Effects of Selenium and L-Carnitine on Oxidative Stress in Blood of Rat Induced by 2.45-GHz Radiation from Wireless Devices

The levels of blood lipid peroxidation, glutathione peroxidase, reduced glutathione, and vitamin C were used to follow the level of oxidative damage caused by 2.45 GHz electromagnetic radiation in rats. The possible protective effects of selenium and L-carnitine were also tested and compared to untreated controls. Thirty male Wistar Albino rats were equally divided into five groups, namely Groups A₁ and A₂: controls and sham controls, respectively; Group B: EMR; Group C: EMR + selenium, Group D: EMR + L-carnitine. Groups B–D were exposed to 2.45 GHz electromagnetic radiation during 60 min/day for 28 days. The lipid peroxidation levels in plasma and erythrocytes were significantly higher in group B than in groups A₁ and A₂ (p?<?0.05), although the reduced glutathione and glutathione peroxidase values were slightly lower in erythrocytes of group B compared to groups A₁ and A₂. The plasma lipid peroxidation level in group A₂ was significantly lower than in group B (p?<?0.05). Erythrocyte reduced glutathione levels (p?<?0.01) in group B; erythrocyte glutathione peroxidase activity in group A₂ (p?<?0.05), group B (p?<?0.001), and group C (p?<?0.05) were found to be lower than in group D. In conclusion, 2.45 GHz electromagnetic radiation caused oxidative stress in blood of rat. L-carnitine seems to have protective effects on the 2.45-GHz-induced blood toxicity by inhibiting free radical supporting antioxidant redox system although selenium has no effect on the investigated values.     

Alpha-lipoic acid supplementation: tissue glutathione homeostasis at rest and after exercise.

Antioxidant nutrients have demonstrated potential in protecting against exercise-induced oxidative stress. alpha-Lipoic acid (LA) is a proglutathione dietary supplement that is known to strengthen the antioxidant network. We studied the effect of intragastric LA supplementation (150 mg/kg, 8 wk) on tissue LA levels, glutathione metabolism, and lipid peroxidation in rats at rest and after exhaustive treadmill exercise. LA supplementation increased the level of free LA in the red gastrocnemius muscle and increased total glutathione levels in the liver and blood. The exercise-induced decrease in heart glutathione S-transferase activity was prevented by LA supplementation. Exhaustive exercise significantly increased thiobarbituric acid-reactive substance levels in the liver and red gastrocnemius muscle. LA supplementation protected against oxidative lipid damage in the heart, liver, and red gastrocnemius muscle. This study reports that orally supplemented LA is able to favorably influence tissue antioxidant defenses and counteract lipid peroxidation at rest and in response to exercise.     

Optimization of selenium status by a single intraperitoneal injection of Se in Se-deficient rat: possible application to burned patient treatment

In order to investigate the efficiency of a single selenium (Se) administration in restoring selenium status, Se and antioxidant enzymes were studied in an animal model of Se depletion. In Se-depleted animals receiving or not a single parenteral administration of Se, plasma, red blood cell (RBC), and tissue Se levels were measured concurrently with glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. The oxidative stress was assessed by thiobarbituric acid-reactive species (TBARs), total thiol groups, glutathione, and tocopherol measurements. Our study showed that Se depletion with alterations in the antioxidant defense system (Se and GPx activity decreases) led to an increase of lipid peroxidation, a decrease of the plasma vitamin E level, and SOD activation. Sodium selenite injection resulted after 24 h in an optimal plasma Se level and a reactivation of GPx activity. In liver, brain, and kidney, Se levels in injected animals were higher than those in reference animals. However, this single administration of Se failed to decrease free radical damage induced by Se depletion. Therefore, in burned patients who exhibit an altered Se status despite a daily usually restricted Se supplementation, the early administration of a consistent Se amount to improve the GPx activity should be of great interest in preventing the impairment of the antioxidant status.     

Effect of selenium supplementation on some blood biochemical parameters in male rats

The long-term effect of selenium supplementation on blood glutathione peroxidase (GSH-Px) activity and plasma TBARS’ production (as an index of peroxidation) was evaluated in 15-mo-old male rats fed a diet supplemented with 0.25 or 0.50 ppm selenium, for 12 mo. A group of nonsupplemented age-matched rats was the control. In addition, triglycerides, phospholipids, total and free cholesterol, HDL-cholesterol, and HDL-phospholipid levels were measured in plasma. Plasma testosterone levels were also determined in order to control the aging process in these animals. The GSH-Px activity and the peroxidation level were unchanged in all the groups. However, concerning the lipid parameters, a decrease in triglycerides concentration was observed in both treated groups (p<0.05). Therefore, in these experimental conditions, despite no observed changes in parameters related to lipid peroxidation, selenium seems to be involved with triglycerides metabolism, eventually improving the triglycerides status of aged animals.     

<Emphasis Type="SmallCaps">l</Emphasis>-Carnitine Blood Levels and Oxidative Stress in Treated Phenylketonuric Patients

Aims l-Carnitine exerts an important role by facilitating the mitochondrial transport of fatty acids, but is also a scavenger of free radicals, protecting cells from oxidative damage. Phenylketonuria (PKU), an inborn error of phenylalanine (Phe) metabolism, is currently treated with a special diet consisting of severe restriction of protein-enriched foods, therefore potentially leading to l-carnitine depletion. The aim of this study was to determine l-carnitine levels and oxidative stress parameters in blood of two groups of PKU patients, with good and poor adherence to treatment. Methods Treatment of patients consisted of a low protein diet supplemented with a synthetic amino acids formula not containing Phe, l-carnitine, and selenium. l-Carnitine concentrations and the oxidative stress parameters thiobarbituric acid reactive species (TBARS) and total antioxidant reactivity (TAR) were measured in blood of the two groups of treated PKU patients and controls. Results We verified a significant decrease of serum l-carnitine levels in patients who strictly adhered to the diet, as compared to controls and patients who did not comply with the diet. Furthermore, TBARS measurement was significantly increased and TAR was significantly reduced in both groups of phenylketonuric patients relatively to controls. We also found a significant negative correlation between TBARS and l-carnitine levels and a significant positive correlation between TAR and l-carnitine levels in well-treated PKU patients. Conclusions Our results suggest that l-carnitine should be measured in plasma of treated PKU patients, and when a decrease of this endogenous component is detected in plasma, supplementation should be considered as an adjuvant therapy.     

Oxidative stress and antioxidant status in mouse kidney: effects of dietary lipid and vitamin E plus iron

The purpose of this study was to determine the effects of dietary fat, vitamin E, and iron on oxidative damage and antioxidant status in kidneys of mice. Sixty 1-month-old male Swiss-Webster mice were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g all-rac-alpha-tocopherol acetate or 0.74 g ferric citrate per kilogram of diet for 4 weeks. Significantly (P < 0.05) higher levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), and conjugated dienes were found in the kidneys of mice fed with fish oil compared with mice fed lard irrespective of vitamin E status. Mice maintained on a vitamin E-deficient diet had significantly higher renal levels of TBAR, but not conjugated dienes, than the supplemented group. Fish oil fed mice receiving vitamin E supplementation had lower levels of alpha-tocopherol than did mice in the lard fed group. Significantly higher levels of ascorbic acid were also found in the kidneys of mice fed with fish oil than were found in mice fed lard. The levels of protein carbonyls and glutathione (GSH), and activities of catalase, superoxide dismutase, selenium (Se)-GSH peroxidase, and non-Se-GSH peroxidase were not significantly altered by dietary fat or vitamin E. Dietary iron had no significant effect on any of the oxidative stress and antioxidant indices measured. The results obtained provide experimental evidence for the pro-oxidant effect of high fish oil intake in mouse kidney and suggest that dietary lipids play a key role in determining cellular susceptibility to oxidative stress.     

Dietary chitosan supplementation attenuates isoprenaline-induced oxidative stress in rat myocardium

Despite considerable advances in diagnosis and management over the last three decades, acute myocardial infarction continues to be a major public health problem. It is predicted that ischemic heart diseases will constitute the major disease-burden worldwide in the year 2020. In the present study, an attempt has been made to examine the effects of dietary chitosan supplementation on lipid peroxidation and cardiac antioxidant defense system in isoprenaline-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Dietary chitosan intake significantly attenuated the isoprenaline-induced lipid peroxidation and maintained the level of reduced glutathione at near normal. Its administration demonstrated an antioxidant effect by maintaining the activities of myocardial glutathione dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (superoxide dismutase and catalase) at levels comparable to that of controls. The results of the present study indicate that the salubrious effects of dietary supplementation of chitosan is probably related to a counteraction of free radicals and/or to normal maintenance of the activities of free radical enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation.     

Effect of dietary selenium deficiency on the in vitro fertilizing ability of mice spermatozoa

Selenium is an essential micronutrient for mammals, being integral part of antioxidant system. The aim of the study was to evaluate the effect of selenium deficiency on in vitro fertilization (IVF) capacity of spermatozoa and on oxidative stress in these cells. Male C57BL/6N mice were maintained on selenium-deficient or selenium-sufficient diets (0.02 or 0.2 ppm of selenium as selenomethionine, respectively) for 4 months. Liver glutathione peroxidase activity measurements were used to confirm selenium deficiency. Sperm quality and IVF capability among both groups were evaluated. To assess oxidative damage, lipid peroxidation as malondialdehyde production was determined in spermatozoa as well as the testes. Ultrastructural analyses of spermatozoa nuclei using transmission electron microscopy were also performed. The percentage of eggs fertilized with sperm from selenium-deficient mice was significantly decreased by approximately 67%. This reduced fertilization capacity was accompanied by increased levels of lipid peroxidation in both the testes and sperm, indicating that selenium deficiency induced oxidative stress. Consistent with this finding, spermatozoa from selenium-deficient animals exhibited altered chromatin condensation. Deficiency in dietary selenium decreases the reproductive potential of male mice and is associated with oxidative damage in spermatozoa.     

Selenium Supplementation Modulates Zinc Levels and Antioxidant Values in Blood and Tissues of Diabetic Rats Fed Zinc-Deficient Diet

Diabetes mellitus is associated to a reduction of antioxidant defenses that leads to oxidative stress and complications in diabetic individuals. The present study was undertaken to investigate the effect of selenium on blood biochemical parameters, antioxidant enzyme activities, and tissue zinc levels in alloxan-induced diabetic rats fed a zinc-deficient diet. The rats were divided into two groups; the first group was fed a zinc-sufficient diet, while the second group was fed a zinc-deficient diet. Half of each group was treated orally with 0.5 mg/kg sodium selenite. Tissue and blood samples were taken from all animals after 28 days of treatment. At the end of the experiment, the body weight gain and food intake of the zinc-deficient diabetic animals were lower than that of zinc-adequate diabetic animals. Inadequate dietary zinc intake increased glucose, lipids, triglycerides, urea, and liver lipid peroxidation levels. In contrast, serum protein, reduced glutathione, plasma zinc and tissue levels were decreased. A zinc-deficient diet led also to an increase in serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and liver glutathione-S-transferase and to a decrease in serum alkaline phosphatase activity and glutathione peroxidase. Selenium treatment ameliorated all the values approximately to their normal levels. In conclusion, selenium supplementation presumably acting as an antioxidant led to an improvement of insulin activity, significantly reducing the severity of zinc deficiency in diabetes.     

Interrelationship between oxidative damage and antioxidant enzyme activities: an easy and rapid experimental approach

This article describes a method for determining some antioxidant enzyme activities (catalase and/or glutathione peroxidase) and the oxidative status (protein oxidative damage and/or lipid peroxidation) of human blood. However, the main objective of the work is to illustrate the relationship between antioxidant defences and oxidative damage, showing to students their correlation and the general importance of the biochemical regulation in health and diseases.     

Changes observed in antioxidant system in the blood of postmenopausal women with breast cancer.

From experimental studies and epidemiological data, it can be inferred that lipid peroxidation is increased in cancer patients. Cases of post-menopausal, untreated women with benign and malignant breast tumours, were compared with their age matched controls in their serum lipid peroxides, antioxidant vitamins (E and C), serum selenium and serum ceruloplasmin. Erythrocyte and its membrane lipid peroxidation and antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase) levels were also analyzed. Significant increase in circulating lipid peroxides, ceruloplasmin and significant decrease in antioxidant vitamins and selenium were observed in breast cancer women. The erythrocyte and its membrane lipid peroxidation was increased significantly and severe impairment of antioxidant potential was observed in breast cancer women.     

Selenium and Vitamin E Modulates Cigarette Smoke Exposure-Induced Oxidative Stress in Blood of Rats

Cigarette smoke contains about 5,000 chemicals that include organic and metallic compounds. The current study was undertaken to investigate the effects of selenium and vitamin E on oxidative stress-induced damage in rats exposed to cigarette smoke. Forty male rats were equally divided into four groups. The first and second groups were used as control and cigarette smoke groups, respectively. Selenium was administered to rats constituting the third group for 27 days. The Se and vitamin E combination was given to animals in fourth group for 27 days. All groups except the control, were exposed to cigarette smoke starting at the third day of the experiment and continuing for 27 days. The blood samples from all groups were taken at the end of 27 days. Plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were higher in the cigarette smoke group than in the control, although erythrocytic superoxide dismutase and glutathione peroxidase activities were lower in the cigarette smoke group than in the control. The plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were lower in cigarette smoke+Se+VE group than in the cigarette smoke group, although erythrocytic superoxide dismutase activity and glutathione peroxidase activity in selenium and vitamin E-administered groups were higher than in the exposed to cigarette smoke group. High-density lipoprotein-cholesterol level was not affect by selenium and vitamin E administrations. In conclusion, selenium and vitamin E seem to have protective effects on the cigarette smoke-induced blood toxicity by supporting the enzymatic antioxidant redox systems.     

Effect of maternal fluoride exposure on developing CNS of rats: protective role of Aloe vera, Curcuma longa and Ocimum sanctum

Fluoride is toxic to neuronal development and its excessive intake during pregnancy cause adverse effects on neonatal development. The present study examined the presence of oxidative stress during maternal exposure of fluoride and the therapeutic strategy of Aloe vera, Curcuma longa and Ocimum sanctum extracts in functional prevention of fluoride led oxidative stress. The pregnant Wistar rats were exposed to 100 ppm fluoride in drinking water and pups born to them were supplemented with phytoextracts daily. On 21st postpartum day, the pups were sacrificed to analyse fluoride and oxidative stress markers. Fluoride exposure significantly increased its accumulation, lipid peroxidation and decreased the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase and glutathione levels in discrete regions of the central nervous system (CNS) of pups indicating oxidative stress and inhibited antioxidant defense. The results implied the vulnerability of developing CNS to fluoride toxicity. On phytoextract supplementation, the oxidant devastation was suppressed by regaining antioxidant homeostasis near normal level proving efficacy and therapeutic strategy. Among the phytoextracts supplemented the Ocimum sanctum is found to be more effective.     

Lipid peroxidation products,and vitamin and trace element status in patients with cancer before and after chemotherapy,including adriamycin

Adriamycin is a potent chemotherapeutic agent used in the treatment of human neoplastic diseases. A major side effect limiting the use of this drug is its toxic effect on the heart. Several hypotheses have been proposed to explain the cardiotoxicity of Adriamycin. However, the most plausible hypothesis seems to be the reduction of Adriamycin and free radical production, which induces lipid peroxidation and oxidative damages in the heart. We have thus undertaken this preliminary study to investigate Adriamycin-induced lipid peroxidation by the measurement of plasma thiobarbituric acid reactant materials and antioxidant systems, namely glutathione content, glutathione peroxidase activity, and vitamin and trace element status, in patients with cancer before and after chemotherapy, including Adriamycin. The concentration of thiobarbituric acid reactant materials in plasma of patients with cancer was higher than in controls and was further increased after chemotherapy. Blood glutathione and plasma glutathione peroxidase activity, as well as plasma zinc and selenium in patients with cancer, were decreased, but not further modified by chemotherapy. However, only zinc and selenium levels reached a significant level. In contrast, plasma vitamin E and β-carotene levels were not significantly increased in patients with cancer. Finally, plasma vitamin A and copper levels were not modified either in patients with cancer or by chemotherapy.     

Protective effect of esculetin on hyperglycemia-mediated oxidative damage in the hepatic and renal tissues of experimental diabetic rats

Diabetes mellitus is the most common serious metabolic disorder and it is considered to be one of the five leading causes of death in the world. Hyperglycemia-mediated oxidative stress plays a crucial role in diabetic complications. Hence, this study was undertaken to evaluate the protective effect of esculetin on the plasma glucose, insulin levels, tissue antioxidant defense system and lipid peroxidative status in streptozotocin-induced diabetic rats. Diabetic rats exhibited increased blood glucose with significant decrease in plasma insulin levels. Extent of oxidative stress was assessed by the elevation in the levels of lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP) and conjugated dienes (CD); reduction in the enzymic antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST); nonenzymic antioxidants Vitamin C, E and reduced glutathione (GSH) were observed in the liver and kidney tissues of diabetic control rats as compared to control rats. Oral supplementation of esculetin to diabetic rats for 45 days significantly brought back lipid peroxidation markers, enzymic and nonenzymic antioxidants to near normalcy. Moreover, the histological observations evidenced that esculetin effectively rescues the hepatocytes and kidney from hyperglycemia mediated oxidative damage without affecting its cellular function and structural integrity. These findings suggest that esculetin (40 mg/kg BW) treatment exerts a protective effect in diabetes by attenuating hyperglycemia-mediated oxidative stress and antioxidant competence in hepatic and renal tissues. Further, detailed studies are in progress to elucidate the molecular mechanism by which esculetin elicits its modulatory effects in insulin signaling pathway.     

Selenium supplementation sensitizes renca cells to tert-butylhydroperoxide induced loss of viability

Mouse renal carcinoma (renca) cells growing exponentially in foetal bovine serum (1%) supplemented with selenium (1 microM, sodium selenite) were exposed to oxidative insult. It was found that glutathione peroxidase activity increased (44%), while the activities of catalase, glutathione disulfide reductase, and level of total glutathione did not change due to selenium supplementation. Selenium supplementation made renca cells susceptible to tert-butylhydroperoxide induced cell death, while it did not affect the viability when the cells were exposed to hydrogen peroxide. It suggested that the contribution of glutathione peroxidase in antioxidant defense mechanism of renca cells was possibly not crucial and the function of catalase might be important especially against hydrogen peroxide.     

Dietary vitamin C supplementation decreases blood pressure in DOCA-salt hypertensive male Sprague Dawley rats and this is associated with increased liver oxidative stress

The effects of a vitamin C supplemented diet on blood pressure, body and liver weights, liver antioxidant status, iron and copper levels were investigated in DOCA-salt treated and untreated Sprague-Dawley (SD) male rats after 8 weeks of treatment. Vitamin C supplementation had no effect on blood pressure in SD rats but induced a significant decrease in blood pressure in DOCA-salt treated rats, the decrease being more efficient at 50 mg/kg of vitamin C than at 500 mg/kg. Hepatic lipid peroxidation and iron levels were significantly increased in DOCA-salt hypertensive rats whereas total hepatic antioxidant capacity (HAC), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were decreased. Vitamin C supplementation did not affect the overall antioxidant defences of control SD rat livers. In contrast, vitamin C supplementation accentuated the DOCA-salt induced accumulation of liver iron and lipid peroxidation. This occurred without any notable aggravation in the antioxidant deficiency of vitamin C supplemented DOCA-salt treated rat livers. Our data suggest that DOCA-salt treatment induces an accumulation of iron in rat livers which is responsible for the prooxidant effect of vitamin C. The normalization of blood pressure in DOCA-salt treated rats by vitamin C supplementation appears thus independent from liver antioxidant status.     

Human selenium-containing single-chain variable fragment with glutathione peroxidase activity protects NIH3T3 fibroblast against oxidative damage

Ultraviolet B (UVB medium wave, 280–315 nm) induces cellular oxidative damage and apoptosis by producing reactive oxygen species (ROS). Glutathione peroxidase functions as an antioxidant by catalyzing the reduction of hydrogen peroxide, the more important member of reactive oxygen species. A human selenium-containing single-chain variable fragment (se-scFv-B3) with glutathione peroxidase activity of 1288 U/μmol was generated and investigated for its antioxidant effects in UVB-induced oxidative damage model. In particular, cell viability, lipid peroxidation extent, cell apoptosis, the change of mitochondrial membrane potential, caspase-3 activity and the levels of intracellular reactive oxygen species were assayed. Human se-scFv-B3 protects NIH3T3 cells against ultraviolet B-induced oxidative damage and subsequent apoptosis by prevention of lipid peroxidation, inhibition of the collapse of mitochondrial membrane potential as well as the suppression of the caspase-3 activity and the level of intracellular ROS. It seems that antioxidant effects of human se-scFv-B3 are mainly associated with its capability to scavenge reactive oxygen species, which is similar to that of the natural glutathione peroxidase.     

Selenium and Topiramate Attenuates Blood Oxidative Toxicity in Patients with Epilepsy: A Clinical Pilot Study

It is well known that oxidative stress plays an important role in the etiology of epilepsy. We investigated effects of selenium (Se) and topiramate (TPM) combination supplementation on antioxidant and oxidant values in control and patients with epilepsy and refractory epilepsy. For the aim, we used control (n?=?19), epilepsy + TPM (n?=?19), epilepsy + TPM + Se (n?=?15) groups. We also used control (n?=?15), refractory epilepsy (n?=?15), and refractory epilepsy + Se (n?=?8) groups. TPM (0.2 mg/daily) and Se, as sodium selenite (twice daily with 0.1 mg doses), were orally supplemented to the patients for 45 days. Erythrocyte lipid peroxidation levels were higher in refractory epilepsy groups than in control although its level and seizure numbers were decreased in TPM and TPM + Se supplemented groups of the patients. The erythrocyte reduced glutathione (GSH), glutathione peroxidase (GSH-Px), plasma total antioxidant status (TAS), and vitamin E concentration in refractory epilepsy group were lower than in control. However, the erythrocyte and plasma TAS, erythrocyte GSH and GSH-Px, and plasma vitamins A and C values were increased either by Se or Se + TPM in epilepsy and refractory epilepsy groups. There were no effects of TPM and Se on plasma β-carotene values in the groups. In conclusion, TPM and selenium caused protective effects on the epilepsy and refractory epilepsy-induced oxidative injury by inhibiting free radical production and supporting antioxidant redox system.     

Lipid peroxidation and antioxidant status in blood of patients with uterine myoma, endometrial polypus, hyperplastic and malignant endometrium

Oxidative stress is considered to be involved in pathogenesis of many disorders of the female genital tract. In this study, we explored the lipid peroxidation levels and antioxidant enzyme activities in women diagnosed with different forms of uterine diseases in order to evaluate the extent of oxidative stress in blood of such patients. Blood samples of healthy subjects and gynecological patients were collected and subjected to assays for superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and lipid hydroperoxides. The results show that alterations of measured parameters vary with the enzyme type and diagnosis. However, both reduction in antioxidants and elevation of lipid peroxidation were observed in general. Lipid hydroperoxides level was negatively correlated to superoxide dismutase and glutathione peroxidase activities, as well as positively correlated to catalase activity. In addition, the lipid hydroperoxides/ glutathione peroxidase ratio was found to be increased, according to the type of uterine disease. The obtained results show that perturbation of antioxidant status is more pronounced in blood of patients with premalignant (hyperplastic) and malignant (adenocarcinoma) lesions, compared to those with benign uterine changes such as polypus and myoma.