glutathione in methacrylonitrile (MeAN)-intoxicated Wistar rats was correlated with the levels of lipid peroxidation products. Optimum changes were observed 30 min and 60 min after oral administration of MeAN at dosages of 50 mg/kg body weight per day (0.25 LD₅₀) and 100 mg/kg body weight per day (0.5 LD₅₀). An increase in lipid peroxidation products, decrease in the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), and decrease in reduced glutathione (GSH) were observed. These studies suggest that the membrane lipid peroxidation observed in MeAN intoxication is related, in part, to a compromised antioxidant defense system.     

The effects of oxcarbazepine on oxidative stress in epileptic patients

In the present study, erythrocyte lipid peroxidation, superoxide dismutase, glutathione peroxidase and catalase activities were determined in epileptic patients receiving oxcarbazepine monotherapy for 1 year and normal controls. Glutathione peroxidase, catalase, superoxide dismutase and malondialdehyde activities were investigated in a control group (15 normal healthy adults) and a group of 13 epileptic patients, before and after 1 year of oxcarbazepine treatment. The values of glutathione peroxidase and superoxide dismutase activities were statistically significant after 1 year of therapy and pretreatment. The values of malondialdehyde were significantly different from the normal subjects and pretreatment patients values. This study suggests that the antioxidant systems of epileptic patients receiving oxcarbazepine therapy for 1 year were significantly affected.     

Effect of l-ascorbic acid on antioxidant defense system in testes of albino rats exposed to nickel sulfate

We studied the effect of oral supplementation with L-ascorbic acid (50 mg/100 g body weight) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced lipid peroxidation in the testes of Wister strain male albino rats. Testicular lipid peroxide and glutathione (GSH) levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated. Nickel sulfate treatment significantly increased the level of testicular lipid peroxide and decreased all antioxidant enzymes activities and GSH concentration. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on testicular lipid peroxide and GSH concentration as well as antioxidant enzymatic defense system.     

汉防己甲素对大鼠肝保护和抗氧化作用研究

目的:使用汉防己甲素评价对四氯化碳诱导的大鼠肝损伤的保护作用以及抗氧化作用。方法:每日给予四氯化碳损伤大鼠不同的浓度汉防己甲素剂量分别为20,60,100mg/kg,随后检测血清和组织中谷胱甘肽(GSH),谷胱甘肽过氧化物酶,过氧化氢酶(CAT),超氧化和物歧化酶(SOD),谷胱甘肽S-转移酶(GST),脂质过氧化效应等指标,体外抗氧化使用使用超氧化物和过氧化物清除实验评价。结果:与对照组和四氯化碳模型组比较后发现,汉防己甲素在所用剂量下均显示出较为理想的肝保护和抗氧化效应。进一步的体外过氧化自由基清除和超氧化自由基清除实验表明,汉防己甲素较维生素C有更为优越的清除活性。结论:汉防己甲素能有效保护四氯化碳对大鼠造成的肝损伤,其保护机制可能与抗氧化和自由基清除密切相关。     

Erythrocyte redox status in streptozotocin diabetic rats: effect of Casearia esculenta root extract

The present study was aimed to investigate the effect of Casearia esculenta root extract on erythrocyte lipid peroxidation and to assess the status of antioxidants in red blood cells of streptozotocin (STZ) diabetic rats. The study showed a significant elevation (p < 0.05) of erythrocyte thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation and significant reduction (p < 0.05) in reduced glutathione (GSH), ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in the STZ diabetic rats. The study also observed significant reduction in membrane cholesterol and phospholipid content in STZ diabetic rats. By oral administration of C. esculenta (200 and 300 mg/kg body wt.) for 45 days to the diabetic rats these values approached almost normal levels. A dose of 300 mg/kg body weight C. esculenta extract showed better antioxidant effects than 200 mg/kg body weight.     

Influence of naringenin on oxytetracycline mediated oxidative damage in rat liver

Naringenin is a naturally occurring citrus flavanone, which has been reported to have a wide range of pharmacological properties. The present work was carried out to evaluate the effect of naringenin on antioxidant and lipid peroxidation status in liver of oxytetracycline-intoxicated rats. Intraperitonial administration of oxytetracycline 200 mg/kg for 15 days resulted a significant elevation in serum hepatospecific markers such as aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and bilirubin and the levels of lipid peroxidation markers (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) in liver. Oxytetracycline also caused a significant reduction in the activities of superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione (GSH), vitamin C and vitamin E in liver. Oral administration of naringenin (50 mg/kg b.w.t.) with oxytetracycline significantly decreased the activities of serum aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and the levels of bilirubin along with significant decrease in the levels of lipid peroxidation markers in the liver. In addition, naringenin significantly increased the activities of superoxide dismutase, catalase and GSH peroxidase as well as the level of GSH, vitamin C and vitamin E in liver of the oxytetracycline-treated rats. Our results demonstrate that naringenin exhibited antioxidant property and decrease the lipid peroxidation against oxytetracycline-induced oxidative stress in liver.     

Hepatoprotective effect of rhinax on antitubercular drug-induced hepato-toxicity in rats

Rhinax, a polyherbal formulation, exhibited hepatoprotective function when tested against antitubercular drug-induced hepatotoxicity in rats. Suppression of GSH and antioxidant enzymes "superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), gultathionle peroxidase (GPx) and glutathione S-transferase (GST) were noticed in the liver of antitubercular chemotherapeutic agents (namely isoniazid, rifampicin and pyrazinamide) treated animals accompanied with an increase in cytochrome P-450 contents and increased production of lipid peroxidation. Rhinax afforded hepatoprotection by inhibiting lipid peroxidation and, as a result, the animals showed improved antioxidant status.     

Combined effects of vitamin C, vitamin E, and sodium selenate supplementation on absolute ethanol-induced injury in various organs of rats

In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.     

Relationships between tissue concentrations of polycyclic aromatic hydrocarbons and antioxidative responses of marine mussels, Perna viridis

Local mussels, Perna viridis, were transplanted from a relatively clean site to various polluted sites in Hong Kong. After a 30-day field exposure, different antioxidant parameters including glutathione S transferase (GST), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), NADPH DT-diaphorase (DT-d), glutathione (GSH) and lipid peroxidation were quantified, and tissue concentrations of benzo[a]pyrene (B[a]P) as well as a total of five polycyclic aromatic hydrocarbons (PAHs) with potential carcinogenicity were determined for individual mussels. Results indicated that: (1) tissue concentrations of B[a]P and total PAHs from the same site were highly variable; (2) gill SOD, DT-d and lipid peroxidation showed no response to tissue pollutants; (3) the majority of the antioxidant parameters were induced by increasing tissue pollutant concentrations; and (4) amongst the various parameters, oxyradical scavenger GSH best correlated with tissue concentrations of pollutants.     

4-Methylthiobenzoic Acid Protection against Cisplatin Nephrotoxicity: Antioxidant System

This study investigates the changes in renal antioxidant systemafter cisplatin administration and the nephroprotection with4-methylthiobenzoic acid (MTBA). Male Wistar rats were injectedwith (1) vehicle control, (2) cisplatin, (3) MTBA, and (4) cisplatinplus MTBA. Rats were euthenized 3 days post-treatment and kidneywas isolated and analyzed for platinum concentration, malondialdehyde (MDA), glutathione (GSH and GSSG), superoxide dismutase(SOD), catalase (CAT), and glutathione peroxidase (GSH-Px).Plasma creatinine increased 508% following cisplatin administrationalone, which decreased to 189% with MTBA. Cisplatin-treatedrats showed a depletion of renal GSH levels (53%), while cisplatinplus MTBA-injected rats had GSH values close to those of thecontrols. SOD, CAT, and GSH-Px activities decreased 36, 29,and 38%, respectively, and MDA levels increased 212% followingcisplatin administration, which were restored to control levelsafter MTBA treatment. The renal platinum level depleted significantlywith MTBA treatment. The data suggest that cisplatin nephrotoxicityis mediated by depletion in GSH concentration and by impairedactivities of SOD, CAT, and GSH-Px, increased lipid peroxidation,and plasma creatinine levels. The protection offered by MTBAagainst cisplatin nephrotoxicity is related to the reductionin plasma creatinine levels, prevention of GSH depletion andlipid peroxidation, and restoring antioxidant enzyme activityin the kidneys of rats.     

In vitro effects of CB1 receptor ligands on lipid peroxidation and antioxidant defense systems in the rat brain

The in vitro effects of arachidonyl-2-chloroethylamide (ACEA; a selective CB(1)-receptor agonist) and N-piperidin-l-yl)-5-(4-chlorophenyl)-1-(2,4-cochlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716A; a selective CB(1)-receptor antagonist) on lipid peroxidation (spontaneous and Fe (2+)-induced), total glutathione (GSH)-level and activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase and glutathione reductase) in the rat brain were studied. The effects of these CB(1)-induced), total glutathione (GSH)-level and activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase and glutathione reductase) in the rat brain were studied. The effects of these CB(1)-ligands in Fenton system (generating *OH radicals) were also examined. The cannabinoids did not change the total GSH-level and were without effects on the activity of antioxidant enzymes in the rat brain. These results proved a lack of in vitro pro-oxidant activity of the CB(1)-receptor ligands, as well as a lack of direct effects on GSH and enzyme molecules. ACEAand SR141716A were without effect on spontaneous lipid peroxidation, but decreased the Fe(2+)-induced brain lipid peroxidation and OH-provoked deoxyribose degradation in Fenton system. It can be suggested that the tested cannabinoids possess a metal-chelating activity, which might contribute to an antioxidant activity. The data, obtained in this study offer a background for investigation of the in vivo effects of these CB(1)-receptor ligands on antioxidant defense systems in the brain of healthy animals and animals, previously subjected to oxidative stress.     

羊栖菜多糖对L_(615)小鼠LPO含量及GR、GSH—PX、CAT和SOD活性的影向

本文报道了羊栖菜多糖(SFPS)对L_(615)小鼠全血及肝脾脂质过氧化物(LPO)含量以及对各胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GSH—PX)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)等酶活性的影响。结果表明,SFPS可显著降低L_(615)小鼠全血及肝脾LPO的含量,增加CAT、SOD的酶活性,提示SFPS具有清除L_(615)小鼠体内自由基,抗脂质过氧化作用。本文结果提示,SFPS的这些作用可能是其抗白血病作用的机理之一。     

Brain lipid peroxidation and antioxidant status after acute methacrylonitrile intoxication

The status of brain antioxidant enzymes and glutathione in methacrylonitrile (MeAN)-intoxicated Wistar rats was correlated with the levels of lipid peroxidation products. Optimum changes were observed 30 min and 60 min after oral administration of MeAN at dosages of 50 mg/kg body weight per day (0.25 LD50) and 100 mg/kg body weight per day (0.5 LD50). An increase in lipid peroxidation products, decrease in the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), and decrease in reduced glutathione (GSH) were observed. These studies suggest that the membrane lipid peroxidation observed in MeAN intoxication is related, in part, to a compromised antioxidant defense system.     

Effects of hormone replacement therapy on lipid peroxides and oxidation system in postmenopausal women

A short-term evaluation of 6 months of estrogen therapy on oxidant status in 38 postmenopausal women was conducted. The levels of serum lipid peroxidation products, glutathione (GSH) status, and glutathione-related enzymes were evaluated before and after 6 months of hormone replacement therapy. After 6 months of estrogen treatment there was a significantly increased concentration of thiobarbituric acid-reactive substances (TBARS), which are an end product of lipid peroxidation. This was accompanied by a significant increase in the activity of glutathione peroxidase (GSH-Px). However, the activities of glutathione reductase (GSSG-R) and superoxide dismutase (SOD) were significantly decreased and total protein thiols were reduced. Data suggest that hormone replacement therapy in postmenopausal women is associated with oxidant mechanisms.     

Protective Effects of Zinc on Oxidative Stress Enzymes in Liver of Protein-Deficient Rats

Persons afflicted with protein malnutrition are generally deficient in a variety of essential micronutrients like zinc, copper, iron, and selenium, which in turn affects number of metabolic processes in the body. To evaluate the protective effects of zinc on the enzymes involved in oxidative stress induced in liver of protein-deficient rats, the current study was designed. Zinc sulfate at a dose level of 227mg/L zinc in drinking water was administered to female Sprague–Dawley normal control as well as protein-deficient rats for a total duration of 8 weeks. The effects of zinc treatment in conditions of protein deficiency were studied on rat liver antioxidant enzymes, which included catalase, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), glutathione reduced (GSH), and glutathione-S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic activities of catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase and the levels of lipid peroxidation. A significant inhibition in the levels of reduced glutathione and the enzyme activity of superoxide dismutase has been observed after protein deficiency in normal rats. Interestingly, Zn treatment to protein-deficient animals lowered already raised activity catalase, glutathione peroxidase, and glutathione-S-transferase and levels of lipid peroxidation to significant levels when compared to protein-deficient animals. Also, Zn treatment to the protein-deficient animals resulted in a significant elevation in the levels of GSH and SOD activity as compared to their respective controls, thereby indicating its effectiveness in regulating their levels in adverse conditions. It has also been observed that concentrations of zinc, copper, iron, and selenium were found to be decreased significantly in protein-deficient animals. However, the levels of these elements came back to within normal limits when zinc was administrated to protein-deficient rats. This study concludes that zinc has thepotential to regulate the activities of oxidative stress enzymes as well as essential hepatic elements.