Co-administration Of Selenium Research Articles

Protective effects of selenium against cypermethrin induced hepatorenal damage in Sprague Dawley rats

Introduction: Alpha-Cypermethrin is a synthetic pyrethroid insecticide. Pyrethroids are derived from pyrethrins, which are toxic components found in the Chrysanthemum cinerariaefolium flowers. They have been employed in agriculture, home and veterinary formulations to control the insect vectors of disease, agricultural insects and topically applied to eradicate veterinary pests. The extensive use of pyrethroids in agriculture results in severe pyrethroid poisonings in developing countries. Objectives: This study aimed to evaluate the serum biochemical changes induced by oral exposure of cypermethrin and the protective effects of selenium in female Sprague-Dawley rats. Methodology: The female rats (n=20) were equally divided into four groups. Group 1, 2, 3 and 4 received 1 ml corn oil, 55 mg/kg/b.w of cypermethrin, 1 ppm of sodium selenite, both cypermethrin and sodium selenite respectively for 21 days. The serum was utilized for estimation of alkaline phosphatase (ALP), alanine transaminase (ALT), urea, creatinine and bilirubin by using Selectra E (Germany). Levels of sodium (Na+) and potassium (K+) in serum were measured using Easylyte (Na+/K+) analyzer (Japan). Results: Results obtained showed that activities of ALP and ALT were significantly (P<0.05) elevated in cypermethrin treated rats. Total bilirubin, urea and creatinine were insignificantly elevated due to cypermethrin administration. Also, selenium reduced the harmful effects of cypermethrin in the combined treatment group in some parameters. Conclusion: Oral exposure of cypermethrin induces injuries in liver and kidney of rats as well as alterations in the levels of serum electrolytes which were modulated by selenium co-administration.

Preventive effects of selenium against cypermethrin induced haematological toxicity in Sprague-Dawley rats

Purpose: Cypermethrin (class II) belongs to pyrethroid insecticides which have been in wide use to control various pests including moth pests of cotton, fruit and vegetable crops. This study was aimed to investigate the effects of cypermethrin on haematology of female rats and their modulation by co-administration of sodium selenite. Methodology: Four equal groups of female rats were made (n=20). Group 1 received 1 ml corn oil, Group 2 was administered 55 mg/kg/b.w of cypermethrin, Group 3 was provided with 1 ppm of sodium selenite and Group 4 was given both cypermethrin and sodium selenite. Haematological analysis of blood samples was performed employing Sesmex Kx-21 (Japan). Results: Red blood cell (RBC) count, haemoglobin concentration (Hb) and hematocrit (Hct) were significantly reduced (P<0.05) due to cypermethrin treatment which indicates that rats were suffering from anaemia. While, the rest of the hematological parameters i.e. platelet count (PLT), number of lymphocytes, white blood cell (WBC) count, platelet larger cell ratio (P-LCR), RBC distribution width (RDW), mean platelet volume (MPV), platelet distribution width (PDW), lymphocyte percentage (LYM), mean corpuscular haemoglobin concentration (MCHC), mean corpuscular haemoglobin (MCH) and mean corpuscular volume (MCV) were non-significantly affected. Selenium coadministration with cypermethrin was found to restore the levels of above-mentioned parameters to those found in control group. Conclusion: Hence, it can be concluded from this study that cypermethrin administration can cause hematological alterations in rats. Co-administration of selenium provided protection against cypermethrin toxicity to some extent.

Selenium attenuates diclofenac-induced testicular and epididymal toxicity in rats.

The adverse effect of diclofenac administration on the male reproductive organ in both humans and rats has been reported. Selenium, a trace element vital in nutrition, plays a significant part in cellular redox homeostasis, including male reproduction. However, the impact of selenium on male reproductive toxicity associated with diclofenac administration is lacking in the literature. The current investigation assessed the modulatory effects of selenium on diclofenac-mediated reproductive toxicity in rats. Rats were treated for fourteen consecutive days, either with diclofenac (10mg/kg) or co-treated with selenium (0.125 and 0.25mg/kg) body weight. Sperm parameters, enzymes of testicular function, luteinizing, follicle-stimulating hormone and testosterone were assessed in addition to oxidative stress indices and histopathological changes. Selenium significantly alleviated diclofenac-induced decreases in sperm count and motility, testicular function enzymes and levels of luteinizing hormone and testosterone in serum. Moreover, selenium co-administration at 0.125 and 0.25mg/kg inhibited the diclofenac-induced decrease of antioxidant enzyme activities and increased oxidative stress parameters-lipid peroxidation, reactive nitrogen and oxygen species-in epididymis and testes of rats. Selenium (0.25mg/kg) alone ameliorated diclofenac-mediated histological injuries in exposed rats. Collectively, selenium enhanced testicular and epididymal function in diclofenac-treated rats by suppressing nitrosative and oxidative stress in rats.

Chromium-Induced Hepatotoxicity and Potential Protective Effect of Selenium in Adult Male Albino Rat: A Histological, Immuno-Histochemical and Molecular Study

Abstract Background: Chromium (Cr) is a main environmental contaminant, famous for its major poisonous effects. Cr (VI) induces variable health hazards. Selenium (Se) is a micronu-trient with anti-oxidant activity. Aim of Study: This study aims to demonstrate the protecting role of selenium in chromium-induced hepatotoxicity in adult male albino rat. Material and Method: Thirty six adult healthy male albino rats 3-6 months of age were divided into four groups (9 animals for each): Group I (control): Fed on balanced diet and water; group II (Se-group): Received daily dose of sodium selenite (0.25mg/kg B.W, dissolved in distilled water); group III (Cr-treated): Received daily dose of potassium dichromate (700ppm equivalent to 67mg/kg B.W, in distilled water); group IV; received potassium dichromate in combination with sodium selenite (as mentioned in groups II & III respectively). Blood samples were drawn from tail vein for biochemical examinations, and after sacrifice fresh liver specimens were collected for histological, immunohistochemical studies and real-time RT-PCR analysis of oxidative stress genes. Results: Chromium motivated oxidative stress process, through producing significant down regulation of the gene expression levels of the anti-oxidant genes (CAT, SOD1 and GPx) as compared to control rats, thus inducing different hepatic histopathological changes in the form of loss of the normal arrangement of hepatocytes with dilated central vein. Dilated congested portal vein with thick wall and mononuclear cellular infiltrations were noticed. In addition, fatty degener-ation, vacuolization and degeneration of hepatocytes were observed. Moreover, bile ducts showed proliferation and stratifications of their epithelial lining and some sinusoids showed slight dilatation. These histopathological changes were associated with high statistical significant increase in serum level of (ALT, AST and total bilirubin) in group III (Cr -treated) as compared with groups (I and II). Se co - admin-istration with Cr in group IV showed less histopathological disturbances and induced a statistical significant decrease in serum level of (ALT, AST and total bilirubin) as compared with group III (Cr-treated). Such changes may be attributed to up regulation of gene expression levels of anti-oxidants genes (CAT, SOD1 and GPx) under influence of Se. in com-parison to group III (Cr -treated). Conclusion: Chromium-induced oxidative stress, biochem-ical, histopathological and immunohistochemical hepatic disturbances which were less manifested by co-administration of selenium.

Co-administration of Selenium with Inorganic Mercury Alters the Disposition of Mercuric Ions in Rats.

Mercury (Hg) is a common environmental toxicant to which humans are exposed regularly through occupational and dietary means. Although selenium supplementation has been reported to prevent the toxic effects of Hg in animals, the mechanisms for this prevention are not well understood. The purpose of the current study was to determine the effects of selenium on the disposition and toxicity of Hg. Wistar rats were injected intravenously with a non-nephrotoxic dose (0.5μmolkg-1) or a nephrotoxic dose (2.5μmolkg-1) of HgCl2 (containing radioactive Hg) with or without co-administration of sodium selenite (Na2SeO3). Twenty-four hours after exposure, rats were euthanized, and organs were harvested. Co-administration of SeO32- with HgCl2 reduced the renal burden of Hg and the urinary excretion of Hg while increasing the amount of Hg in blood and spleen. We propose that Hg reacts with reduced selenite in the blood to form large Hg-Se complexes that are unable to be filtered at the glomerulus. Consequently, these complexes remain in the blood and are able to accumulate in blood-rich organs. These complexes, which may have fewer toxic effects than other species of Hg, may be eliminated slowly over the course of weeks to months.

Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington's Disease.

Systemic administration of 3-nitropropionic acid (3-NPA) is commonly used to induce Huntington's disease (HD)-like symptoms in experimental animals. Here, the potential neuroprotective efficiency of rutin and selenium (RSe) co-administration on 3-NPA-induced HD-like symptoms model in mice was investigated. 3-NPA injection evoked severe alterations in redox status, as indicated via increased striatal malondialdehyde and nitric oxide levels, accompanied by a decrease in levels of antioxidant molecules including glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase. Moreover, 3-NPA potentiated inflammatory status by enhancing the production of interleukin-1β, tumor necrosis factor-α, and myeloperoxidase activity. Pro-apoptotic cascade was also recorded in the striatum as evidenced through upregulation of cleaved caspase-3 and Bax, and downregulation of Bcl-2. 3-NPA activated astrocytes as indicated by the upregulated glial fibrillary acidic protein and inhibited brain-derived neurotrophic factor. Furthermore, perturbations in cholinergic and monoaminergic systems were observed. RSe provided neuroprotective effects by preventing body weight loss, oxidative stress, neuroinflammation, and the apoptotic cascade. RSe inhibited the activation of astrocytes, increased brain-derived neurotrophic factor, and improved cholinergic and monoaminergic transmission following 3-NPA intoxication. Taken together, RSe co-administration may prevent or delay the progression of HD and its associated impairments through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory effects.

Impact of selenium co-administration on methylmercury exposed eleutheroembryos and adult zebrafish (Danio rerio): Changes in bioaccumulation and gene expression

Mercury still represents one of the most hazardous threats for the aquatic ecosystem due to its high toxicity, and the fact that it can be easily incorporated into the food chain by accumulation in fish as MeHg. On the other hand, selenium is a micronutrient that is part of different antioxidant enzymes that regulate the cellular redox state, and whose complex interaction with Hg has been extensively studied from a toxicological point of view. In order to evaluate the protective effect of Se(IV) co-administration against MeHg accumulation and toxicity, we have selected an in-vivo model at two developmental stages: zebrafish eleutheroembryos and adult fish. Embryos were exposed during 48 h to MeHg (5 or 25 μg/l) and a concentration of Se (IV) representing a molar ratio close to one (2.5 or 12.5 μg/l), while adult zebrafish were exposed during 72 h to either 25 μg/l of MeHg alone or co-exposed with 12.5 μg/l of Se (IV). A significant decrease in MeHg bioaccumulation factor was observed in eleutheroembryos co-exposed to Se(IV). A time-dependent accumulation of MeHg was observed in all the analyzed organs and tissues of adult fish, which was significantly reduced in the muscular tissue and the intestine by Se(IV) co-administration. However, such protection against MeHg bioaccumulation was not maintained in the brain and liver. The data derived from the gene expression analysis also demonstrated the protective effect of Se(IV) against MeHg-induced oxidative stress and the activation of different defense mechanisms by Se(IV) co-administration.

Lithium disturbs homeostasis of essential microelements in erythrocytes of rats: Selenium as a protective agent?

Selenium is an essential element which shows protective properties against diverse harmful factors. Lithium compounds are widely used in medicine, but, in spite of undoubted beneficial effects, treatment with these compounds may lead to severe side effects, including renal, gastrointestinal, neurological, endocrine and metabolic disorders. This study was aimed at evaluating the influence of selenium and/or lithium on lithium, iron, zinc and copper content in rats' erythrocytes as well as estimate the action of additional selenium on lithium exposure effects. The experiment was performed on four groups of rats (six animals each): control - received saline; Li - received 2.7mg Li/kg b.w. as lithium carbonate; Se - received 0.5mg Se/kg b.w. as sodium selenite; Se+Li - received simultaneously 0.5mg Se/kg b.w. and 2.7mg Li/kg b.w. (sodium selenite and lithium carbonate). The administration was performed for three weeks, once a day by stomach tube, in form of water solutions. In erythrocytes the content of lithium, iron, zinc and copper was determined using flame atomic absorption spectroscopy. Lithium treatment insignificantly disturbed iron and zinc homeostasis as well as markedly increased lithium accumulation and copper content in rat erythrocytes. Selenium coadministration reversed those effects. The beneficial effect of selenium on disturbances of studied microelements homeostasis as well as on preventing lithium accumulation in erythrocytes in Li receiving animals allows suggesting that further research on selenium application as an adjuvant in lithium therapy is worth carrying on.

The Influence of Lithium and/or Selenium Treatment on Homeostasis of Chosen Bioelements in Rats

Lithium is widely used in medicine and the therapy is often long term. Apart from beneficial effects, its application can cause diverse side effects. The current study was performed with the aim of the evaluation of the effect of lithium and/or selenium administration on magnesium, calcium and silicon levels in rats. The study was performed on rats divided into four groups (six animals each): control—received saline, Li—received Li2CO3 (2.7 mg Li/kg b.w.), Se—received Na2SeO3·H2O (0.5 mg Se/kg b.w.), and Li+Se—received simultaneously Li2CO3 and Na2SeO3·H2O (2.7 and 0.5 mg Se/kg b.w.). The administration was performed in form of water solutions by a stomach tube once a day for 6 weeks. In the organs (liver, kidney, brain, spleen, heart, lung and femoral muscle), the concentrations of magnesium, calcium and silicon were determined. Lithium significantly increased Ca in the kidney, brain and spleen. Coadministration of selenium reversed this effect. No changes of magnesium in organs were observed. Silicon was affected only in spleen—an increase vs. control was observed in all studied groups. The beneficial influence of coadministration of selenium in case of calcium lets us suggest that an issue of its possible use as an adjuvant alleviating side effects in lithium-treated subjects is worth being continued.

Evaluation of Some Biochemical Parameters and Brain Oxidative Stress in Experimental Rats Exposed Chronically to Silver Nitrate and the Protective Role of Vitamin E and Selenium.

Due to undesirable hazardous interactions with biological systems, this investigation was undertaken to evaluate the effect of chronic exposure to silver on certain biochemical and some oxidative stress parameters with histopathological examination of brain, as well as the possible protective role of selenium and/or vitamin E as nutritional supplements. Thirty six male rats were divided into six groups of six each: the first group used as a control group. Group II given both vitamin E (400 mg/kg) of diet and selenium (Se) (1 mg/L) in their drinking water. Group III given silver as silver nitrate (AgNO3) (20 mg/L). Group IV given vitamin E and AgNO3. Group V given both AgNO3 and selenium. Group VI given AgNO3, vitamin E and Se. The animals were in the same exposure conditions for 3 months. According to the results which have been obtained; there was an increase in serum lactate dehydrogenase (LDH), lipase activities and cholesterol level, a decrease in serum total protein, calcium and alkaline phosphatase (ALP) activity in Ag-intoxicated rats. Moreover, the findings showed that Ag+ ions affected antioxidant defense system by decreasing superoxide dismutase (SOD) activity and increasing vitamin E concentration with a high level of malondialdehyde (MDA) in brain tissue. The histological examination also exhibited some nervous tissue alterations including hemorrhage and cytoplasm vacuolization. However, the co-administration of selenium and/or vitamin E ameliorated the biochemical parameters and restored the histological alterations. In conclusion, this study indicated that silver could cause harmful effects in animal body and these effects can be more toxic in high concentrations or prolonged time exposure to this metal. However, selenium and vitamin E act as powerful antioxidants which may exercise adverse effect against the toxicity of this metal.

Homeostasis of chosen bioelements in organs of rats receiving lithium and/or selenium

Lithium is an essential trace element, widely used in medicine and its application is often long-term. Despite beneficial effects, its administration can lead to severe side effects including hyperparathyroidism, renal and thyroid disorders. The aim of the current study was to evaluate the influence of lithium and/or selenium treatment on magnesium, calcium and silicon levels in rats’ organs as well as the possibility of using selenium as an adjuvant in lithium therapy. The study was performed on rats divided into four groups (six animals each): control-treated with saline; Li-treated with Li2CO3 (2.7 mg Li/kg b.w.); Se-treated with Na2SeO3·H2O (0.5 mg Se/kg b.w.); Se + Li-treated simultaneously with Li2CO3 and Na2SeO3·H2O (2.7 mg Li/kg b.w. and of 0.5 mg Se/kg b.w., respectively). The administration was performed in form of water solutions by stomach tube once a day for 3 weeks. In the organs (liver, kidney, brain, spleen, heart, lung and femoral muscle) the concentrations of magnesium, calcium and silicon were determined. Magnesium was increased in liver of Se and Se + Li given rats. Lithium decreased tissue Ca and co-administration of selenium reversed this effect. Silicon was not affected by any treatment. The beneficial effect of selenium on disturbances of calcium homeostasis let suggest that further research on selenium application as an adjuvant in lithium therapy is worth being performed.

The protective influence of selenium on oxidant disturbances in brain of rats exposed to lithium.

For more than sixty years lithium carbonate has been used in medicine. However, during its administration different side effects including oxidative stress can occur. Selenium belongs to essential elements possessing antioxidant properties. This study aimed at evaluating if selenium could be used as a protective adjuvant in lithium therapy. The experiment was performed on four groups of Wistar rats: I (control), II (Li), III (Se), IV (Li + Se) treated with saline, lithium carbonate (2.7 mg Li/kg b.w.), sodium selenite (0.5 mg Se/kg b.w.) and lithium carbonate (2.7 mg Li/kg b.w.) + sodium selenite (0.5 mg Se/kg b.w.), respectively. All substances were administered as water solutions by stomach tube for 3 or 6 weeks. Catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) as well as malonyldialdehyde (MDA) were determined in brain homogenates. Lithium slightly enhanced MDA and depressed CAT and SOD after 6 weeks as well as GPx after 3 weeks. Selenium co-administration showed tendency to restore the disturbed parameters. Selenium alone and given with lithium significantly increased GPx vs. Li-treated group after 3 weeks. Having regarded the outcomes of this study, the research on application of selenium during lithium treatment seems to be worth continuation.

The investigation of the possible protective influence of selenium on antioxidant barrier in heart of rats exposed to lithium.

Selenium is an essential element possessing antioxidant properties and the treatment with it has displayed protective effects against toxicity of different substances occurring in the environment and food as well as against the side effects of some drugs. Lithium is used in medicine although numerous side effects can occur during therapy, including disturbances of the heart. For these reasons studies to find protective adjuvants have been performed. In the current study the possibility of selenium (as sodium selenite) application as a protective adjuvant in lithium treatment was studied. Male Wistar rats were treated: control - with saline; Li-group - with Li2CO3 (2.7 mg Li/kg b.w.); Se-group - with Na2SeO3 (0.5 mg Se/kg b.w.); Li+Se-group simultaneously with Li2CO3 and Na2SeO3 (2.7 mg Li/kg b.w. and 0.5 mg Se/kg b.w., respectively) by a stomach tube for a period of three weeks, once a day. In heart homogenate activities of antioxidant enzymes - catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), concentrations of low-molecular-weight antioxidants - ascorbic acid (AA) and reduced glutathione (GSH) as well as total antioxidant status (TAS) values were determined. GPx/SOD and CAT/SOD ratios were evaluated. In comparison with control selenium caused no significant changes of the studied parameters except for GPx, whereas lithium slightly disturbed TAS and markedly GPx, CAT and CAT/SOD ratio. In Li-treated rats co-administration of selenium displayed tendency towards restoring the impaired parameters. The results suggest that research on selenium application as an adjuvant in lithium therapy is worthy to be continued.

Effect of sodium selenite on chosen anti- and pro-oxidative parameters in rats treated with lithium: A pilot study

BackgroundSelenium is an essential element of antioxidant properties. Lithium is widely used in medicine but its administration can cause numerous side effects including oxidative stress. The present study aimed at evaluating if sodium selenite could influence chosen anti- and pro-oxidant parameters in rats treated with lithium. MethodsThe experiment was performed on four groups of Wistar rats: I (control) – treated with saline; II (Li) – treated with lithium (2.7mgLi/kg b.w. as Li2CO3), III (Se) – treated with selenium (0.5mgSe/kg b.w. as Na2SeO3), IV (Li+Se) – treated with Li2CO3 and Na2SeO3 together at the same doses as in group II and III, respectively. All treatments were performed by stomach tube for three weeks in form of water solutions. The following anti- and pro-oxidant parameters: total antioxidant status (TAS) value, catalase (CAT) activity, concentrations of ascorbic acid (AA) and malonyldialdehyde (MDA) in plasma as well as whole blood superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured. ResultsSelenium given alone markedly enhanced whole blood GPx and diminished plasma CAT vs. control. Lithium significantly decreased plasma CAT and slightly increased AA vs. control. Selenium co-administration restored these parameters to the values observed in control animals. Furthermore, selenium co-administration significantly increased GPx in Li-treated rats. All other parameters (TAS, SOD and MDA) were not affected by lithium and/or selenium. ConclusionFurther research seems to be warranted to decide if application of selenium as an adjuvant in lithium therapy is worth considering.

Selenium partially prevents cisplatin-induced neurotoxicity: A preliminary study

Cisplatin is an anticancer drug and it has neurotoxic effects. On the other hand, the neuroprotective effect of selenium was observed in previous studies. However, the effect of selenium on cisplatin-induced neurotoxicity has not been studied yet. Therefore, we aimed to investigate whether selenium prevent cisplatin-induced neurotoxicity. Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12mg/kg/day, i.p.) was administered for 3 days to CS and CSE groups. Also, CSE group received via oral gavage 3mg/kg/day (twice-a-day as 1.5mg/kg) selenium 5 days before of cisplatin injection and continued for 11 consecutive days. The same volumes of saline were intraperitoneally and orally administered to C group at same time. At the end of experimental protocol, electrophysiological and histopathological examinations were performed. The nerve conduction velocity, amplitude of compound action potential and number of axon of CS group were significantly lower than the C group. However, the same parameters of CSE group were significantly higher than the CS group. Although, cisplatin has a peripheral neurotoxic effect in rats, this effect was partially prevented by selenium treatment. Thus, it appears that co-administration of selenium and cisplatin may be a useful approach to decrease severity of peripheral neurotoxicity.

Ameliorative effect of selenium on carbendazim induced oral sub-chronic testicular toxicity in bucks

In the present investigation, ameliorative effect of selenium (Se), an antioxidant, on oral sub chronic toxicity of carbendazim (CBZ) was assessed by studying various indices of antioxidant defense system. Goat bucks were randomly divided into four groups of four animals each. Group I served as control, Group II was orally administered carbendazim at the dose rate of 50mg/kg, Group III was orally administered selenium in the form of sodium selenite at the dose rate of 0.05mg/kg and Group IV was orally administered carbendazim along with selenium at same dose rates for 90 consecutive days. Prolonged administration of carbendazim produced oxidative stress as evidenced by increased lipid peroxidation (LPO) and significant decrease in the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). The co-administration of selenium with carbendazim produced less marked alterations in the indices of antioxidant status. Carbendazim resulted in significant alteration in sperm count, live sperm percent and also produced sperm abnormalities. Carbendazim co-administered with selenium lead to partial restoration of sperm count and live sperm per cent and resulted in diminished sperm abnormalities. Carbendazim produced anti-androgenic effect as depicted by significant decrease in testosterone level. On the contrary, bucks co-administered with carbendazim and selenium resulted in partial restoration of testosterone level. Thus, from the findings of present investigation it can be concluded that carbendazim leads to testicular oxidative stress as well as antiandrogenic effect and selenium supplementation partially protect from carbendazim induced testicular toxicity.

Effects of Nutritional and Excessive Levels of Selenium on Red Blood Cells of Rats Fed a High Cholesterol Diet

In this study, we investigated the effects of selenium (Se) on the properties of erythrocytes and atherogenic index in the presence and absence of high cholesterol diet (HCD). The effect of selected two different doses (1 μg and 50 μg Se/kg/body weight) on HCD-induced oxidative stress was investigated. The hemolysis of the erythrocytes of the HCD rats as well as by high levels of selenium or their combination was markedly increased. Likewise, atherogenic index and plasma glutathione peroxidase (GPx) activity were significantly increased in the same groups of rats compared to control ones. In contrast, paraoxonase activity, glutathione levels and protein thiol levels, catalase, GPx, and superoxide dismutase activities were significantly decreased in rats that received the HCD, high selenium dose, or their combination. Malondialdehyde and protein carbonyl levels in the plasma and red blood cells were significantly increased by HCD and high selenium dose administration. Co-administration of selenium at low dose with or without an HCD restored all of the investigated parameters to near-normal values. The results of this study suggest that excess selenium administration with HCD worsens the atherogenic index and enhances formation of oxidized red blood cells. At dosage levels in the nutritional range such as 1 μg Se/kg body weight, selenium ameliorates the atherogenic index and preserves the antioxidant capacity of the erythrocytes.

Co-administration of selenium but not iron prevents fluoride toxicity in rats

Fluoride toxicity is known to be associated with oxidative stress, altered antioxidant defense mechanism and DNA damage. The current study was undertaken to evaluate the efficacy of co-administration of selenium (6.3μM) and iron (7.2μM) with fluoride (50ppm) in preventing fluoride-induced oxidative injury, DNA damage and in reducing body fluoride burden in rats. The data suggested that sodium fluoride administration, (50ppm, in drinking water) in rats led a significant oxidative stress which is evident from elevated levels of reactive oxygen species (ROS), lipid peroxidation (TBARS) and reduced activities of antioxidants such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in rats. Co-administration of selenium with fluoride led to a significant recovery in blood and tissue ROS and TBARS levels accompanied by restored activities of antioxidant enzymes studied. Interestingly, selenium also exhibited a remarkable effect in preventing DNA damage in blood and fluoride accumulation in blood and soft tissues. In contrast, administration of iron with fluoride provided significant beneficial effects on blood oxidative stress and DNA damage but failed in reducing tissue oxidative stress conditions and fluoride concentration. Thus, present study provides some useful data concerning beneficial role of selenium against fluoride toxicity by virtue of its ability to eliminate fluoride from target organs and providing recovery in altered biochemical variables.

Dimethoate Induced Oxidative Damage and Histopathological Changes in lung of Adult rats: Modulatory Effects of Selenium and/or Vitamin E

ObjectiveTo determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound. MethodsAdult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E. ResultsExposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage. ConclusionWe concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.

Selenium as a modulator of membrane stability parameters and surface changes during the initiation phase of 1,2-dimethylhydrazine induced colorectal carcinogenesis

The present study evaluated the modulatory potential of selenium on colonic surface abnormalities and membrane fluidity changes following 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis. Rats were segregated into four groups viz., normal control, DMH treated, selenium treated, and DMH + selenium treated. Initiation of molecular events leading to colon carcinogenesis was started following weekly subcutaneous injections of DMH (30 mg/Kg body weight) for 10 weeks. Selenium in the form of sodium selenite was supplemented to rats at a dose level of 1 PPM in drinking water, ad libitum for the entire duration of the study. Brush border membranes were isolated from the colon of rats and the viscosity as well as fluidity parameters were assessed using the membrane extrinsic fluorophore pyrene. DMH treatment resulted in a significant increase in lipid peroxidation. Reduced glutathione levels (GSH) and the activities of glutathione reductase (GR), glutathione transferase (GST), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were found to be significantly decreased following DMH treatment. On the other hand, supplementation with selenium to DMH treated rats resulted in a significant decrease in the levels of lipid peroxidation but caused a significant increase in the levels of GSH as well in the activities of GR, GST, SOD, CAT, and GPx. The results further, demonstrated a marked decrease in membrane microviscosity following DMH treatment. On the other hand, a significant increase was observed in the excimer/monomer ratio and fluidity parameter of DMH treated rats when compared to normal control rats. However, the alterations in membrane microviscosity and the fluidity parameters were significantly restored following selenium treatment. Further, histological as well as colon surface alterations were also observed following DMH treatment, which however were greatly prevented upon selenium co-administration. The study, therefore, concludes that selenium proves as a useful in modulating the colonic surface abnormalities and membrane stability following DMH induced colon carcinogenesis.