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PubMed2006

[Effect of treatment with selenium electrophoresis on biochemical indices in patients suffering from ischaemic cardiac disease with a stable stenocardia of tension].

Disturbances in lipid metabolism, intensification of lipid peroxidize oxidation and functions of sympatho-adrenal system play an important role in the development and progressing of ischaemic cardiac disease. As a result of investigations it has been established that microelement--selenium has an antiatherogenic action and suppresses peroxidize oxidation of lipids. The effect of treatment with selenium electrophoresis in patients suffering from ischaemic cardiac disease with a stable stenocardia of tension has been studied. Total of 76 patients with ICS:SST of I-II functional classes (FC) have been investigated. It has been established that treatment with selenium electrophoresis provokes a reduction of overall cholesterol, triglycerides and beta-lipoproteins content in blood serum, as well as a decrease of cholesterol amount in beta-lipoproteins, lipoproteins of low and very low density and diene conjugates in blood serum and adrenaline and norepinephrine excretion with urine; increase of lipoprotein amount of high density in blood serum, activity of catalase and selenium excretion with urine. Above-said positive changes in biochemical data were more pronounced for the ICS:SST of the first FC.

Adult↗
PubMed2004

High dietary intake of sodium selenite induces oxidative DNA damage in rat liver.

One mechanism for the cancer-chemopreventive effects of high selenium (Se) intake is hypothesized to be antioxidant protection of DNA. In this work we examine DNA oxidation in whole animals as a function of dietary Se intake and carcinogen administration. Weanling male Sprague-Dawley rats were fed a basal, Torula yeast-based, Se-deficient diet supplemented with 0, 0.15, or 2.0 ppm Se as sodium selenite for 10 wk. They were then injected with 0, 0.1, or 10 mg /kg body weight of the pro-oxidant carcinogen N-nitrosodiethylamine. High levels of carcinogen and high levels of selenite intake each increased concentration of 8-hydroxy-2'-deoxyguanosine in liver DNA. Se-dependent glutathione peroxidase I gene expression and enzyme activity were dramatically reduced by dietary Se deficiency but were unaffected by carcinogen administration. There were no significant main or interactive effects of Se or carcinogen on activity or gene expression of the DNA repair enzyme 8-oxoguanine glycosylase I. These results do not support the hypothesis that high Se intake may be cancer-preventive by inhibiting oxidative DNA damage. Rather than inhibiting oxidative DNA damage, these findings suggest that high dietary intake of inorganic Se may promote in vivo DNA oxidation.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1998

Selenium and liver cirrhosis.

Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.

Animals↗
PubMed2006

Selenium in critical illness.

PURPOSE OF REVIEW: Selenium is a trace element essential to human health. Critical illness is associated with the generation of oxygen free radicals resulting in a condition of oxidative stress. Supplementing critically ill patients with antioxidant nutrients may improve survival. Selenium levels can be low due to redistribution to high-priority organs and dilution associated with aggressive resuscitation of the patient. The purpose of this review is to investigate the benefit of selenium supplementation in critically ill patients. RECENT FINDINGS: Most of the selenium-supplementation trials were performed in relatively small patient populations presenting with trauma, sepsis, burns and adult respiratory distress syndrome. Widely varying doses of selenium of between 200 and 1000 microg were used, either alone or in combination with other antioxidants. Significant improvements have been demonstrated in length of hospital stay, rate of infection and need for haemodialysis in these patients. However, no trial has demonstrated a statistically significant improvement in mortality. Two recent meta-analyses suggest a trend towards reduced mortality with selenium supplementation. SUMMARY: Selenium, by supporting antioxidant function, may be associated with a reduction in mortality. To demonstrate this large, well-designed randomized trials are required.

Antioxidants↗
PubMed1981

Oxidative degradation of 6-selenoguanosine in aqueous solutions.

The degradation of 6-selenoguanosine (NSC 137679) (I) in water and in various buffer systems was investigated. Drug degradation in aqueous media was monitored by high-pressure of I in various chromatography. Some kinetic aspects of the degradation of I in various buffer systems at 25 degrees also were studied spectrophotometrically. The degradation, which requires oxygen, involves autoxidation of I to the corresponding diselenide, which produces a selenide and metallic selenium in the presence of oxygen. This degradation pathway differs from that reported fro the oxidation of related thio compounds.

Chemistry, Pharmaceutical↗
PubMed1989

[Correction of selenium deficiency in patients with renal failure undergoing hemodialysis].

Plasma selenium levels (p Se) as well as glutathione peroxidase activity in plasma (p GPx) and in erythrocytes (e GPx) were measured in 39 haemodialysis patients. Glutathione peroxidase is a selenium-dependent enzyme which protects cells against oxidation. The mean level values obtained were significantly lower in patients than in controls: p Se: 38 +/- 14 versus 88 +/- 17 micrograms/l; p GPx: 15 +/- 32 versus 334 +/- 41 IU/l; e GPx: 19 +/- 4 versus 26 +/- 4 IU/g Hb. These values were found to correlate significantly with the duration of dialysis and with the type of membrane utilized. The total muscular mass was significantly smaller in patients with the lowest p Se or p GPx values. At echocardiography, septal hypertrophy correlated with both p Se and p GPx. Twenty patients were supplemented with sodium selenite administered orally at the end of each haemodialysis session during 6 months. After this period, muscular mass and septal hypertrophy were decreased and the echocardiographic contractility parameters were improved, albeit not significantly.

Adult↗
PubMed2002

The investigation of prooxidant-antioxidant balance in serum of children with family histories of essential hypertension.

It has been accepted that essential hypertension is associated with a loss of the balance between prooxidation and antioxidation. Thus, excessive oxygen free radical production may be an early event in the pathogenesis of hypertension. To compare lipid peroxidation and antioxidant system in serum of children of essential hypertensive and normotensive parents. Serum malondialdehyde (MDA) levels were measured spectrofluorometrically. Antioxidant activity, glutathione peroxidase, selenium levels in serum were measured as indices of antioxidant power. The peroxidation of apo B containing lipoproteins (VLDL+LDL) was measured as the susceptibility to oxidation in vitro. Serum MDA levels increased, but no marked differences in total antioxidant activity, glutathione peroxidase activity, selenium levels and VLDL+LDL oxidation were found in serum of children with family histories of essential hypertension as compared to children of normotensive parents.

Adolescent↗
PubMed1997

[Selenium, antioxidant status and radical/reactive oxygen species in medicine].

BACKGROUND: In all organisms with a metabolism of oxygen, radicals/reactive oxygen species appear. Normally a balance exists between formation and destruction of radicals. Many diseases show a disturbance of this balance with the destruction of biological structures. Results in patients with sepsis, terminal renal failure, bone marrow transplantation and cancer are given. CONCLUSION: To avoid a possible pro-oxidative effect (vitamins C and E) and intoxications (selenium), before substitution a monitoring is necessary.

Antioxidants↗
PubMed2000

Host nutritional status and its effect on a viral pathogen.

The nutritional status of the host has long been associated with both severity and susceptibility to infectious disease. The accepted model system proposes that inadequate nutrition impairs the functioning of the immune system, thus resulting in increased susceptibility to infection. However, current work suggests that not only can the nutritional status of the host affect the immune response, but it can also affect the viral pathogen. In a mouse model, a benign strain of coxsackievirus B3 became virulent and caused myocarditis in selenium- and vitamin E-deficient mice. This change in pathogenicity was due to mutations in the viral genome, which changed an avirulent virus into a virulent one. Once these mutations occurred, even mice with normal nutriture developed disease from the mutated virus. These results suggest that the oxidative stress status of the host can have a profound influence on a viral pathogen.

Animals↗
PubMedDate not supplied

[Selenium: the biological role and antioxidant activity].

Selenium is essential trace element, sulphur analogue with high chemical activity, component of some selenoproteins and enzymes: glutathione peroxidase and other peroxidases, blood and tissue proteins. As to their biological action mechanism selenium and its compounds are antioxidants. Selenium is active immunomodulator, much more potent anti-oxidant than vitamins E, C and A, beta-carotene, but much more toxic. It takes part in thyroxine conversion to triiodethyronine in thyroid hormone biosynthesis. As sperm antioxidant selenium protected its motility and fertility. Selenium is a serious factor of biological and antioxidant protection of vascular endothelium, of low-density lipoproteins, protection of DNA, chromosomes. As food component selenium is an exceptional agent of protection from atherosclerosis, coronary ischemic disease and cancer. Some hydrobionts, liver, kidney, meal, corn and garlic, onion, cabbage, broccoli are dietary products with high content of selenium.

Animals↗
PubMed2004

Oxidant and antioxidant levels in preterm newborns with idiopathic hyperbilirubinaemia.

OBJECTIVES: Newborns, particularly preterm infants, have limited antioxidant protective capacity. The organism's defence system against reactive oxygen species including vitamins A, E and C, trace element selenium (Se) and enzymes, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) are essential components of the antioxidant system against the oxidative injury to the cellular membranes of erythrocytes. In this study, our aim was to compare the oxidant nitric oxide (total plasma nitrite level as an indicator of nitric oxide (NO)), antioxidant vitamins and selenium and erythrocyte antioxidant enzymes in premature babies with hyperbilirubinaemia with healthy preterms. METHODS: Twenty preterm infants with newborn jaundice were included in the study group, while 15 preterm infants without jaundice were enrolled in the control group. We evaluated the mean plasma levels of, respectively, the total nitrite as an indicator of NO, bilirubin, vitamins A, E, C and selenium, and the activity of erythrocyte antioxidant enzymes such as CAT, SOD and GSH-Px of preterm infants with idiopathic hyperbilirubinaemia and compared to those of the control group. RESULTS: The mean plasma total nitrite and total serum bilirubin levels and blood reticulocyte counts of the study group were found to be significantly higher than those of the control group (P < 0.001, P < 0.001 and P < 0.05, respectively). Furthermore, the activity of erythrocyte antioxidant enzymes (all P < 0.001) and the mean plasma levels of the antioxidant vitamins A, E, and C (P < 0.05, P < 0.05 and P < 0.001, respectively) and selenium (P < 0.001) of the study group were all found to be significantly lower than those of the control group. CONCLUSION: We hypothesize that low antioxidants in pretem babies may predispose them to increased oxidative stress, and cause hyperbilirubinaemia.

Antioxidants↗
PubMed1987

The effects of humic acid on the chemical and biological properties of selenium in the environment.

To shed light on the causes of Kaschin-Beck disease, which can be prevented by supplementation of the diet with sodium selenite, the interactions between inorganic selenium compounds (selenite and selenate) and humic/fulvic acid were investigated. Selenate was found to be slowly reduced to selenite by humic acid in acidic solution. Selenite was adsorbed on manganese dioxide and iron(III) oxide from solution to a much greater degree than on kaolin, humic acid, Yongshu soil, or silicon dioxide. Feeding mice a diet supplemented with sodium selenite increased the selenium concentration in the kidney, liver, spleen, lung, heart and blood. A diet containing sodium selenite and fulvic acid caused the selenium concentrations in the organs, with the exception of the spleen, to be lower than observed with the selenite-only diet. Selenium and fulvic acid increase the activity of glutathione peroxidase. Sodium selenite and fulvic acid injected in combination into the abdominal cavity of mice and rats were less toxic than either substance alone. Selenite and fulvic acid applied separately enhanced the luminosity of photobacterium phosphoreum T-3 at low concentrations but depressed the luminosity at higher concentrations. Selenite and fulvic acid in combination caused a larger enhancement and a smaller depression of the luminosity than observed with either substance alone. The hypothesis is formulated that Kaschin-Beck disease is caused by selenium levels insufficient to prevent the toxic effects of the organic compounds present in the drinking water of the regions in which the disease is endemic.

Animals↗
PubMed1976

Influence of dietary peroxides, selenium and vitamin E on glutathione peroxidase of the gastrointestinal tract.

The influence of dietary peroxides, vitamin E and selenium on glutathione peroxidase (GSH-Px) activity in the gastrointestinal tract of the rat was investigated. Feeding 7% oxidized stripped corn oid (peroxide value 1,000) in a diet adequate in selenium and vitamin E increased the specific activity of GSH-Px in the stomach mucosa. Feeding oxidized oil produced an increase in the wet weight of the intestinal mucosa which was associated with a decrease in the specific activity of the enzyme. Total GSH-Px activity in the intestinal mucosa was unchanged or moderately increased. These changes were unaffected by the presence of vitamin E in the diet. Dietary peroxides had no effect on GSH-Px activity in the plasma or in the perirenal and paraepididymal adipose tissues. Subacute vitamin E deficiency had no consistent effect on the activity of the enzyme in several tissues examined. In rats fed a Se deficient diet glutathione peroxidase activity decreased markedly in most tissues but only slightly in the intestinal mucosa. The moderate decrease in the intestine may be explained by the accessibility of residual dietary Se to the mucosal cells. The role of Se in the detoxification of peroxides in foods and the response of gastrointestinal GSH-Px to dietary peroxides are discussed.

Adipose Tissue↗