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PubMed1978

Interaction between cadmium and selenium in rat plasma.

The metabolism of (75)Se-labeled SeO(3) (2-) and its conversion by intact rat erythrocytes in vitro to a form which complexes with Cd and plasma proteins were studied. By utilizing both excess SeO(3) (2-) and N-ethylmaleimide to lower erythrocyte reduced glutathione (GSH) concentrations, it was shown that the uptake and metabolism of SeO(3) (2-) were GSH-dependent, the probable intermediate being glutathione selenotrisulfide (GSSeSG). Secondary release of selenium by rat erythrocytes had no relation to the erythrocyte transport of oxidized glutathione (GSSG). While fluoride depressed and chromate increased GSSG transport, chromate, a glutathione reductase inhibitor, decreased selenium release. This release appeared to be secondary to a reaction catalyzed by glutathione reductase. The similarity of I(50) values for chromate's inhibition of glutathione reductase and for the inhibition of selenium release further suggested a relationship between these two events. H(2)Se or a similar product of GSSeSG reduction is proposed to be the active product of SeO(3) (2-) metabolism by rat erythrocytes. By use of gel-filtration and ion-exchange methods it was noted that the incubation of H(2)Se with cadmium and plasma produced a Cd-Se complex indistinguishable from that produced by incubation of Cd, SeO(3) (2-), plasma, and erythrocytes in vitro, or that noted following the administration of Cd and SeO(3)in vivo. A mechanism whereby the tissue distribution and toxicity of cadmium are altered by selenium is suggested.

Animals↗
PubMed2005

Damage of zinc fingers in DNA repair proteins, a novel molecular mechanism in carcinogenesis.

Zinc finger motifs participate in protein-nucleic acid and protein-protein interactions in many groups of proteins, including those involved in DNA repair. The Zn(II) ion, bonded tetrahedrally to cysteine thiolates and/or histidine imidazole groups, maintains the three-dimensional structure, crucial for the function of the domain. Zinc fingers can thus be compromised by a substitution of Zn(II) with another metal ion or by a release of Zn(II), due to the oxidation of thiolate donors. The latter may result from an action of redox-active metals or other oxidative agents. Studies in cell cultures and ex vivo demonstrated that soluble compounds of definite carcinogenic metals and metalloids, such as arsenic, cadmium and nickel, and putative carcinogens, including cobalt and lead, inhibit zinc finger containing DNA repair proteins. Further experiments demonstrated that these metals, as well as endogeneous oxidative substances, including hydrogen peroxide, nitrosoglutathione, and reducible selenium compounds damage or distort zinc finger domains. This reactivity can therefore be regarded as a novel molecular mechanism in carcinogenesis.

Animals↗
PubMed1999

Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells.

The mechanisms involved in the anti-carcinogenic activity of selenium remain to be elucidated. In the present study, we examined sodium selenite-induced oxidative stress and apoptosis in a human hepatoma cell line (HepG2). Sodium selenite (10 microM) exerted clear cytotoxic effect, as shown by the significant increase of lactate dehydrogenase leakage. Selenite-induced DNA alterations in apoptosis were studied by: 1. comet assay; 2. TdT-mediated dUTP nick end-labeling assay. In addition, characteristic apoptotic morphological alterations were also observed in selenite-treated cells. Our results clearly show that Se-induced cell death occurs predominantly in the form of apoptosis. Selenite-induced oxidative stress was evaluated by the measurement of reactive oxygen species production using lucigenin-dependent chemiluminescence. The involvement of glutathione in selenite-induced oxidative stress was further demonstrated by the concurrent decline of intracellular reduced glutathione and increase of oxidized glutathione contents in Se-treated cells. Moreover, the finding that selenite-induced oxidative stress and apoptosis was significantly attenuated by superoxide dismutase, catalase and deferoxamine provides additional evidence to suggest that Se-induced oxidative stress mediates the induction of apoptosis, a mechanism related to the anti-carcinogenic and chemopreventive effect of Se.

Apoptosis↗
PubMed1991

In situ bacterial selenate reduction in the agricultural drainage systems of western Nevada.

Dissimilatory in situ selenate reduction to elemental selenium in sediments from irrigated agricultural drainage regions of western Nevada was measured at ambient Se oxyanion concentrations. Selenate reduction was rapid, with turnover rate constants ranging from 0.04 to 1.8 h-1 at total Se concentrations in pore water of 13 to 455 nM. Estimates of removal rates of selenium oxyanions were 14.38, and 155 mumol m-2 day-1 for South Lead Lake, Massie Slough, and Hunter Drain, respectively.

Agriculture↗
PubMed1986

Menadione- (2-methyl-1,4-naphthoquinone-) dependent enzymatic redox cycling and calcium release by mitochondria.

The results presented in this paper reveal the existence of three distinct menadione (2-methyl-1,4-naphthoquinone) reductases in mitochondria: NAD(P)H:(quinone-acceptor) oxidoreductase (D,T-diaphorase), NADPH:(quinone-acceptor) oxidoreductase, and NADH:(quinone-acceptor) oxidoreductase. All three enzymes reduce menadione in a two-electron step directly to the hydroquinone form. NADH-ubiquinone oxidoreductase (NADH dehydrogenase) and NAD(P)H azoreductase do not participate significantly in menadione reduction. In mitochondrial extracts, the menadione-induced NAD(P)H oxidation occurs beyond stoichiometric reduction of the quinone and is accompanied by O2 consumption. Benzoquinone is reduced more rapidly than menadione but does not undergo redox cycling. In intact mitochondria, menadione triggers oxidation of intramitochondrial pyridine nucleotides, cyanide-insensitive O2 consumption, and a transient decrease of delta psi. In the presence of intramitochondrial Ca2+, the menadione-induced oxidation of pyridine nucleotides is accompanied by their hydrolysis, and Ca2+ is released from mitochondria. The menadione-induced Ca2+ release leaves mitochondria intact, provided excessive Ca2+ cycling is prevented. In both selenium-deficient and selenium-adequate mitochondria, menadione is equally effective in inducing oxidation of pyridine nucleotides and Ca2+ release. Thus, menadione-induced Ca2+ release is mediated predominantly by enzymatic two-electron reduction of menadione, and not by H2O2 generated by menadione-dependent redox cycling. Our findings argue against D,T-diaphorase being a control device that prevents quinone-dependent oxygen toxicity in mitochondria.

2,4-Dinitrophenol↗
PubMed1995

[Reactive oxygen species in the pathogenesis of gastrointestinal tumors. A follow-up study].

UNLABELLED: Development and growth of gastrointestinal tumors seems to correlate closely with the formation of reactive oxygen intermediates (ROI). It is known, that oxygen-free-radicals are able to induce a precancerous stage and tumor growth by damaging DNA or changing the protein and lipid structure. To investigate, whether the cellular formation of oxygen-free radicals plays a role in the pathogenesis of colorectal carcinoma, we performed the study presented here. 40 patients with colorectal carcinoma were studied over a period of 6 months (before operation, 10 days after operation, 3 months later, 6 months later). Oxygen-free radicals were determined by chemiluminescence response in the whole blood, in granulocytes and in monocuclear blood cells (MBC). At the same time the trace elements selenium, Copper and Zinc, known to play an important role as antioxidants, were measured. RESULTS: We observed, that the ability of granulocytes for phagocytosis was depleted. However, this effect could be reversed as demonstrated in in vitro stimulation assays. After 6 months the phagocytosis by granulocytes achieved again normal values. Simultaneously a dramatic increase in superoxide-anions generated by mononuclear blood cells was seen. This increase was still obvious after 6 month. Independent of the tumor state selenium deficiency was found in all patients. Since no substitution of selenium was performed after operation, this deficiency was not normalised. CONCLUSION: The ability for phagocytosis and therefore the immune response is reduced in a reversible manner. In addition reactive superoxide-anions, that are able to induce tumors, are formed. This risk is increased in the absence of selenium. Thus, clinical follow-up studies are needed to determine subclinical tumor relapses and to investigate the role of oxidative stress by chemi-luminescence. As consequence of this study selenium substitution seems to be indicated.

Aged↗
PubMed1995

Asthma and oxidant stress: nutritional, environmental, and genetic risk factors.

A considerable body of evidence suggests that oxidant stress results in inflammation and tissue damage in the respiratory system, and later in immune damage, and that individuals with lowered cellular reducing capacity are at increased risk to develop asthma. Reducing capacity in the erythrocyte is generated through the pentose phosphate pathway and this pathway also generates a major portion of the reducing capacity in all cells of the body. Therefore, dietary, environmental, and genetic factors which diminish cellular reducing capacity will increase tissue vulnerability to oxidant stress and are likely to increase asthma risk. Dietary selenium deficiency lowers red cell glutathione peroxidase activity and is associated with an increased risk for asthma, and low dietary intakes of vitamins C and E also appear to increase asthma risk. High body iron stores increase free radical production and may also elevate asthma risk. Environmental lead exposure depresses the activities of a several enzyme systems that influence cellular reducing capacity (glucose-6-phosphate dehydrogenase, NAD synthetase, glutathione peroxidase, superoxide dismutase, catalase) and consequently may increase asthma risk. Genetically-determined low activity of glucose-6-phosphate dehydrogenase lowers cellular reducing capacity and may also heighten asthma risk. Simple dietary and environmental interventions may significantly reduce oxidant stress and prevent or minimize the development of asthmatic symptoms and should prove to be a cost effective approach to asthma management in addition to current pharmacological strategies.

Asthma↗
PubMed2002

Chemoprevention of carcinoma prostate: a review.

PURPOSE: Chemoprevention of prostate cancer is the administration of agents to prevent, inhibit, or delay progression of prostate cancer. Opportunities exist for testing various types of chemopreventive interventsion. MATERIAL AND METHODS: The authors reviewed the relevant articles published in the last twenty years and studied the biology of the prostate cancer. An attempt is made to identify intermediate markers and surrogate endpoint markers. The various interventions and initial clinical trial results are described. End points for evaluation are mainly based on changes in PSA, changes of histological precursors, or time of onset of clinical disease. RESULTS: Nutritional factors such as reduced fat intake, vitamin A, vitamin E, vitamin C, vitamin D, Lycopene and selenium may have a protective effect against prostate cancer. CONCLUSION: Numerous studies implicate dietary and nutritional factors in the onset and progression of prostate cancer. Hence, it is possible that bioactive compounds (anti-oxidants) like vits. A, C, D, E, minerals like selenium and carotenoids like lycopene can be a part of chemopreventive strategies for prostate cancer. Ongoing studies on nutrition and prostate cancer may bring the required evidence to support what is still only a hypothesis at present. However, absolute recommendation will have to await the results of long term prospective clinical trials.

Animals↗
PubMed2000

The effect of selenium and/or vitamin E treatments on radiation-induced intestinal injury in rats.

Cytotoxic effects of ionizing radiation on gastrointestinal epithelium may be related to oxidative stress. In this study, we wanted to investigate the effects of selenium, vitamin E and selenium plus vitamin E pretreatments prior to whole abdominal irradiation on intestinal injury. Irradiation caused increased lipid peroxide and decreased GSH levels in the intestine. Intestinal superoxide dismutase and glutathione peroxidase activities were increased, but glutathione transferase activity decreased following irradiation. Selenium and/or vitamin E pretreatments ameliorated these disturbances in prooxidant-antioxidant balance. This amelioriation has been verified with histopathological findings. These results indicate that antioxidant pretreatments prior to irradiation may have some beneficial effects against irradiation-induced intestinal injury.

Animals↗
PubMed1993

Interaction of adriamycin aglycones with isolated mitochondria. Effect of selenium deficiency.

Adriamycin (AdM) aglycones have dramatic effects on isolated heart mitochondria, oxidizing pyridine nucleotides, modifying sulfhydryl groups, and triggering a permeability transition of the inner membrane that results in free passage of solutes smaller than 1500 Da. In this investigation, the role of glutathione (GSH) peroxidase in these actions of the aglycones was evaluated, by comparing mitochondria from selenium-deficient and selenium-supplemented rats, with the following results. Selenium deficiency was without effect on the permeability transition of heart mitochondria, followed via Ca2+ release and triggered by AdM aglycone or by t-butyl hydroperoxide (TBH) or H2O2, both of which are authentic substrates of the peroxidase. The permeability transition of liver mitochondria was delayed by selenium deficiency regardless of the triggering agent; however, substantial triggering by the aglycone and TBH persisted in mitochondria from selenium-deficient animals. Selenium deficiency inhibited thiol modification elicited by AdM aglycone and H2O2 in heart mitochondria and by the aglycone, TBH, and possibly H2O2 in liver mitochondria. It would thus appear that AdM aglycone, TBH, and H2O2 can induce the permeability transition of isolated heart mitochondria via a process (or processes) distinct from the catalytic activity of the peroxidase. Furthermore, even in liver, where involvement of the peroxidase is observed, mechanisms other than the GSH cycle can contribute to transition induction by the aglycone and by TBH. Finally, mitochondrial-SH group modification by the aglycones appeared not to be causally linked to induction of the permeability transition. This laboratory has suggested that the effects of aglycone metabolites of AdM on mitochondria mediate the cardiotoxicity that limits use of the parent drug. The data presented in this paper argue against the involvement of GSH peroxidase in that process. They are in agreement with in vivo studies, which have generally failed to find evidence for amelioration of AdM cardiotoxicity in selenium-deficient animals.

Animals↗
PubMed1999

[Significance of selenium in intensive care medicine. Clinical studies of patients with SIRS/sepsis syndrome].

Selenium is an essential component of the intracellular antioxidant system as a structural component of the active center of the glutathione peroxidase enzymes. These selenoenzymes play a major role in protecting cells against peroxidation, especially lipid peroxidation and selenium seems to play a direct role in the regulation of inflammatory processes. In conditions of systemic inflammatory response or sepsis, patients are exposed to severe oxidative stress. These patients already have both, a decreased plasma selenium and glutathione peroxidase activity at admission to the ICU as has been shown in several studies. The degree of selenium deficiency is correlated with the severity of disease and the incidence of mortality. The reason for the low plasma selenium levels is unknown. Especially it would be of interest a) if the low plasma selenium is the consequence of the systemic inflammatory response with distribution of selenium in other compartments of the body, b) most important, whether the substitution of selenium might improve the outcome and decrease the mortality rate of these patients. In 2 independently performed intention-to-treat studies including patients with systemic inflammatory response syndrome or sepsis a beneficial effect of selenium supplementation on multiple organ function and outcome could already be demonstrated as well as a tendency of an improved mortality rate. A prospective analytical study clearly could demonstrate the inverse relationship between low plasma selenium and morbidity and mortality of patients with SIRS/sepsis. The results of these studies are so convincing, that we propose a randomized, prospective, double blind multicenter phase-III study including patients with systemic inflammatory response syndrome or sepsis to investigate, whether a high-dose selenium substitution in addition to the recommended treatment strategies for patients with sepsis improves outcome and mortality rate of these patients.

APACHE↗
PubMed2005

Non-invasive monitoring of oxidant stress in alcoholic liver disease.

OBJECTIVE: In alcoholic liver disease (ALD), progression from initial steatosis, through hepatitis to cirrhosis is well described, resulting in 20,000 deaths in the UK annually. However, pathological mechanisms are not well understood and drug trials have led to conflicting results. It has been established that alcohol consumption increases hepatic free radical production and oxidant stress has been implicated in the disease process. MATERIAL AND METHODS: Markers of lipid peroxidation, antioxidant status, hepatic fibrogenesis, inflammation and liver function were measured in blood and urine from 24 patients with established alcoholic cirrhosis and in 49 age- and sex-matched controls. RESULTS: In the ALD group, lipid peroxidation markers 8-isoprostane and malondialdehyde were significantly increased (p<0.001), as was the ratio of oxidized to reduced glutathione (p=0.027). The antioxidants selenium, glutathione (whole blood and plasma) and vitamins A, C and E were all significantly decreased (p<0.001); median plasma glutathione levels were only 19% of control levels. Type III procollagen peptide (PIIINP), a serum marker of hepatic fibrogenesis, and C-reactive protein (CRP) were both increased (p<0.001). Urinary 8-isoprostane correlated positively with PIIINP, CRP and markers of cholestasis (alkaline phosphatase and bilirubin) and negatively with glutathione (whole blood), vitamins A and E and albumin. CONCLUSIONS: Oxidant stress, as reflected in blood and urine by a wide range of pro- and antioxidant markers, is a significant feature of alcoholic cirrhosis, providing a mechanism by which alcohol intake may be linked to hepatic inflammation and fibrosis. Non-invasive markers could prove valuable in monitoring response to treatment during clinical trials.

Adult↗
PubMed2006

Plasma selenium concentration and glutathione peroxidase activity in HIV-1/AIDS infected patients: a correlation with the disease progression.

AIMS AND OBJECTIVES: To find a correlation, if any, between the concentration of plasma selenium and erythrocyte activity in HIV-infected patients with the progression of the disease. MATERIALS AND METHODS: Plasma selenium concentration and erythrocyte glutathione peroxidase (GSH-Px) activity were measured in 62 HIV-1 seropositive patients before commencing antiretroviral drug. Thirty (30) age-matched and apparently healthy HIV-1/11 seronegative subjects were recruited as control subjects. HIV-1 seropositive patients were classified according to the Centre for Disease Control and Prevention (CDC) Criteria. RESULTS: The mean plasma selenium concentrations of 0.53+/-0.06_mol/L and 0.71+/-0.10_mol/L were significantly reduced (P<0.001) in HIV- 1 patients with CD4+ count of <200 lym/mm3 and that of 200-499 lym/mm3 respectively when compared with the controls which is 1.01+/-0.10_mol/L. The mean erythrocyte GSH-Px activity of 15.1+/-2.4 U/g Hb and 20.7+/-3.7U/g Hb of HIV-1 seropositive patients with CD4+ count of <200 lym/mm3 and 200-499 lym/mm3 respectively were significantly reduced (P<0.001) compared with 31.5+/-4.5 U/g Hb for the control. Our results clearly show that there is reduced scavenging antioxidant i.e Selenium and GSH-Px which will lead to oxidative stress in the HIV-1 patients when compared with controls, and decrease significantly with the progression of disease, i.e. AIDS<symptomatics<asymptomatics<controls. HIV-1 subtype variants have no significant influence in both parameters. CONCLUSION: The inclusion of selenium micronutrient which is essential for the activity of erythrocyte GSH-Px as an adjuvant in the management of HIV seropositive patients to prevent additional damage that can be caused by free radicals will be of immense benefit.

Acquired Immunodeficiency Syndrome↗
PubMed1982

Recovery of endogenous selenium from fish tissues by open system dry ashing.

Quantitative recovery of endogenous selenium from fish tissues following dry ashing techniques has not been confirmed. An open system dry ashing procedure, using oxidative fusion with Mg(NO3)2 X 6H2O in the presence of MgO, was tested for recovery of selenium from National Bureau of Standards (NBS) Reference Materials (tuna and oyster) and selected fish tissues. Recovery after dry ashing and hydride analysis was complete from NBS Bovine Liver, Tuna, and Oyster Tissues, as well as from Food and Drug Administration cod, haddock, perch, and flounder research materials. Endogenous selenium, injected into rainbow trout (Salmo gairdneri) as 75Se, was recovered after ashing from liver, ovaries, gastrointestinal tract, muscle, bile, and carcass, 3 and 10 days post-injection. Results indicate that open vessel oxidative fusion is a rapid, simple technique applicable to quantitative recovery of selenium from organoselenium compounds that exist in various aquatic species. The diluted digestate is readily amenable to conventional hydride generation analysis.

Animals↗