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PubMed2003

A complex of antioxidant vitamins effectively inhibits free-radical oxidation of LDL phospholipids in blood plasma and membrane structures of the liver and myocardium.

Antioxidant effect of a complex preparation including antioxidant vitamins C, E, provitamin A and selenium was studied on the model of Cu(2+)-initiated free-radical oxidation of LDL isolated from human blood plasma. The antioxidant effect of combined administration of alpha-tocopherol+ascorbic acid and alpha-tocopherol+beta-carotene is far more pronounced that the antioxidant effect of individual components of these cocktails. Moreover, in the model system the combined action of all antioxidant components completely inhibited free-radical oxidation of LDL. A 30-day course of peroral administration of antioxidant vitamin cocktail and selenium to rats pronouncedly enhanced the antioxidant potential of liver and completely suppressed free-radical processes in the myocardium. It is suggested that preparations containing antioxidant vitamins and selenium can be perspective for prevention and complex therapy of atherosclerosis.

Animals↗
PubMed1991

Cigarette smoking-nutritional implications.

Although the effects of cigarette smoking on a variety of diseases, from cancer through emphysema and cardiovascular illness are well documented, direct effects on the levels of macro- and micronutrients in the body are reported less frequently. In fact, imbalances in these nutrients may have a role in many of the pathological conditions attributed to smoking. Tobacco smoke contains numerous compounds emitted as gases and condensed tar particles, many of them being oxidants and prooxidants, capable of producing free radicals thus enhancing lipid peroxidation in biological membranes. Vitamin E, vitamin C, B-carotene and selenium are involved in the overall cellular anti-oxidant defense against deleterious effects of reactive oxygen species. Smoking has been shown to lower the level of vitamin C and B-carotene in plasma. Cadmium, naturally found in tobacco, decreases the bioavailability of selenium and acts antagonistically to zinc, a cofactor for the antioxidant enzyme, superoxide dismutase. Vitamin E, the principle lipid-soluble antioxidant, may be at suboptimal levels in tissues of smokers. In addition, tobacco constituents have been shown to reduce levels of several vitamins of the B-complex. Nutritional status in smokers may be further compromised by an inadequate diet. Data from the Second National Health and Nutrition Examination Survey indicates that smokers are less likely to consume fruits and vegetables, particularly those high in vitamin C and carotenes. Cessation of smoking is the obvious solution to ending cigarette-related problems. In the world as it is, however, the medical community should be responsible for making recommendations to lower the risk in smokers to tobacco related diseases. Nutritionists could have a role in this process. There exists a lively debate as to where levels of nutrients should be set. Additional vitamin C has already been recommended for smokers. Should other antioxidants also be increased? Arguments for the against are considered.

Disease↗
PubMed1983

Interactions between selenium and mercury in mice: marked retention in the lung after inhalation of metallic mercury.

The distribution of 203Hg after inhalation of radioactive metallic mercury (4.3 mumol 203Hg0/kg body wt. for 1 h) was studied in saline (control) and selenite (10 mumol/kg body wt. intraperitoneally, i.p.) pretreated male C57BL mice by means of whole-body autoradiography and scintillation counting. Selenite pretreatment did not apparently change the immediate uptake and distribution of 203Hg (presumably inorganic Hg after oxidation in the different organs) but markedly increased the retention time in the whole body. The most marked retention was seen in the lungs where the selenite-pretreated animals had 200 times higher concentration as compared to control animals 14 days after inhalation. In other organs the corresponding value ranged between 1 (brain) and 12 (spleen). Selenite-pretreated and control animals showed the same low rate of exhalation of 203Hg after the inhalation period, while the latter animals eliminated significantly more through the urine and faeces (measured only during the first 24 h). When inversely radioactive selenite (75Se-selenite) was injected i.v. into animals 1 h earlier exposed to non-radioactive Hg0 (by inhalation), the lung concentration of 75Se after 24 h was 4 times higher than that of control animals. When radioactive mercury was injected i.v. in the form of 203HgCl2 (4.3 mumol/kg body wt.), selenite (10 mumol/kg body wt., i.p.) increased the retention time in the body, more so than after 203Hg0 inhalation. In this case the mercury was retained especially in the serum, red pulp of the spleen and liver (reticulo-endothelial system). 75Se-selenite injected i.v. after i.p. administration of non-radioactive HgCl2 in the same doses as above similarly accumulated more in serum, spleen and liver as compared to control animals. It is presumed that while injected selenite and inorganic mercury (Hg2+) interact strongly in the serum, increasing each other's uptake and retention especially in the reticulo-endothelial system, inorganic mercury retained in various organs after oxidation of Hg0 upon inhalation interacts with selenium mainly intracellularly. This occurs especially in the lungs, where initially high concentrations of mercury are found after inhalation.

Animals↗
PubMed2000

Scavengers for peroxynitrite: inhibition of tyrosine nitration and oxidation with tryptamine derivatives, alpha-lipoic acid and synthetic compounds.

The inhibitory effects of various endogenous and synthetic compounds on the nitration and oxidation of L-tyrosine by peroxynitrite were examined. Nitrating and oxidizing activities were monitored by the formation of 3-nitrotyrosine and dityrosine with a HPLC-UV-fluorescence detector system, respectively. Glutathione, serotonin and synthetic sulfur- and selenium-containing compounds inhibited both the nitration and oxidation reaction of L-tyrosine effectively. However, 5-methoxytryptamine, melatonin and alpha-lipoic acid only inhibited the nitration reaction, and enhanced the formation of an oxidation product. This is important evidence that there are different intermediates in the nitrating and oxidizing reactions of L-tyrosine by peroxynitrite. It was suggested that 5-methoxytryptamine, melatonin and alpha-lipoic acid reacted only with the nitrating intermediate of peroxynitrite and inhibited nitration of L-tyrosine. Actually, the DNA strand breakage, which is believed to be a typical reaction of hydroxyl radical-like species, caused by peroxynitrite was not effectively inhibited by 5-methoxytryptamine. 5-Methoxytryptamine, melatonin and alpha-lipoic acid were viewed as useful reagents for investigating the mechanisms of damage by peroxynitrite in vitro.

Antioxidants↗
PubMed2002

Selenium-based pharmacological agents: an update.

The biochemistry and pharmacology of selenium is a subject of intense current interest, particularly from the viewpoint of public health. Selenium, long recognised as a dietary antioxidant, is now known to be an essential component of the active sites of several enzymes, including glutathione peroxidase and thioredoxin reductase, which catalyse reactions essential to the protection of cellular components against oxidative and free radical damage. A low concentration of selenium in plasma has been identified as a risk factor for several diseases, including cancer, cardiovascular disease, osteoarthritis and AIDS, and several large-scale selenium supplementation human trials are now underway. Evidence is emerging that, at least in the case of cancer, the antitumorigenic effect of selenium supplementation arises at least in part from enhanced production of specific selenium-containing metabolites, not just from maximal expression of selenoenzymes. Therefore a number of novel pharmaceutical agents which are selenium-based or which target specific aspects of selenium metabolism are under development. Among these are orally-active antihypertensive agents, anticancer, antiviral, immunosuppressive and antimicrobial agents, and organoselenium compounds which reduce oxidative tissue damage and edema. It can be anticipated that as our understanding of the basic biology and biochemistry of selenium increases, the coming years will bring further development of new selenium-based pharmaceutical agents with therapeutic potential toward a variety of human diseases.

Animals↗
PubMed1996

Attenuation of oxidation and nitration reactions of peroxynitrite by selenomethionine, selenocystine and ebselen.

The effect of the selenium-containing compounds selenomethionine, selenocystine and ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one] on the oxidation of dihydrorhodamine 123 caused by peroxynitrite and on the nitration of 4-hydroxyphenylacetate by peroxynitrite was studied in comparison with their sulphur analogues methionine, cystine and ebsulfur [2-phenyl-1,2-benzisothiazol-3(2H)-one]. The selenocompounds protected dihydrorhodamine 123 from oxidation and 4-hydroxyphenylacetate from nitration more effectively than their sulphur analogues. Sodium selenite exhibited no effect. These observations are corollaries to the recent finding [Roussyn, Briviba, Masumoto and Sies (1996) Arch. Biochem. Biophys. 330, 216-218] that selenium-containing compounds are efficient in protecting against peroxynitrite-induced DNA single-strand breaks.

Azoles↗
PubMed2000

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

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

Animals↗
PubMed1993

Contribution to the pathobiochemistry of furazolidone-induced oxidative toxicity in chickens.

Furazolidone (F) and its 5-nitrofuran derivatives, occasionally used in veterinary and human medicine, are active against some microorganisms. This drug is considered to be mutagenic in special bacterial test systems. For public health reasons, the presence of F and other 5-nitrofuran residues in edible mammalian and poultry tissues is strictly prohibited. One-month-old experimental chickens (n = 2 x 25) were fed 300 mg.kg-1 furazolidone for 3 days. A separate subgroup (n = 11) was used for monitoring the kinetics of F in the blood plasma. Liver, lung and blood plasma samples taken from the experimental and control chickens after treatment were tested for glutathione-peroxidase (GSH-Px), glutathione reductase (GSH-R), catalase (CAT), superoxide dismutase (SOD) activities, reduced and oxidized glutathione (GSH and GSSG), malondialdehyde (MDA), alpha-tocopherol (vE), selenium (Se) and F concentrations. On post-treatment day 2, SOD activity was significantly lowered in the liver only. GSH-Px did not show any characteristic change in any of the tissues. CAT and GSH-R activities were significantly reduced in both organs until post-treatment day 5. At the same time, a significant decrease of GSH accompanied by an increase in GSSG concentration, was found in both tissues. Oral F treatment produced a transient increase in lipid peroxidation levels measured by the formation of MDA. Alpha-tocopherol content significantly decreased in both organs by post-treatment day 2. Se concentrations showed an insignificant rate of decrease. F concentration in the blood plasma reached its peak already 30 min after treatment. In the liver and lungs, F decreased sharply, reaching the detection limit between days 2-5 after treatment. Furazolidone administered per os was found to alter the in vivo antioxidative enzymatic defense mechanisms. Increased lipid peroxidation and the concomitant oxidative stress may affect the functional integrity of the tissues.

Animals↗
PubMed1996

Selenite incubated with NADPH and mammalian thioredoxin reductase yields selenide, which inhibits lipoxygenase and changes the electron spin resonance spectrum of the active site iron.

Selenite and selenodiglutathione (GS-Se-SG) efficiently inhibited 5-lipoxygenase activity in sonicates of human monoclonal B-lymphocytes. The apparent IC50 of GS-Se-SG was 0.5 microM. The inhibitory effect of these compounds was observed within 10 min of incubation. In order to elucidate if the mechanism of inhibition by these compounds was result of direct interference with lipoxygenase or indirectly mediated by cellular factors, pure 15-lipoxygenase from soybeans was used as a model system for enzyme assays and electron spin resonance (ESR) measurements. Incubation of 15-lipoxygenase with a mixture of human placenta thioredoxin reductase (TR) or calf-thymus TR, selenite, and NADPH blocked the activity of the enzyme. Neither TR and NADPH nor selenite inhibited soybean lipoxygenase when incubated separately. These results suggest that selenite must be reduced to selenide in order to inhibit 5- and 15-lipoxygenase activities. Preincubation anaerobically of 15-lipoxygenase with chemically generated selenide (6 microM) resulted in a strong inhibition of activity, in assays with arachidonic acid in the presence of oxygen. In contrast, selenide exposed to air prior to preincubation did not inhibit the enzyme. Since selenide is known to be efficiently oxidized by oxygen and to form elemental selenium the results evidence that selenide was the inhibitor of lipoxygenase activity in the anaerobic preincubations. After incubation with TR, NADPH, and selenite or with chemically generated selenide, the ESR spectrum of 15-lipoxygenase changed: the dominant axial component with a peak at g = 6.1 decreased, and a rhombic form with a feature at g = 4.28 grew. The results suggest that selenide produced by the reduction of selenite reduces the active site iron to the ESR invisible state and changes the ligation geometry of the oxidized form.

Arachidonate 15-Lipoxygenase↗
PubMed1998

Effects of mild chronic heat exposure on the concentrations of thiobarbituric acid reactive substances, glutathione, and selenium, and glutathione peroxidase activity in the mouse liver.

To determine whether mild and chronic heat stress leads to oxidative stress and to differentiate such effects of different exposure periods, we kept male ICR-mice at an ambient temperature of either 35 degrees C or 25 degrees C for 6 hours, 3 days, or 7 days and measured the concentrations of thiobarbituric acid reactive substances (TBARS), glutathione (GSH), selenium (Se), and glutathione peroxidase (GSH-Px) activities in the liver. Since the food consumption of the heat-exposed group was only half that of the control, we prepared pair-fed groups, which were kept at 25 degrees C and whose food consumption were limited to those of the heat-exposed group for the 3-day and the 7-day exposure. TBARS concentrations of the liver was significantly higher in the heat group than the control after the 3-day exposure, while there was no significant difference among the groups after the 7-day exposure. There was no significant difference in GSH concentrations between the heat-exposed group and the control after the 7-day exposure, when the GSH concentration of the pair-fed group was significantly lower than that of the control. Hepatic cytosolic Se GSH-Px activity in the heat group was significantly less than that in the control group after the 6-hour exposure and it tended to be lower in the heat group than that of the control group after the 7-day exposure, while there was no difference in the total GSH-Px activity among the three groups. Our results showed that mild and chronic heat exposure may cause oxidative damage to organisms and that GSH-related anti-oxidative systems would play an important role to defensive reaction.

Animals↗
PubMed1995

Atherogenic and anti-atherogenic factors in the human diet.

New atherosclerosis causative factors and preventive modalities have been identified. Atherogenic factors include lipid oxidation products, such as cholesterol oxidation products, malonaldehyde and other aldehydes; trans-fatty acids; some saturated fatty acids (lauric, myristic and possibly palmitic acids); and myristic acid plus cholesterol. Lipid oxidation products are well suited to induce arterial damage, based on their known cytotoxic effects; evidence also indicates the possibility of plaque promotion and stimulation of thrombogenesis. Anti-atherogenic factors include antioxidants, fish oils and other polyunsaturates (if protected from oxidation), fibre and trace minerals such as copper, manganese, selenium and zinc. Iron is unique, being considered as both a potential promoter of atherosclerosis (component of ferritin, conceivably inducing lipid oxidation) and a possible anti-atherogenic component (of antioxidant enzyme catalase). It is apparent that an entire new series of research challenges has been uncovered.

Antioxidants↗
PubMed2004

[Advanced glycation end products accelerate atherosclerosis via enhancement of oxidative stress].

OBJECTIVE: To investigate the effect of advanced glycation end products (AGE) on atheromatous plaque formation and its possible mechanisms. METHODS: Fifty rabbits were randomly divided into five groups of 10 rabbits: group A, fed with hypercholesterolemic diet and injected intravenously with AGE modified rabbit serum albumin (AGE-RSA); group B, fed with hypercholesterolemic diet and injected with unmodified RSA; group C, fed with hypercholesterolemic diet; group D, fed with normal diet alone: and group E, fed with normal diet and injected with AGE-RSA. Ten weeks after the rabbits were killed. Their aortas were taken out and stained with Sudan red IV. The extent of atheromatous plaques in the aortas en face was evaluated by computer-assisted morphometry and by histologic examination. Photoshop system was used to measure the percentage of atheromatous plaques in the area of tunica intima. The depositions of AGE, malondialdehyde modified low-density lipoprotein (MDA-LDL), oxidized low-density lipoprotein (ox-LDL) and expression of receptor of AGE (RAGE) in aortic tissue were detected by using immunohistological staining. The circulating AGE, blood lipids, serum selenium glutathione peroxydase (SeGSHPx) activity, malonyldialdehyde (MDA), and oxidized LDL (ox-LDL) were detected before the experiment and after the rabbits were killed. RESULTS: (1) The relative plaque area was significantly increased in group A (50% +/- 8%) compared with in group B (21% +/- 7%) and group C (29% +/- 6%). No plaque could be found in animals fed with normal diet (group D) even in those receiving repeated injections of AGE-RSA (group E). Depositions of ox-LDL, MDA-LDL and AGE in atherosclerotic lesions increased and RAGE expression were upregulated in the rabbits fed with hypercholesterolemic diet and injected with AGE-RSA (group A) compared with the other four groups. (2) All hypercholesterolemic rabbits showed comparable serum levels of triglyceride and cholesterol. However, the serum levels of AGE, ox-LDL and MDA were significantly higher and the serum level of SeGSHPx was relatively lower in group A compared with those in the other four groups. (3) The serum level of AGE was directly correlated with the serum ox-LDL (r = 0.459, P < 0.01) or serum MDA concentration (r = 0.423, P < 0.05), and inversely correlated with the serum level of SeGSHPx (r = - 0.448, P < 0.01). A close correlation was found between the serum level of AGE and endothelium RAGE expression (r = 0.384, P < 0.05) and deposition area of AGE (r = 0.468, P < 0.05) in aorta. CONCLUSION: AGE accelerates the atheromatous plaque formation through induction of oxidative stress and upregulation of RAGE.

Animals↗
PubMed1991

Role of selenium-dependent glutathione peroxidase in protecting against t-butyl hydroperoxide-induced damage in hepatocytes.

The role of the selenoenzyme glutathione peroxidase (Se-GSHPx) in protecting against oxidative injury was studied in hepatocytes isolated from rats fed either a low-selenium (Se-) or a selenium-adequate (Se+, control) diet. In rats fed Se- diet for eight weeks the selenium content of plasma and liver was lowered to 15 and 8%, respectively. No Se-GSHPx and only 5% of total GSHPx activity was detected in Se- hepatocytes. However, the Se- hepatocytes were as resistant as the Se+ cells to oxidative injury by 0.8 mM tert-butyl hydroperoxide (t-BuOOH), or 0.2 mM t-BuOOH plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), an inhibitor of oxidized glutathione (GSSG) reductase. Only at 1.5 mM t-BuOOH or at 0.5 mM t-BuOOH with BCNU were cell damage and lipid peroxidation more evident in Se- cells. At all t-BuOOH concentrations used the depletion of cellular glutathione (GSH) was similar in magnitude in Se- and Se+ cells, but Se+ cells released more glutathione (mainly GSSG), obviously due to their higher Se-GSHPx activity. These results suggest that hepatocytes devoid of Se-GSHPx activity maintain a high capacity to resist peroxidative attack, either via residual (non-Se)GSHPx activity or other compensatory GSH-associated detoxication mechanisms.

Animals↗
PubMed2004

Comparative in vitro uptake of zinc by erythrocytes of normal vs Type 2 diabetic individuals and the associated factors.

Diabetes is an oxidative stress-related disorder in which erythrocyte zinc uptake may vary as compared to healthy individuals. Since zinc is one of the important antioxidant trace metals, some functional indices of erythrocyte zinc status, ie in vitro zinc uptake, osmotic fragility and glucose uptake, were compared in Type 2 diabetic subjects (n=43) and healthy controls (n=22). The associations of these indices with plasma levels of antioxidants and micronutrients were examined. The trace metals were analyzed by atomic absorption spectrophotometer. Vitamins were estimated using spectrophotometric and spectroflourometric methods. In vitro zinc uptakes of healthy subjects were 17 to 52% higher (p<0.01) than those for diabetic subjects. The osmotic fragility for diabetic cells was 2.2 to 1.5 times higher than the healthy cells in 0.85-0.5% NaCl solutions (p<0.05). Percent hemolysis at 0.75, 0.65 and 0.55% NaCl had significant negative correlations (p<0.05) with in vitro zinc uptakes and that at 0.50% NaCl had a positive correlation with HbA1c levels (p<0.05). The in vitro zinc uptakes of erythrocytes in healthy subjects showed a strong negative correlation (p<0.01) with percent hemolysis at 0.75, 0.65 and 0.55% NaCl, a positive correlation with plasma zinc (r=0.33, p<0.05) and a strong negative correlation with plasma selenium and iron, hemoglobin and serum ceruloplasmin indicating antagonistic behavior of copper, iron and selenium with zinc uptake (p<0.01). Furthermore, erythrocyte super oxide dismutase (SOD), plasma ascorbic acid and status of riboflavin and thiamine were negatively correlated with in vitro zinc uptakes of erythrocytes in healthy subjects (p<0.01). These associations in the diabetic subjects were weaker than normal. Erythrocyte zinc uptake and osmotic fragility could be biomarkers of long-term zinc status and decrease of zinc uptake may be one of the features of diabetic patients.

Adult↗
PubMed1998

[Selenium status and bronchopulmonary dysplasia in premature infants <1,500 g].

Selenium is an essential component of the antioxidant enzyme glutathione peroxidase that protects tissues against oxidative injury by detoxifying peroxides. In preterm infants the risk for selenium deficiency is increased due to insufficient selenium uptake. Low selenium uptake and as a consequence decreased glutathione peroxidase activity may result in an elevated risk for the development of bronchopulmonary dysplasia (BPD). The aim of this prospective study was to investigate the relationship between the selenium status of preterm infants < 1500 g and the incidence of BPD. We determined the selenium plasma levels by means of atomic absorption spectrometry in 34 VLBW infants (mean birth weight 1075 +/- 249 g; mean gestational age 28.6 +/- 2.5 weeks) within the first 5 days of life and later in the age of 4 weeks. The infants received mainly parenteral nutrition and were not specifically supplied with selenium. Postnatally, the selenium plasma level was 34.2 micrograms/l (17.3/50) [median (25/75% quantil)] and dropped after 4 weeks to a median value of 16.1 micrograms/l (5.2/38.4) (p < 0.001). In the infants with BPD (n = 12) the selenium concentration within the first week of life was 45.0 micrograms/l (31.5/55.6) versus 33.2 micrograms/l (20.2/42.4) in the infants without BPD. In the age of 4 weeks of life the median selenium level was not significantly different between the infants with and without BPD - 17.2 micrograms/l (10.3/22.5) versus 14.8 micrograms/l (8.8/22.6).

Bronchopulmonary Dysplasia↗
PubMed2004

Blood oxidative stress status in patients with macrophagic myofasciitis.

The study aimed at determining the presence of an oxidative stress in patients with macrophagic myofasciitis (MMF), a new inflammatory myopathy with suspected toxic etiology related to aluminium hydroxide-containing vaccines. A total of 30 MMF patients (nine males, 21 females; aged 42+/-14 years), whose diagnosis was confirmed by deltoid biopsy, have been included and compared to 38 sex- and age-matched healthy control subjects (10 males, 28 females; aged 43+/-8 years). The blood oxidative stress status has been evaluated by assaying six parameters: plasma lipid peroxidation products (thiobarbituric acid-reactive substances: TBARS) and antioxidant defense systems: plasma vitamin E and glutathione peroxidase (GSH-Px) activity, erythrocyte GSH-Px and Cu,Zn-superoxide dismutase (SOD) activities. Plasma selenium was also determined as a trace element essential to the activity of GSH-Px. Statistical significance was evaluated by the Mann-Whitney test. Plasma GSH-Px activity, selenium and vitamin E concentration were significantly lower in MMF group than in controls (P=0.004, P=0.003 and P=0.009, respectively), with a positive correlation in MMF patients between plasma GSH-Px activity and selenium concentration (rho=0.0001). The other parameters of oxidative stress did not significantly differ between both groups. A macrophage activation could occur in MMF, consequently to chronic stimulation by aluminium-containing vaccines, and could participate to the lower values of selenium and vitamin E observed in comparison with controls. Nevertheless, since no deficiency in these elements has been observed, no supplementation is to be considered.

Adult↗
PubMed1980

Interactions of vitamin E and selenium with mercury and silver.

It is well established that the toxicity of silver and methylmercury is suppressed by the presence of low levels of vitamin E or selenium in the diet, but little is known of the mechanisms involved. Silver induces a conditioned deficiency of selenium in rats, as shown by its effects on tissue levels of selenium and glutathione peroxidase (a selenoprotein), but methylmercury does not. Supplements of selenium do not decrease mercury levels in tissues of animals given methylmercury, and animals given selenium plus methylmercury may accumulate high levels of mercury without signs of toxicity. Although an equimolar accumulation of selenium and mercury in tissues sometimes occurs and could lead to mutual detoxification, such a coaccumulation is not always linked to protection. The only known functions of vitamin E and selenium are related to the prevention of oxidative damage. It is possible that their protective effects against heavy metals may involve such functions, thus accounting for the protection afforded by low levels of the nutrients against high levels of the metal toxicants.

Animals↗