Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes

Organophosphate (OP) pesticides such as dimethoate and malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is possible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated orally with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to oral administration of a single low dose of dimethoate and/or malathion (0.01% LD(50)). The result showed that treatment with OP increased lipid peroxidation (LPO) in erythrocytes, however, vitamin E pretreated rats administered OP's showed decreased LPO in erythrocytes. The increase in the activities of superoxide dismutase (SOD) and catalase (CAT) and total-SH content in erythrocytes from dimethoate and/or malathion treated rats as compared to control appears to be a response towards increased oxidative stress. Vitamin E pretreated animals administered OP's showed a lowering in these parameters as compared to OP treated rats which indicates that vitamin E provide protection against OP-induced oxidative stress. The glutathione-S-transferase (GST) activity in erythrocytes was inhibited in OP intoxicated rats which partially recovered in vitamin E pretreated animals administered OP's. Inhibition in erythrocyte and serum acetylcholinesterase (AChE) activity was not relieved in vitamin E pretreated rats administered OP's probably due to the competitive nature of enzyme inhibition by OP's. The results show that vitamin E may amelierate OP-induced oxidative stress by decreasing LPO and altering antioxidant defense system in erthrocytes.     

Protection against ischemia-reperfusion induced oxidative stress by vitamin E treatment.

The rat heart protection offered by vitamin E against oxidative stress after ischaemia-reperfusion was studied by using a new methodological approach. Functional recovery of hearts from ischaemia-reperfusion was correlated with a traditional index of oxidative stress such as lipid peroxidation and with antioxidant capacity and susceptibility to oxidants of the tissue evaluated by enhanced chemiluminescence techniques. Rats were treated with ten daily i.m. injections of 100 mg/kg body weight of vitamin E. The functional recovery during reperfusion (20 min, following 45 min ischaemia) of Langendorff preparations from control (vehicle-injected) and vitamin E treated rats was evaluated in terms of heart rate, left ventricular developed pressure (LVDP), double product (= heart rate. LVDP) and coronary flow recovery. Vitamin E treatment significantly improved functional recovery of heart rate, LVDP, double product and coronary flow. It also increased the level of vitamin E and reduced the levels of both malondialdehyde and hydroperoxides in the heart tissue at the end of the ischaemia-reperfusion protocol. In contrast, it did not affect the antioxidant capacity and the response of heart homogenates to in vitro oxidative stress measured after ischaemia-reperfusion. These results show a protective action of vitamin E treatment against lipid peroxidation and cardiac dysfunction associated with ischaemia-reperfusion. Although the precise mechanism of this protection is not evident, our model in part suggests a role of vitamin E other than as a free radical scavenger.     

Protective effects of vitamin E against atrazine-induced genotoxicity in rats

Atrazine (2-chloro-4-(ethylamino)-6-(isopropylamino)-s-triazine) is one of the most commonly used herbicides to control grasses and weeds. The widespread contamination and persistence of atrazine residues in the environment has resulted in human exposure. Vitamin E is a primary antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. The present study was undertaken to investigate the protective effect of vitamin E against atrazine-induced genotoxicity. Three different methods: gel electrophoresis, comet assay and micronucleus test were used to assess the atrazine-induced genotoxicity and to evaluate the protective effects of vitamin E. Atrazine was administered to male rats at a dose of 300 mg/kg body weight for a period of 7, 14 and 21 days. There was a significant increase (P<0.001) in tail length of comets from blood and liver cells treated with atrazine as compared to controls. Co-administration of vitamin E (100 mg/kg body weight) along with atrazine resulted in decrease in tail length of comets as compared to the group treated with atrazine alone. Micronucleus assay revealed a significant increase (P<0.001) in the frequency of micronucleated cells (MNCs) following atrazine administration. In the animals administrated vitamin E along with atrazine there was a significant decrease in percentage of micronuclei as compared to atrazine treated rats. The increase in frequency of micronuclei in liver cells and tail length of comets confirm genotoxicity induced by atrazine in blood and liver cells. In addition, the findings clearly demonstrate protective effect of vitamin E in attenuating atrazine-induced DNA damage.     

Efficacy of piperine, an alkaloidal constituent from Piper nigrum on erythrocyte antioxidant status in high fat diet and antithyroid drug induced hyperlipidemic rats

The main aim of this study was to investigate the effect of piperine on erythrocyte antioxidant status in high fat diet (HFD) and antithyroid drug induced hyperlipidemic rats. Male Wistar rats were divided into eight groups. The first four groups were fed a control diet and in addition were given respectively 1% carboxymethyl cellulose (CMC); 10 mg/kg body weight carbimazole (CM); 10 mg CM + 40 mg/kg body weight piperine and 10 mg CM + 2 mg/kg body weight atorvastatin (ATV). A similar pattern was followed for the next four groups except that they were all fed HFD instead of the control diet. Erythrocyte osmotic fragility, total cholesterol, phospholipids, lipid peroxidation products, enzymic and non-enzymic antioxidant status were studied in all experimental groups. Significantly increased osmotic fragility, total cholesterol/phospholipid ratio, thiobarbituric acid reactive substances and lipid hydroperoxides were observed in the plasma and erythrocytes of HFD fed and CM treated rats compared to the control. Superoxide dismutase, catalase, glutathione peroxidase, vitamin E and reduced glutathione in erythrocytes and vitamin C in the plasma were also significantly lowered in HFD fed, antithyroid drug treated rats compared to control animals. Concurrent piperine supplementation along with HFD and antithyroid drug administration normalized erythrocyte osmotic fragility, reduced lipid peroxidation, and improved the enzymic and non-enzymic antioxidant status compared to those rats that did not receive piperine. Thus, our results indicate that piperine supplementation markedly protects erythrocytes from oxidative stress by improving the antioxidant status in HFD fed antithyroid drug treated rats.     

Effects of Dietary Supplementation with Vitamin C and Vitamin E and Their Combination on Growth Performance,Some Biochemical Parameters,and Oxidative Stress Induced by Copper Toxicity in Broilers

This study investigated effects of dietary supplementation with vitamin C, vitamin E on performance, biochemical parameters, and oxidative stress induced by copper toxicity in broilers. A total of 240, 1-day-old, broilers were assigned to eight groups with three replicates of 10 chicks each. The groups were fed on the following diets: control (basal diet), vitamin C (250 mg/kg diet), vitamin E (250 mg/kg diet), vitamin C + vitamin E (250 mg/kg?+?250 mg/kg diet), and copper (300 mg/kg diet) alone or in combination with the corresponding vitamins. At the 6th week, the body weights of broilers were decreased in copper, copper + vitamin E, and copper + vitamin C + vitamin E groups compared to control. The feed conversion ratio was poor in copper group. Plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase activities, iron, copper concentrations, and erythrocyte malondialdehyde were increased; plasma vitamin A and C concentrations and erythrocyte superoxide dismutase were decreased in copper group compared to control. Glutathione peroxidase, vitamin C, and iron levels were increased; aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and copper levels were decreased in copper + vitamin C group, while superoxide dismutase, glutathione peroxidase, and vitamin E concentrations were increased; aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase were decreased in copper with vitamin E group compared to copper group. The vitamin C concentrations were increased; copper, uric acid, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and malondialdehyde were decreased in copper + vitamin C + vitamin E group compared to copper group. To conclude, copper caused oxidative stress in broilers. The combination of vitamin C and vitamin E addition might alleviate the harmful effects of copper as demonstrated by decreased lipid peroxidation and hepatic enzymes.     

Effect of vitamin E on the response to ischemia-reperfusion of Langendorff heart preparations from hyperthyroid rats

Hyperthyroidism has been reported to decrease heart antioxidant capacity and increase its susceptibility to in vitro oxidative stress. This may affect the heart response to ischemia-reperfusion, a condition that increases free radical production. We compared the functional recovery from in vitro ischemia-reperfusion (Langendorff) of hearts from euthyroid (E), hyperthyroid (H, ten daily intraperitoneal injections of T3, 10 microg/100g body weight), vitamin E-treated (VE, ten daily intramuscular injections, 20 mg/100g body weight) and hyperthyroid vitamin E-treated (HVE) rats. We also determined lipid peroxidation, tissue antioxidant capacity and the tissue capability to face an oxidative stress in vitro. A significant tachycardia was displayed during reperfusion following 20 min ischemia by the hyperthyroid hearts, together with a low recovery of left ventricular developed pressure (LVDP) and left ventricular dP/dt(max). When H hearts were paced at 300 beats/min, the functional recovery (LVDP and dP/dt(max)) was close to 100% and significantly higher than in E paced hearts. At the end of the ischemia-reperfusion protocol, myocardium antioxidant capacity was significantly lower, whereas lipid peroxidation and the susceptibility to in vitro oxidative stress were higher in the T3 treated (H) than in euthyroid rats. The in vitro tachycardic response, the reduction in the antioxidant capacity and the increase in lipid peroxidation were prevented by treatment of hyperthyroid rats with vitamin E (HVE). These results suggest that the tachycardic response to reperfusion following chronic T3 pretreatment was associated with the reduced capability of the heart to face oxidative stresses in hyperthyroidism.     

Effect of Tridax procumbens on liver antioxidant defense system during lipopolysaccharide-induced hepatitis in D-galactosamine sensitised rats

The present study was carried out to assess the effect of chloroform insoluble fraction of ethanolic extract of Tridax procumbens (TP) against D-Galactosamine/Lipopolysaccharide (D-GalN/LPS)-induced hepatitis in rats. Induction of rats with D-GalN/LPS (300 mg/kg body weight/30 microg/kg body weight) led to a marked increase in lipid peroxidation as measured by thiobarbituric acid reactive substances (TBARS) in liver. Further there was a decline in the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferase and the levels of non-enzymic antioxidants namely reduced glutathione, vitamin C and vitamin E. These biochemical alterations were normalised upon pretreatment with TP extract. Thus, the above results suggest that TP (300 mg/kg body weight orally for 10 days) is very effective in allievating the D-GalN/LPS-induced oxidative stress suggesting its antioxidant property.     

Veratric acid ameliorates hyperlipidemia and oxidative stress in Wistar rats fed an atherogenic diet

An investigation was made to reveal the protective effects of veratric acid (VA), a phenolic acid against atherogenic diet-induced hyperlipidemic rats. Male albino Wistar rats were fed with atherogenic diet (4% cholesterol, 1% cholic acid, and 0.5% 2-thiouracil) daily for 30 days and treated with VA (40 mg/kg body weight) daily for a period of 30 days. Rats fed with atherogenic diet showed significant (P < 0.05) elevation in the level of plasma lipids, systolic and diastolic blood pressure, oxidative stress markers (thiobarbituric acid reactive substances, lipid peroxides) and significant (P < 0.05) reduction in the activities of enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (vitamin C, vitamin E, and reduced glutathione) antioxidants in erythrocytes, plasma, and tissues (liver, kidney, and aorta). Oral administration of VA (40 mg/kg body weight) for 30 days to atherogenic diet fed rats markedly attenuates systolic, diastolic blood pressure and lipid peroxidation products. Further, VA treatment significantly improved enzymatic and non-enzymatic antioxidants levels and showed beneficial effects on lipid profile in atherogenic diet rats. All the above alterations were supported by histopathological observations. These results indicate that oral administration of VA ameliorates atherogenic diet-induced hyperlipidemia in rats by its free radical scavenging; improving the antioxidants and lipid lowering properties.     

Regulation of expression of antioxidant enzymes by vitamin E and curcumin in <Emphasis Type="SmallCaps">l</Emphasis>-thyroxine-induced oxidative stress in rat renal cortex

The present study investigates the antioxidative effects of vitamin E and curcumin against l-thyroxine (T₄)-induced oxidative stress in renal cortex of adult male rats. Rats were made hyperthyroid by administration of l-thyroxine (0.0012%) in their drinking water for 30 days. Vitamin E (200 mg/kg body weight/day) and curcumin (30 mg/kg body weight/day) were supplemented singly or in combination orally for 30 days along with l-thyroxine treatment. The elevated level of oxidative stress parameters (lipid peroxidation and protein carbonylation) and decline level of small antioxidant molecules (reduced glutathione and ascorbic acid) in renal cortex of T₄-treated rats were restored back by supplementation of vitamin E or/and curcumin. Increased superoxide dismutase and catalase activities in kidney cortex of T₄-treated rats were ameliorated in response to vitamin E or/and curcumin treatment. The elevated translated product of Cu/Zn-SOD, Mn-SOD and catalase in T₄-treated rats were differentially reduced by the administration of vitamin E and curcumin independently or in combination. Cu/Zn-SOD expression was ameliorated by both vitamin E and curcumin independently or in combination, whereas Mn-SOD expression was ameliorated by the supplementation of vitamin E or curcumin independently. However, the expression of catalase was alleviated by only supplementation of vitamin E to T₄-treated rats. The results suggest that both vitamin E and curcumin may play an important role in protecting T₄-induced oxidative stress in rat renal cortex by differentially modulating the activities of antioxidant enzymes and oxidative stress parameters.     

Vitamin E prevents nonylphenol-induced oxidative stress in testis of rats

In the present study we have investigated if administration of nonylphenol-induced oxidative stress in various subcellular fractions of adult rat testis and the effect of vitamin E on reactive oxygen species mediated nonylphenol toxicity. Male rats were administered orally with nonylphenol at 1, 10 and 100 microg/kg body weight per day for 45 days with and without supplementation of vitamin E (20 mg/kg body weight). In nonylphenol-treated rats the activities of antioxidant enzymes superoxide dismutase and glutathione reductase decreased significantly while the levels of lipid peroxidation increased significantly in the crude homogenate and in the mitochondrial and microsome-rich fractions of testis. Co-administration of nonylphenol and vitamin E did not cause changes in the activities of antioxidant enzymes in various subcellular fractions of rat testis. The results suggest that graded doses of nonylphenol elicit depletion of antioxidant defence system in rat testis, indicating nonylphenol induced oxidative stress in the testis of rats which could be reversed by the administration of vitamin E.     

Change in the concentration of vitamins C and E in rat tissues by paraquat administration

Paraquat causes lung injury by oxidative stress. After 48 h of intraperitoneal administration of paraquat (50 mg/kg of body weight) to rats, the vitamin C concentration in the lungs was significantly decreased, while lung vitamin E content was increased after 12 h. These results indicate that vitamin C directly reflected the oxidative stress in the lungs.     

Ameliorative action of melatonin on oxidative damage induced by atrazine toxicity in rat erythrocytes

Excessive generation of reactive oxygen species (ROS) can induce oxidative damage to vital cellular molecules and structures including DNA, lipids, proteins, and membranes. Recently, melatonin has attracted attention because of their free radical scavenging and antioxidant properties. The aim of this study was to evaluate the possible protective role of melatonin against atrazine-induced oxidative stress in rat erythrocytes in vivo. Adult male albino rats of Wistar strain were randomly divided into four groups. Control group received isotonic saline; melatonin (10 mg/kg bw/day) group; atrazine (300 mg/kg of bw/day) group; atrazine + melatonin group. Oral administration of atrazine and melatonin was given daily for 21 days. Oxidative stress was assessed by determining the glutathione (GSH) and malondialdehyde (MDA) level, and alteration in antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G-6-PD) in the erythrocytes of normal and experimental animals. A significant increase in the MDA levels and decrease in the GSH was observed in the atrazine treated animals (P < 0.05). Also, significant increase in the activities of SOD, CAT, GPx, and GST were observed in atrazine treated group compared to controls (P < 0.05). Moreover, significant decrease in protein, total lipids, cholesterol, and phospholipid content in erythrocyte membrane were demonstrated in atrazine treated rats. Administration of atrazine significantly inhibits the activities of G-6-PD and membrane ATPases such as Na(+)/K(+)-ATPase, Mg(2+)-ATPase, and Ca(2+)-ATPase (P < 0.05). Scanning electron microscopic (SEM) examination of erythrocytes revealed morphological alterations in the erythrocytes of atrazine treated rats. Furthermore, supplementation of melatonin significantly modulates the atrazine-induced changes in LPO level, total lipids, total ATPases, GSH, and antioxidant enzymes in erythrocytes. In conclusion, the increase in oxidative stress markers and the concomitant alterations in antioxidant defense system indicate the role of oxidative stress in erythrocytes of atrazine-induced damage. Moreover, melatonin shows a protective role against atrazine-induced oxidative damage in rat erythrocytes.     

Influence of ferulic acid on circulatory prooxidant-antioxidant status during alcohol and PUFA induced toxicity.

In recent years, there has been an escalation in alcohol abuse and inevitably, alcohol related disorders are becoming an increasingly important cause of morbidity and mortality. Alcohol is known to induce a dose dependent increase in lipid peroxidation. Alcohol related disabilities are more pronounced when taken along with diet rich in polyunsaturated fatty acid (PUFA). The present work aims at analysing the protective role of ferulic acid (FA), a naturally occurring nutritional component on alcohol and PUFA induced oxidative stress. Two different doses of ferulic acid, 20 mg/kg body weight and 40 mg /kg body weight were used for the study. The results showed that the levels of oxidative markers; thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and levels of copper (Cu) and ferritin were increased significantly in plasma of alcohol, thermally oxidised PUFA (DeltaPUFA) and alcohol + DeltaPUFA groups, which were decreased significantly on treatment with both the doses of ferulic acid. The activities of enzymic antioxidants viz. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and non enzymic antioxidants like vitamin C, vitamin E, and reduced glutathione (GSH) and the levels of zinc (Zn) were significantly decreased in alcohol, DeltaPUFA and alcohol + DeltaPUFA groups which were improved significantly on treatment with both the doses of FA. The reduction in oxidative stress was more significant in 20 mg/kg body weight treatment groups compared to 40 mg/kg body weight. Thus from the results obtained, we conclude that FA effectively protects the system against alcohol and PUFA induced oxidative stress.     

Lipid peroxidation, vitamins C, E and reduced glutathione levels in patients with pulmonary tuberculosis

The present study examined the relationship between lipid peroxidation and vitamin C, vitamin E and reduced glutathione levels in plasma, erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients and an equal number of age-and sex-matched healthy subjects. Enhanced plasma, erythrocytes and erythrocyte membrane lipid peroxidation with concomitant decline in vitamin C, vitamin E and reduced glutathione levels were found in pulmonary tuberculosis patients. The elevated lipid peroxidation and decreased vitamin C, vitamin E and reduced glutathione levels indicate the potential of oxidative damage to erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients.     

Olive oil supplemented with vitamin E affects mitochondrial coenzyme Q levels in liver of rats after an oxidative stress induced by adriamycin.

In this study we have evaluated the supplementation of olive oil with vitamin E on coenzyme Q concentration and lipid peroxidation in rat liver mitochondrial membranes. Four groups of rats were fed on virgin olive, olive plus 200 mg/kg of vitamin E or sunflower oils as lipid dietary source. To provoke an oxidative stress rats were administered intraperitoneally 10 mg/kg/day of adriamycin the last two days of the experiment. Animals fed on olive oil plus vitamin E had significantly higher coenzyme Q and vitamin E levels but a lower mitochondrial hydroperoxide concentration than rats fed on olive oil. Retinol levels were not affected, by either different diets or adriamycin treatment. In conclusion, an increase in coenzyme Q and alpha-tocopherol in these membranes can be a basis for protection against oxidation and improvement in antioxidant capacity.     

Galangin,a dietary flavonoid,improves antioxidant status and reduces hyperglycemia-mediated oxidative stress in streptozotocin-induced diabetic rats

Objective: To examine the effect of galangin on hyperglycemia-mediated oxidative stress in streptozotocin (STZ)-induced diabetic rats.

Methods: Diabetes was induced by intraperitoneal administration of low-dose STZ (40?mg/kg body weight (BW)) into male albino Wistar rats. Galangin (8?mg/kg BW) or glibenclamide (600?µg/kg BW) was given orally, once daily for 45 days to normal and STZ-induced diabetic rats.

Results: Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes. The levels of insulin and non-enzymatic antioxidants (vitamin C, vitamin E, reduced glutathione) and the activity of enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase (GST)) were decreased significantly in diabetic control rats. These altered plasma glucose, insulin, lipid peroxidation products, enzymatic and non-enzymatic antioxidants ions were reverted to near-normal level after the administration of galangin and glibenclamide.

Conclusion: The present study shows that galangin decreased oxidative stress and increased antioxidant status in diabetic rats, which may be due to its antidiabetic and antioxidant potential.     

Involvement of oxidative stress in the impairment in biliary secretory function induced by intraperitoneal administration of aluminum to rats

We have shown that aluminum (Al) induces cholestasis associated with multiple alterations in hepatocellular transporters involved in bile secretory function, like Mrp2. This work aims to investigate whether these harmful effects are mediated by the oxidative stress caused by the metal. For this purpose, the capability of the antioxidant agent, vitamin E, to counteract these alterations was studied in male Wistar rats. Aluminum hydroxide (or saline in controls) was administered ip (27 mg/kg body weight, three times a week, for 90 d). Vitamin E (600 mg/kg body weight) was coadministered, sc. Al increased lipid peroxidation (+50%) and decreased hepatic glutation levels (-43%) and the activity of glutation peroxidase (-50%) and catalase (-88%). Vitamin E counteracted these effects total or partially. Both plasma and hepatic Al levels reached at the end of the treatment were significantly reduced by vitamin E (-40% and -44%, respectively;p< 0.05). Al increased 4 times the hepatic apoptotic index, and this effect was fully counteracted by vitamin E. Bile flow was decreased in Al-treated rats (-37%) and restored to normality by vitamin E. The antioxidant normalized the hepatic handling of the Mrp2 substrates, rose bengal, and dinitrophenyl-S-glutathione, which was causally associated with restoration of Mrp2 expression. Our data indicate that oxidative stress has a crucial role in cholestasis, apoptotic/necrotic hepatocellular damage, and the impairment in liver transport function induced by Al and that vitamin E counteracts these harmful effects not only by preventing free-radical formation but also by favoring Al disposal.     

The effect of vitamin E supplementation on reduction of lymphocyte DNA damage induced by T-2 toxin and deoxynivalenol in weaned pigs

The objective of the present study was to establish the effect of deoxynivalenol (DON) and T-2 toxin on lipid peroxidation, lymphocyte DNA fragmentation and immunoglobulin production in weaned pigs, and furthermore, to evaluate the potential of vitamin E (α-tocopheryl acetate) in prevention of toxin mediated changes. Forty-eight weaned castrated male crossbred pigs (mean live weight at the beginning of the experimental period was 11.7 kg) were randomly assigned to five experimental groups: control (without toxin and vitamin E), T-2 (3 mg/kg T-2 toxin), T-2 + E (3 mg/kg T-2 toxin + 100 mg/kg vitamin E), DON (4 mg/kg DON) and DON + E (4 mg/kg DON + 100 mg/kg vitamin E). After 14 days of treatment blood was collected for analysis. Lipid peroxidation was studied by assays of malondialdehyde (MDA), total antioxidant status (TAS) of plasma and erythrocyte glutathione peroxidase (GPx). DNA damage in lymphocytes was measured by comet assay. Serum immunoglobulin levels were evaluated by enzyme-linked immunosorbent assay (ELISA) and the hepatotoxicity was studied by measuring plasma liver enzyme levels (alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl-transferase (GGT). Production parameters of both DON groups were significantly impaired in comparison to the control. DON significantly increased the amount of DNA damage in lymphocytes by 28%. Moreover, the levels of TAS were lowered by addition of DON. T-2 toxin significantly impaired daily live weight gain and feed conversion, increased the amount of DNA damage in lymphocytes by 27%, decreased total serum IgG and did not alter plasma TAS. Plasma and 24-h urinary malondialdehyde (MDA) excretion rate and erythrocyte Gpx levels did not differ among the groups. Supplementation with vitamin E did not improve production parameters impaired by DON and T-2 toxin and only partially protected lymphocyte DNA from toxin impact. To our knowledge, these are the first data on genotoxic effects of moderate doses of DON and T-2 toxin on pig lymphocytes. The effect of DON and T-2 toxin on the immune system was reflected as a change in immunoglobulin synthesis, which might be toxin and species specific. According to other results no major induction of oxidative stress could be proven. Enhancement of antioxidant status with vitamin E in the case of DON and T-2 toxin intoxication can be beneficial for remaining the lymphocyte DNA integrity.     

Acephate induced oxidative damage in erythrocytes

The effect of oral administration of acephate (360 mg/kg body weight), for 15 days, daily, was investigated on the erythrocytes of male rats. Activities of acetyl cholinesterase and glucose-6-phosphate dehydrogenase decreased, while those of glutathione-s-transferase and glutathione reductase increased. Decreased glutathione content and increased lipid peroxidation suggest that there was increased oxidative stress in the erythrocytes of treated animals. Increased cholesterol/phospholipid ratio in the erythrocyte membranes and morphological changes in RBCs (scanning electron microscopy studies) were observed in acephate treated animals. The results clearly suggest that acephate induced oxidative stress in erythrocytes leads to morphological changes.     

Antistress effects of vitamin E and dimethylsulfoxide during their combined administration in low doses

Low doses of vitamin E (5 mg/kg body weight) and dimethyl sulfoxide (50 mg/kg) given simultaneously orally to albino rats prevented the disturbances of the behaviour and vegetative functions induced by chronic emotional painful stress. The adaptive effect of vitamin E or dimethyl sulfoxide given alone was much lower or altogether absent. The antioxidant combination used decreased the intensity of lipid peroxidation in the brain and blood serum as well as cholesterol content in brain lipids and activated brain superoxide dismutase and nonenzymatic superoxide scavenging activity of the serum. The results obtained suggest that the combination of vitamin E with dimethyl sulfoxide may be used for the treatment of pathological conditions accompanied by lipid peroxidation syndrome.