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PubMed2005

Effects of dietary selenium on post-ischemic expression of antioxidant mRNA.

Cardiac ischemia reperfusion leads to oxidative stress and poor physiological recovery. Selenium deficiency down-regulates thioredoxin reductase (Txnrd) and glutathione peroxidase (Gpx) activity, impairing recovery from ischemia-reperfusion. Furthermore, selenium supplementation has been shown to be cardioprotective and lessens oxidative stress in reperfused rat hearts. In this study we have investigated the role of selenium in the mRNA expression of these, and related antioxidant proteins, post ischemia-reperfusion. Male rats were fed varying doses of selenium for five weeks. Hearts were isolated and perfused using the Langendorff method with 22.5 min of global ischemia and 45 min reperfusion. RNA was extracted for quantitative real-time PCR analysis of glutathione peroxidase (Gpx)-1 and 4, glutathione reductase (Gsr), thioredoxin peroxidase-2 (Prdx2), thioredoxin (Txn) and thioredoxin reductase (Txnrd)-1 and 2 gene expression. Selenium deficiency produced significant reductions in Gpx-1, Gpx-4, Prdx2, Txnrd-1 and Txnrd-2 expression. Conversely, selenium supplementation of 1000 microg/kg significantly up-regulated Gpx-1, Gpx-4, Txn, Txnrd-1 and Txnrd-2 transcription. Our results show selenium modulates the cardiac mRNA expression of thioredoxin and glutathione related enzymes post ischemia-reperfusion, and impacts on tolerance to ischemia-reperfusion.

Animal Nutritional Physiological Phenomena↗
PubMed2003

Modulatory effects of selenium and zinc on the immune system.

Almost all nutrients in the diet play a crucial role in maintaining an "optimal" immune response, and both insufficient and excessive intakes can have negative consequences on the immune status and susceptibility to a variety of pathogens. We summarize the evidence for the importance of two micronutrients, selenium and zinc, and describe the mechanisms through which they affect the immune status and other physiological functions. As a constituent of selenoproteins, selenium is needed for the proper functioning of neutrophils, macrophages, NK cells, T lymphocytes and some other immune mechanisms. Elevated selenium intake may be associated with reduced cancer risk and may alleviate other pathological conditions including oxidative stress and inflammation. Selenium appears to be a key nutrient in counteracting the development of virulence and inhibiting HIV progression to AIDS. It is required for sperm motility and may reduce the risk of miscarriage. Selenium deficiency has been linked to adverse mood states and some findings suggest that selenium deficiency may be a risk factor in cardiovascular diseases. Zinc is required as a catalytic, structural and regulatory ion for enzymes, proteins and transcription factors, and is thus a key trace element in many homeostatic mechanisms of the body, including immune responses. Low zinc ion bioavailability results in limited immunoresistance to infection in aging. Physiological supplementation of zinc for 1-2 months restores immune responses, reduces the incidence of infections and prolongs survival. However, in every single individual zinc supplementation of food should be adjusted to the particular zinc status in views of the great variability in habitat conditions, health status and dietary requirements.

Dietary Supplements↗
PubMed1998

Dietary oxidative stress and the potentiation of viral infection.

Oxidative stress is implicated in the pathogenesis of several viral infections, including hepatitis, influenza, and AIDS. Dietary oxidative stress due to either selenium or vitamin E deficiency increases cardiac damage in mice infected with a myocarditic strain of coxsackievirus B3. Such dietary oxidative stress also allows a normally benign (i.e., amyocarditic) coxsackievirus B3 to convert to virulence and cause heart damage. This conversion to virulence is due to a nucleotide sequence change in the genome of the benign virus, which then resembles more closely the nucleotide sequence of virulent strains. Although it has been known for many years that poor nutrition can affect host response to infection, this is the first report of host nutrition affecting the genetic sequence of a pathogen. Further research is needed to determine whether poor host nutrition plays any role in the emergence of new viral diseases via alterations in he genotype of an infectious agent.

Animals↗
PubMed1992

Exercise-induced oxidant stress in the lung tissue: role of dietary supplementation of vitamin E and selenium.

Strenuous physical exercise in the form of swimming in female albino rats increased the oxidative reactions, probably leading to the generation of oxy-free radicals in the lung tissue. Free radical-mediated lipid peroxidation measured in the form of lipid peroxides increased in the pulmonary tissue in response to exhaustive exercise, indicating such a possibility. Dietary supplementation of vitamin E (Vit.E) and selenium (Se) for a period of 12 weeks reduced the oxidative reactions and the ensuing lipid peroxidation in the pulmonary tissue. Physical exercise in control animals induced the activity of superoxide dismutase (SOD), the superoxide anion radical (O2-.) quencher. However, the SOD levels in nutrient-fed animals at rest and after exercise remained well below the control levels, indicating the decreased generation of oxy-free radicals in them. Similarly, selenium-dependent glutathione peroxidase (Se-GSH Px), the enzyme involved in the reduction of organic and inorganic peroxides, and glutathione S- transferase (GST), the multifunctional protein involved in the detoxification of a number of xenobiotics, were increased in response to exercise in control animals, but were significantly decreased in nutrient-fed animals upon exercise. The induction of GST seems to be more towards the peroxidase activity of GST, i.e., non-selenium glutathione peroxidase (Non-Se-GSH Px), which is primarily involved in the reduction of endoperoxides. The studies thus indicate the induction of oxidative stress in the pulmonary tissue upon exhaustive physical exercise and the effectiveness of vit.E and Se independently and more so in combination in combating the exercise-induced oxidant stress.

Animals↗
PubMed1994

Endogenous skeletal muscle antioxidants.

Skeletal muscle is susceptible to oxidative deterioration due to a combination of lipid oxidation catalysts and membrane lipid systems that are high in unsaturated fatty acids. To prevent or delay oxidation reactions, several endogenous antioxidant systems are found in muscle tissue. These include alpha-tocopherol, histidine-containing dipeptides, and antioxidant enzymes such as glutathione peroxidase, superoxide dismutase, and catalase. The contribution of alpha-tocopherol to the oxidative stability of skeletal muscle is largely influenced by diet. Dietary supplementation of tocopherol has been shown to increase muscle alpha-tocopherol concentrations and inhibit both lipid oxidation and color deterioration. Dietary selenium supplementation has also been shown to increase the oxidative stability of muscle presumably by increasing the activity of glutathione peroxidase. The oxidative stability of skeletal muscle is also influenced by the histidine-containing dipeptides, carnosine and anserine. Whereas carnosine and anserine are affected by diet less than alpha-tocopherol and glutathione peroxidase, their concentrations vary widely with species and muscle type. In pigs, beef, and turkey muscle, carnosine concentrations are greater than anserine, while the opposite is true in rabbit, salmon, and chicken muscle. Anserine and carnosine are found in greater concentrations in muscle high in white fibers, with chicken white muscle containing over fivefold more anserine and carnosine than red muscle. Anserine and carnosine are thought to inhibit lipid oxidation by a combination of free radical scavenging and metal chelation.

Animals↗
PubMed2006

Intradialytic parenteral nutrition: comparison of olive oil versus soybean oil-based lipid emulsions.

Lipid, oxidative and inflammatory parameters are frequently altered in dialysis patients and may be worsened by intravenous lipid emulsions (ILE). We assessed the efficacy and tolerance of olive as compared with standard soybean oil-based ILE during intradialytic parenteral nutrition (IDPN). IDPN mixtures containing amino acids, glucose, and either olive oil (OO group, n 17) or soybean oil-based ILE (SO group, n 18) were administered in a 5-week randomized, double-blind study. On days 0 and 35, patients' nutritional status was assessed by BMI, normalized protein catabolic rate, predialytic creatinine, serum albumin and transthyretin; lipid metabolism by plasma LDL- and HDL-cholesterol, triacylglycerols, phospholipids, apo A-I, A-II, B, C-II, C-III, E and lipoprotein (a); oxidative status by alpha-tocopherol, retinol, selenium, glutathione peroxidase, malondialdehyde and advanced oxidized protein products; inflammatory status by serum C-reactive protein, orosomucoid, IL-2 and IL-6. No serious adverse event was observed. Significant changes were observed from day 0 to day 35 (P<0.05): nutritional criteria improved (albumin in OO; albumin, transthyretin and creatinine in SO); LDL-cholesterol, apo B, C-II, C-III and apo A-I/A-II ratio increased in both groups. HDL-cholesterol decreased in OO; apo E increased and lipoprotein (a) decreased in SO; alpha-tocopherol/cholesterol ratio increased in OO; malondialdehyde decreased in both groups; IL-2 increased in both groups. The between-group comparison only showed the following differences: alpha-tocopherol/cholesterol increased in OO; lipoprotein (a) decreased in SO. From these data, it was concluded that OO- and SO-based IDPNs similarly improved nutritional status and influenced plasma lipid, oxidative, inflammatory and immune parameters.

Aged↗
PubMed1994

Antioxidant status of dairy cows supplemented prepartum with vitamin E and selenium.

Possible relationships among dietary antioxidants, oxidative status, and placental retention were investigated in periparturient dairy cows. During 6 wk prepartum, 16 cows each were given daily by capsule 1000 IU of vitamin E, 3 mg of Se, both vitamin E and Se, or neither (control). alpha-Tocopherol in serum and fast-acting antioxidants in plasma increased, but, in red blood cells, thiobarbituric acid-reactive substances decreased during the last 6 wk before parturition in cows given vitamin E. These measurements were unaffected by supplementation of Se. Cows that had retained placenta > or = 12 h had lower fast-acting antioxidants in plasma and glutathione peroxidase in red blood cells up to 2 wk before calving than did cows that shed fetal membranes in < 12 h. Results suggest that inadequate dietary antioxidants may increase oxidative stress, production of lipid peroxides, and incidence of retained fetal membranes in dairy cows.

Animal Feed↗
PubMedDate not supplied

Hydroxylation of 3-acetyl-2-(2,6-dimethyl-5-heptenyl)oxazolidine by rat liver microsomes. Identification of some isomeric metabolites.

The metabolism of nonradiolabeled, stereoisomeric mixtures of 3-acetyl-2-(2,6-dimethyl-5-heptenyl)oxazolidine (I), a new citronelial-based insect repellent, by induced and uninduced rat liver microsomes has been examined in a NADPH-generating system at a substrate concentration of 1.67 mM. By comparison of retention times and mass spectra of the metabolites with the products from oxidation of I with selenium dioxide, the allylic methyl carbons of the isobutenyl group were identified as the major sites of oxidative metabolism, with two samples of I prepared from different sources of (+/-)-citronelial. Both diastereomeric and E-Z isomeric forms of the metabolites were separated by high resolution capillary gas chromatography with Carbowax 20M-terephthalic acid. Diastereomeric mixtures of unmetabolized I, E alcohol (II), Z alcohol (III), and E aldehyde (IV) were detected in postsincubate extracts. From integration of peak areas, the mean ratio of II to III was 70:30 in 47 extracts.

Alcohols↗
PubMed1990

Protective action of selenium and manganese on xanthine and xanthine oxidase induced oxidative damage to cultured heart cells.

Ventricular myocytes from neonatal Wistar rats were cultured with 80% Dulbecoo's modified Eagle medium and 20% fetal bovine serum. An appropriate amount of xanthine and xanthine oxidase was added to the culture medium to increase the content of free radicals in cardiac cells. Variation in action potential and input impedance of cardiac myocytes indicated the oxidative damage to the membrane. The ultrastructure of heart cells, characteristically the myofilaments and mitochondria, was damaged. Electron spin resonance measurement demonstrated that xanthine and xanthine oxidase elevated the free radical content, while selenium (Se) and manganese (Mn) reduced the free radicals in cultured heart cells. Supplementation of 0.173 microgram/ml Se and 0.1 microgram/ml Mn into the culture medium separately or simultaneously antagonized the damage induced by xanthine and xanthine oxidase. The possible mechanism might be the production of superoxide anion free radical leading to free radical damage to cardiac cells. Se and Mn might play a role as scavengers through glutathione peroxidase and superoxide dismutase respectively and thus protect cardiac cells from free radical damage.

Action Potentials↗
PubMed2003

Role of antioxidant nutrients and lipid peroxidation in premature infants with respiratory distress syndrome and bronchopulmonary dysplasia.

The objective of this study was to determine if newborn premature infants with severe respiratory distress syndrome (RDS) who developed bronchopulmonary dysplasia (BPD) demonstrate, within the first 3 days of life, lower blood levels of antioxidants and higher urine levels of lipid peroxidation products than premature infants who recovered from RDS. Perinatal variables (gestational age, birth weight, and Apgar scores) and antioxidant indices in cord and in third day of life plasma and red blood cell (RBC) samples from healthy premature infants (n = 35), infants with RDS (n = 23) and infants with BPD (n = 23) were examined. Antioxidant indices included selenium, alpha-tocopherol, total and oxidized glutathione, glutathione peroxidase, superoxide dismutase, and urinary malondialdehyde. By inferential statistics, only the perinatal variables and cord plasma selenium distinguished healthy premature infants from premature infants with RDS or BPD. From perinatal variables and antioxidant indices we calculated: (1) cord to third-day-of-life variable differences, (2) variable-to-variable ratios, and (3) ratios of a difference for one variable to a difference for any second variable. Subset regression analysis yielded an equation (adjusted R2 = 0.8839) that correctly predicted infants who developed BPD 100% of the time. Predictor variables for BPD were gestational age, Apgar at 1 min, cord and third-day-of-life RBC selenium, cord total glutathione, cord and third-day-of-life glutathione peroxidase and nine different ratios involving Apgar scores, RBC selenium, total and oxidized glutathione, alpha-tocopherol, glutathione peroxidase, and superoxide dismutase. In this study, there was no relationship between lipid peroxidation and BPD. There was a higher rate of patent ductus arteriosus, congestive heart failure, and retinopathy of prematurity in infants with BPD. This study confirms that low plasma selenium and alpha-tocopherol levels in premature infants (< or = 30 weeks' gestational age or lower) were significantly associated with an increased respiratory morbidity.

Antioxidants↗
PubMedDate not supplied

Reversible cardiomyopathy due to selenium deficiency.

Selenium is an essential trace element and a component of glutathione peroxidase, an enzyme that may help to prevent oxidative damage to cells. Selenium deficiency has been linked to the development of Keshan disease, a dilated congestive cardiomyopathy occurring primarily in children living in rural China. Sporadic cases have been reported in the United States in individuals with poor nutritional intake, mostly in individuals on long-term home parenteral nutrition. This report describes a young black woman with Crohn's disease in whom a congestive cardiomyopathy developed and was subsequently reversed following administration of selenium.

Adult↗
PubMed2006

Selenium and antioxidant defenses as major mediators in the development of chronic heart failure.

Increased oxidative stress is involved in the pathogenesis of chronic heart failure (CHF), the common end result of most cardiac diseases. Selenium is an "essential" trace element, which means that it must be supplied by our daily diet and that its blood and tissue concentrations are extremely low. Selenium has a variety of functions. It is a key component of several functional selenoproteins required for normal health. The best known of these are the antioxidant glutathione peroxidase (GPx) enzymes, which remove hydrogen peroxide and the harmful lipid hydroperoxides generated in vivo by oxygen-derived species. GPx deficiency exacerbates endothelial dysfunction, a major contributing factor in the severity of CHF symptoms, in various conditions such as hyperhomocysteinemia. This suggests that homocysteine may be involved in the CHF associated endothelial dysfunction through a peroxide-dependent oxidative mechanism. Selenium also plays a role in the control of thyroid hormone metabolism and in protection against organic and inorganic mercury. One possible additional mechanism by which low selenium may compromise cardiovascular condition may be through the effect of selenium on the synthesis and activity of deiodinases, enzymes converting thyroxin into the biologically active triiodothyronine. Selenium and iodine actually interact in cardiovascular physiology, and further studies are needed to examine their role, in isolation and in association, in the development of CHF. Thus, selenium (through its role in selenoenzymes, thyroid hormones, and interactions with homocysteine and endothelial function) appears to be a major mediator in several pathways potentially contributing to CHF development.

Antioxidants↗
PubMed2005

Human erythrocyte delta-aminolevulinate dehydratase inhibition by monosaccharides is not mediated by oxidation of enzyme sulfhydryl groups.

The heme pathway enzyme delta-aminolevulinate dehydratase is a good marker for oxidative stress and metal intoxication. This sulfhydryl enzyme is inhibited in such oxidative pathologies as lead, mercury and aluminum intoxication, exposure to selenium organic species and diabetes. Oxidative stress is a complicating factor in diabetes, inducing non-enzymatic glucose-mediated reactions that change protein structures and impair enzyme functions. We have studied the effects of high glucose, fructose and ribose concentrations on delta-ALA-D activity in vitro. These reducing sugars inhibited delta-ALA-D with efficacies in the order fructose=ribose>glucose. The possible mechanism of glucose inhibition was investigated using lysine, DTT, and t-butylamine. Oxidation of the enzyme's critical sulfhydryl groups was not involved because DTT had no effect. We concluded that high concentrations of reducing sugars or their autoxidation products inhibit delta-ALA-D by a mechanism not related to thiol oxidation. Also, we are not able to demonstrate that the formation of a Schiff base with the critical lysine residue of the enzyme is involved in the inhibition of delta-ALA-D by hexoses.

Butylamines↗
PubMed2006

Determination of trace selenium by solid substrate-room temperature phosphorescence enhancing method based on potassium chlorate oxidizing phenyl hydrazine-1,2-dihydroxynaphthalene-3,6-disulfonic acid system.

A new method for the determination of trace selenium based on solid substrate-room temperature phosphorimetry (SS-RTP) has been established. This method was based on the fact that in HCl-KCl buffer solution, potassium chlorate could oxidize phenyl hydrazine to form chloridize diazo-ion after being heated at 100 degrees C for 20 min, and then the diazo-ion reacted with 1,2-dihydroxynaphthalene-3,6-disulfonic acid to form red azo-compound which could emit strong room temperature phosphorescence (RTP) signal on filter paper. Selenium could catalyze potassium chlorate oxidizing the reaction between phenyl hydrazine and 1,2-dihydroxynaphthalene-3,6-disulfonic acid, which caused the sharp enhancement of SS-RTP. Under the optimum condition, the relationship between the phosphorescence emission intensity (DeltaIp) and the content of selenium obeyed Beer's law when the concentration of selenium is within the range of 1.60-320 fg spot-1 (or 0.0040-0.80 ng ml-1 with a sample volume of 0.4 microl). The regression equation of working curve can be expressed as DeltaIp=13.12+0.4839CSe(IV) (fg spot-1) (n=6), with correlation coefficient r=0.9991 and a detection limit of 0.28 fg spot-1 (corresponding to a concentration range of 7.0x10(-13) g ml-1 Se(IV), n=11). After 11-fold measurement, R.S.D. were 2.8 and 3.5% for the samples containing 0.0040 and 0.80 ng ml-1 of Se(IV), respectively. This accurate and sensitive method with good repeatability has been successfully applied to the determination of trace selenium in Chinese wolfberry and egg yolk with satisfactory results. The mechanism of the enhancement of phosphorescence was also discussed.

Animals↗
PubMed1996

Modulation of ultraviolet light-induced oxidative stress in mice skin related to dietary vitamin A and selenium intake.

Weanling female SKH1 hairless mice were randomly divided into 4 groups. Each group was fed a particular regimen for 20 weeks: 1) normal basal diet with 5 IU vitamin A/g and 0.45 microgram selenium/g, 2) vitamin A deficient, 3) selenium deficient, and 4) vitamin A plus selenium deficient. Three hours before being sacrificed, half of the animals were subjected to UV A + B irradiation (3 J/cm2). Superoxide dismutases (SOD), catalase, Se glutathione peroxidase activities were determined in dorsal skin homogenates, as well as the concentrations of GSH and of thiobarbituric acid-reactive substances (TBARS), the latter being an index of lipid peroxidation. Ultraviolet light altered the antioxidant defense of mouse skin tissue: GSH level, catalase and Se glutathione peroxidase activities were lowered and SOD was unequally enhanced according to the nutritional status. Vitamin A and Se deficiencies did not perceptibly aggravate the UV-induced oxidative stress, although the former enhanced the decline of catalase expression induced by the irradiation. Probably through an adaptive mechanism, both dietary deficiencies increased the skin reserve of antioxidant GSH and thus appear to modulate the effects caused by reactive oxygen species.

Animals↗
PubMed2005

Protective effect of curcumin during selenium induced toxicity on dehydrogenases in hepatic tissue.

Selenium administration resulted in a marked decrease in the activity levels of the liver succinate dehydrogenase, malate dehydrogenase, and lactate dehydrogenase while pyruvate dehydrogenase increased significantly (P<0.001) in the wistar rat. The degree of decrease of these enzymes was significantly less (P<0.001) when rats were treated with curcumin, a natural constituent Curcuma longa. Curcumin seems to prevent oxidative damage mediated through selenium and protect the dehydrogenases possibly through its anti-oxidative property.

Administration, Oral↗