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PubMed1982

Selenium bioavailability with reference to human nutrition.

Various aspects of selenium metabolism and nutrition in relation to the question of selenium bioavailability in foods and the diet of man are reviewed. Few published studies exist on selenium metabolism in human subjects, particularly those representative of healthy individuals in the United States. Animal studies reveal that various factors, including the source and chemical form of selenium in foods and feeds, influence selenium bioavailability. However, the quantitative significance of animal assay data for human nutrition is not known. The limited number of published studies in man suggest that the metabolic fate and physiological function of dietary selenite may differ from that of selenomethionine or of food selenium. However, much additional research will be required to establish an adequate picture of the significance of dietary selenium bioavailability in human nutrition and health. Based on initial human experiments carried out at the Massachusetts Institute of Technology, use of stable isotopes of selenium offers promising opportunities for closing the gap of knowledge that now exists concerning the role and significance of factors that determine how the selenium present in foods is used to meet the physiological requirements of the consumer.

Absorption↗
PubMed1983

Endemic selenium intoxication of humans in China.

An endemic disease was discovered in 1961 in parts of the population of Enshi County, Hubei Province of the People's Republic of China. During the years of the highest prevalence, from 1961 to 1964, the morbidity was almost 50% in the 248 inhabitants of the five most heavily affected villages; its cause was determined to be selenium intoxication. The most common sign of the poisoning was loss of hair and nails. In areas of high incidence, lesions of the skin, nervous system, and possibly teeth may have been involved. A case is reported of a middle-aged, female hemiplegic, whose illness and death apparently were related to selenosis. Daily dietary intakes of selenium, estimated after the peak prevalence had subsided, averaged 4.99 (range 3.20 to 6.69) mg and hair and blood selenium levels averaged 32.2 and 3.2 micrograms/ml, respectively. Up to 1000x differences occurred when selenium contents of vegetables, cereals, scalp hair, blood, and urine from the selenosis areas were compared with those from Keshan disease (selenium deficiency) areas. The ultimate environmental source of selenium was a stony coal of very high selenium content (average more than 300 micrograms/g; one sample exceeded 80,000 micrograms/g). Selenium from the coal entered the soil by weathering and was available for uptake by crops because of the traditional use of lime as fertilizer in that region. This particular outbreak of human selenosis was due to a drought that caused failure of the rice crop, forcing the villagers to eat more high-selenium vegetables and maize and fewer protein foods.

Adult↗
PubMed1983

Selenium and acute alcoholism.

Selenium status was investigated in nine inebriated alcoholic subjects by collecting serial samples of blood and urine during hospitalization for alcohol detoxification. The selenium content of various alcoholic beverages and samples of hospital diets was also determined. Mean plasma selenium level and mean urinary excretion of selenium were both significantly lower (p less than 0.01) in alcoholic subjects as compared to the control subjects at the time of admission. Furthermore, the daily dietary intake of selenium before hospitalization was estimated to be below the recommended safe and adequate range in the majority of the alcoholic subjects. The selenium content of various alcoholic beverages was determined to be very low (0.1 to 0.8 microgram/dl). These data suggest that selenium depletion does occur in alcoholic subjects most likely due to poor dietary intake. Selenium depletion in this group of patients is corrected by cessation of ethanol ingestion and adequate dietary intake without additional selenium supplementation.

Adult↗
PubMed1990

Selenium utilization during human lactation by use of stable-isotope tracers.

We examined utilization of selenomethionine (SeMet) and selenite in six lactating (L) and six nonlactating (NL) women, 2-3 mo postpartum, and seven never-pregnant (NP) women by use of stable-isotope tracers. All groups had similar selenium status at the start of the study. Significantly more selenium from SeMet than from selenite was absorbed and appeared in plasma in all groups. Milk contained more selenium from apparently absorbed SeMet than from selenite. More selenium from apparently absorbed selenite than from SeMet appeared in urine of NP and NL subjects whereas L subjects had approximately the same amount of selenium from apparently absorbed selenite and SeMet in their urine. All groups retained significantly more selenium from SeMet than from selenite; L women retained more selenium from selenite than did the other two groups. Absorption and retention of selenium from SeMet in L women did not appear to be significantly different from that in other women, suggesting that selenium requirements during lactation are increased mainly because of milk losses.

Absorption↗
PubMed1993

Selenium and difluoromethylornithine additively inhibit DMH-induced distal colon tumor formation in rats fed a fiber-free diet.

We investigated the effects of difluoromethylornithine, an inhibitor of ornithine decarboxylase (ODC) and selenium supplementation on tumor formation induced by the carcinogen 1,2-dimethylhydrazine (DMH) in Sprague-Dawley rats. A biochemical link between polyamine biosynthesis and selenium metabolism to its cancer preventative form has been suggested by the common requirement of S-adenosylmethionine. One-hundred and twenty male Sprague-Dawley rats were divided into experimental (n = 80) and control (n = 40) groups. Experimental animals received DMH 20 mg/kg s.c. for 20 weeks. Animals were fed either a regular diet (selenium content 0.2 p.p.m.) or a high selenium diet (5 p.p.m.) with or without 0.2% DFMO in the drinking water. At death, week 30, animal weights within experimental or control groups were not different between the four diet treatment groups. Tumor number and incidence in the proximal colon was not affected by DFMO treatment, selenium supplementation or the combined treatment. In contrast, in the distal colon, 19 tumors developed in the DFMO treated group, 22 tumors in the high selenium group and only 12 tumors in the combined high selenium/DFMO treatment group compared to 32 tumors in the regular diet group. Similarly, tumor incidence was decreased by DFMO and selenium supplementation and their effects were additive. In control animals, ODC activity was decreased by DFMO treatment and selenium supplementation in the distal colon and liver, but not the proximal colon. ODC activity of tumor tissue was greater than normal colon tissue from diet paired animals for proximal and distal colon, except for distal colonic tumors in the high selenium/DFMO treatment group. Polyamine content, however, did not correlate with ODC activity in normal or neoplastic tissue. In general, S-adenosylmethionine levels from normal colon and liver tissue were unaffected by diet treatment. Selenium supplementation in combination with DFMO treatment selectively inhibited distal colon tumor formation in rats fed a fiber-free diet.

1,2-Dimethylhydrazine↗
PubMed1976

Effect of selenium on rat growth, growth hormone and diet utilization.

Female rats were fed a selenium-deficient diet composed of Torula yeast, sucrose, vitamins (including tocopheryl acetate) and minerals from weaning and during breeding, gestation and lactation. The offspring were used to study the effects of selenium on growth, diet utilization and growth hormon status. The Torula yeast diet containing 200 IU dl-alpha-tocopheryl acetate was fed alone or supplemented with 0.025 or 0.1 ppm of selenium as selenite. Rats fed the selenium-supplemented diets grew significently faster and consumed significantly more diet than rats fed the unsupplemented diet. Anterior pituitary weights were lower in selenium-deficient rats, but if expressed per unit of body weight, were similar to pituitary weight of selenium-supplemented animals. Total growth hormone in the anterior pituitary was reduced in selenium-deficient rats. A metabolism study indicated that rats allowed ad libitum access to supplemented diets consumed more diet and obtained more metabolizable energy from the diet than rats fed the deficient diet. It the intake of rats fed the supplemented diets was limited to that of rats allowed ad libitum access to deficient diet, growth of rats was similar. However, metabolizable energy content of the diet increased quadratically and nitrogen digestibility increased linearly as thelevel of selenium increased. Selenium deficiency reduced growth primarily by decreased diet consumption, but also reduced the utilization of energy and nitrogen.

Animals↗
PubMed1976

Influence of dietary selenium on lead toxicity in the rat.

An investigation of the influence of dietary selenium (0.015, 0.05, 0.50, 1.0 ppm) on toxicity of dietary lead (0 and 200 ppm) in the young male rat indicated that selenium was mildly protective against the toxic effects of lead, but only up to 0.50 ppm selenium. At the excess selenium dietary level an exaggeration of lead toxicity was observed. Criteria employed to judge the effects of dietary selenium on lead toxicity included tissue lead concentration and urinary delta-aminolevulinic acid excretion. One exception to the exaggeration effect of excess selenium on lead toxicity was the protective effect of selenium on liver delta-aminolevulinic acid dehydratase activity. Since lead depressed kidney selenium concentration, lead may act as an antagonist to selenium metabolism.

Animals↗
PubMed1977

Fatty acid and glucose metabolism in selenium deficient rats and lambs.

Fatty acid analyses were done on tissues of lambs from ewes fed purified diets, and injected with selenium and/or vitamin E in a 2 X 2 factorial treatment. The concentrations of arachidonic acid averaged 9.3% of the total fatty acid content in semitendinosus muscle from lambs given vitamin E and selenium, but averaged 19.4% in this muscle from lambs given vitamin E without selenium. Arachidonic acid comprised 28.3% and 33.7%, respectively, of the total fatty acids in livers from selenium supplemented and deficient rats. Twice as much radioactivity from [1-(14)C]acetate was recovered in rat liver phospholipid arachidonate in selenium deficient rats as in selenium supplemented ones, indicating a greater turnover rate of this fatty acid in deficient rats. Fifty-five percent of dosed 14C-glucose (either [1-(14)C] or [6-(14)C]glucose) was recovered within 3 hours as 14CO2 from selenium deficient rats. This recovery dropped to one-half this value when these rats were fed a diet containing 0.1 ppm selenium for only 7 days. This increased glucose metabolism is suggestive of a greater metabolic rate in selenium deficient animals, which may be responsible for the differences observed in tissue fatty acid composition.

Animals↗
PubMed1987

Effect of selenium depletion and repletion on plasma glutathione and glutathione-dependent enzymes in the rat.

Selenium deficiency has several known biochemical effects. In the rat, these effects include loss of glutathione peroxidase (GSH-Px) activity, increased plasma glutathione concentration and increased liver glutathione S-transferase (GSH S-Tr) activity. The time course of the development of these changes in rats fed selenium-deficient diets and the time course of reversal of these changes in selenium-deficient rats fed graded levels of selenium were determined. As selenium deficiency was produced, liver cytosolic and plasma GSH-Px activities decreased first and were less than 5% of control when plasma glutathione concentration and liver GSH S-Tr activity began to increase. Elevated liver GSH S-Tr activity in selenium-deficient rats was corrected by refeeding selenium at the lowest level of supplementation (0.015 ppm) for 4 wk. GSH-Px activity required a supplementation of 0.10 ppm selenium for correction to control levels in 4 wk. Based on these studies a classification of the severity of selenium deficiency into mild, moderate and severe categories is proposed. In addition, the effect of dietary sulfur amino acid supplementation on plasma glutathione concentration was studied.

Amino Acids, Sulfur↗
PubMed2003

Serum selenium levels in relation to markers of neoplastic progression among persons with Barrett's esophagus.

BACKGROUND: Persons with Barrett's esophagus have a substantially greater risk of esophageal adenocarcinoma than the general population. Higher serum selenium levels have been associated with a reduced risk of several cancers; however, their association with the risk of esophageal adenocarcinoma is unknown. We used a cross-sectional study to investigate the relationship between serum selenium levels and markers of neoplastic progression among persons with Barrett's esophagus. METHODS: Medical history, blood, and esophageal tissue specimens were collected from 399 members of a cohort study of Barrett's esophagus patients undergoing endoscopic surveillance. Serum selenium levels were measured by flameless atomic absorption spectrophotometry. DNA content of tissue samples was measured by flow cytometry. Loss of heterozygosity (LOH) at 9p and 17p, chromosomal regions which include the p16 and p53 tumor suppressors, respectively, was detected by automated fluorescent genotyping. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). All statistical tests were two-sided. RESULTS: Persons with serum selenium levels in the upper three quartiles (i.e., >1.5 micro M) were less likely to have high-grade dysplasia (OR = 0.5, 95% CI = 0.3 to 0.9) or aneuploidy (OR = 0.4, 95% CI = 0.2 to 0.8) than those with levels in the lowest quartile. Serum selenium levels in the upper three quartiles were associated with similar reductions in risk of 17p (p53) LOH (OR = 0.5, 95% CI = 0.2 to 0.9) and increased 4N fraction (OR = 0.6, 95% CI = 0.3 to 1.2). By contrast, serum selenium levels were not associated with 9p (p16) LOH (OR = 1.0, 95% CI = 0.5 to 1.7), a marker that appears early in neoplastic progression. CONCLUSION: Our preliminary results, from a cross-sectional analysis with biologic markers, suggest that higher serum selenium levels may be associated with a reduced risk of esophageal adenocarcinoma among persons with Barrett's esophagus. Because serum selenium was not associated with 9p (p16) LOH, we speculate that selenium may act primarily at later stages of progression toward adenocarcinoma.

Adenocarcinoma↗
PubMed1986

Selenium in reproductive organs, seminal fluid and serum of men and bulls.

The concentrations of selenium in the reproductive organs, seminal fluid and serum of human males and bulls were analysed using an atomic absorption spectrometer with Zeeman background correction. The mean (+/- SD) concentration of selenium in human seminal fluid (33.4 +/- 14.1 micrograms/l, n = 70) was less than half the level detected in serum (78.2 +/- 9.9 micrograms/l, n = 32). In bulls, the mean selenium concentration in seminal fluid (457.4 +/- 108.7 micrograms/l, n = 113) was about nine times higher than in human males, while the level in serum (49.1 +/- 5.1 micrograms/l, n = 94) was significantly (P less than 0.001) lower than in human serum. The selenium concentration (500 +/- 244 micrograms/l) in the bovine seminal vesicle secretions were comparable to those in the seminal fluid and this gland appears to be mainly responsible for the high selenium levels in the seminal fluid. The mean selenium concentration in reproductive tissues of both species was highest in the testes. The distribution of selenium in the bovine epididymis was biphasic. The testicular and epididymal selenium are associated mainly with macromolecules of the spermatogenic cells and spermatozoa. It was concluded that studies in farm and laboratory animals do not necessarily form a reliable basis for conclusions with regard to human male reproduction, since selenium may have a different role and importance in the reproduction of various species.

Adult↗
PubMed2004

Serum selenium levels in acute gastroenteritis of possible viral origin.

Selenium, as an essential micronutrient, is required for the proper functioning of the immune system and its deficiency affects the occurrence, virulence, or disease progression of some viral infections. We conducted a study to determine the serum selenium levels of children with acute gastroenteritis of possible viral origin and the effect of the serum selenium levels on the severity and the morbidity of the disease. The study was performed prospectively on 109 children aged 2-24 months with diarrhea of less than 8 days' duration admitted to the Diarrheal Disease Training and Treatment Unit. Blood samples were taken for selenium measurement on admission and 7-10 days after the end of the disease. Forty-three healthy children formed the control group. The mean serum selenium level on admission (62.41 +/- 13.06 microg/dl) was significantly lower than the mean of the second samples 7-10 days after the end of the diarrhea (81.73 +/- 17.10 microg/dl). The mean of the control group was 74.36 +/- 10.75 microg/dl, which was lower than the mean of the second samples but higher than the first sample. The frequency of vomiting and purging on admission and at the control visit, duration of diarrhea on admission, total duration of diarrhea, dehydration, breastfeeding, sex of the patients, and severity score of the disease did not alter the serum selenium levels. No correlation was detected between serum selenium levels and the parameters above. Further studies about the changes in selenium status during infectious diseases and the effect of selenium status on related mortality and morbidity are required to determine if there is need for supplementation.

Acute Disease↗
PubMed1991

Molecular biology of selenium with implications for its metabolism.

Selenium has a highly specific metabolism centered around its incorporation as selenocysteine into selenoproteins. An outline of this metabolism has emerged from recent molecular biological and biochemical studies of bacteria and animals. A unique tRNA, designated tRNA[Ser]Sec, is charged with L-serine, which is then converted through at least two steps to selenocysteine. With the aid of a unique translation factor, the selenocysteinyl-tRNA[Ser]Sec recognizes specific UGA codons in mRNA to insert selenocysteine into the primary structure of selenoproteins. Turnover of selenoproteins presumably liberates selenocysteine which is toxic in its free form. Selenocysteine beta-lyase catabolizes free selenocysteine and makes its selenium available for reuse. Proteins contain almost all the selenium in animals. Of the known selenoproteins, the glutathione peroxidases contain the most selenium. Cellular and plasma glutathione peroxidases are products of different genes but have 44% identity of amino acid sequence. There is evidence for other proteins of this family. Selenoprotein P is an unrelated protein with multiple selenocysteines in its primary structure. It contains most of the selenium in rat plasma. Studies of the regulation of cellular glutathione peroxidase by selenium have yielded conflicting results, but there is a strong suggestion that mRNA levels of the rodent liver glutathione peroxidase decrease in selenium deficiency. This could be a mechanism for directing selenium to the synthesis of other selenoproteins. Although present knowledge allows construction of an outline of selenium metabolism, several steps have not been characterized and little is known about mechanisms of its regulation.

Animals↗
PubMedDate not supplied

Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection.

GOALS: We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. STUDY: Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. RESULTS: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 +/- 25.97 microg/L and 71 +/- 32.9 microg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 +/- 19.74 microg/g and 2.83 +/- 1.42 microg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 +/- 19.4 microg/g and 7.4 +/- 4.56 microg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 +/- 22.5 microg/g and 22.81 +/- 17.35 microg/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10.3 microg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 +/- 6.44 microg/g vs. 19.13 +/- 22.48 microg/g, respectively; p < 0.05). CONCLUSIONS: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.

Adolescent↗
PubMed1984

Plasma selenium concentration in healthy Japanese children and adults determined by flameless atomic absorption spectrophotometry.

This study showed a rapid and direct method for determining selenium concentration in plasma by flameless atomic absorption spectrophotometry, and differences in plasma selenium concentration in healthy children and adults. A direct method is possible, since selenium is heat stable in the presence of nickel. With this method, the recovery of selenium added to plasma was 100.3 +/- 5.7%, and the relative standard deviation in repeated determinations of pooled plasma selenium was 3.0% and 6.8%. The plasma selenium concentration in adults was 99.4 +/- 12.5 ng/ml, lower than reported concentrations from the United States and Canada, and higher than those from New Zealand. These variations may reflect dietary habits, bioavailability of selenium compounds in diet, racial difference, or different analytical methods. The mean concentration of plasma selenium at 1 to 6 months of age (51.0 +/- 13.1 ng/ml) was significantly lower than in adults (p less than 0.001); it increased gradually and steadily to the adult level with age. This age-related difference of plasma selenium level is similar to that reported previously.

Adolescent↗
PubMed1983

Selenium and immune functions in humans.

Earlier animal experiments have shown that selenium depletion may decrease immune functions. In this human study, 40 volunteers from a population with low serum selenium concentrations were supplemented with selenium or placebo for 11 weeks. Blood samples were drawn at intervals for analysis of selenium status and immune function. At the end of the supplementation period, plasma selenium levels were 74 ng/ml in the placebo group and 169 ng/ml in the supplemented group. The improvement in selenium status was associated with a 57% increase in the activity of platelet glutathione peroxidase in the group supplemented with selenium, but there was no increase in the activity of this enzyme in the placebo-treated subjects. Immune function was measured in vitro by tests of lymphocyte and granulocyte activity. Intracellular killing of Staphylococcus aureus by granulocytes was slightly lower in the placebo group than in the selenium group at the end of the supplementation period (77.2 compared to 85.2%; P less than 0.05). No significant changes were observed in phagocytosis, chemotactic factor generation, antibody or leukocyte migration inhibitory factor production by lymphocytes, or proliferative responses to phytohemagglutinin or concanavalin A. These results suggest that the selenium deficiency of the order found in Finland and some other areas of the world has little, if any, influence on the immune functions measured in this study.

Adult↗
PubMed1990

Reduced selenium in asthmatic subjects in New Zealand.

Selenium is an essential component of glutathione peroxidase, an enzyme that helps protect cells against oxidation damage and modulates the lipoxygenase pathway of arachidonic acid metabolism. Low selenium concentrations might therefore influence the inflammatory process in asthma by reducing the activity of glutathione peroxidase. Whole blood and plasma selenium concentrations and glutathione peroxidase activity have been measured in 56 asthmatic patients and 59 non-asthmatic control subjects in New Zealand, a country with a low dietary selenium intake and a high prevalence of asthma. When compared with control subjects the asthmatic patients had lower values for whole blood selenium concentrations (-4.9, 95% confidence interval -10.2 to 0.4 ng/ml) and glutathione peroxidase activity (-3.3, 95% CI -5.8 to -0.8 units/g Hb). There was a 1.9 and 5.8 fold increased risk of asthma in subjects with the lowest range of whole blood selenium concentration and glutathione peroxidase activity respectively (95% CI 0.6 to 5.6 and 1.6 to 21.2). Levels were lower in patients and control subjects without an atopic predisposition, but were not affected by prednisone use. Similar differences between the asthmatic and control subjects were not observed for selenium concentration or glutathione peroxidase activity measured in plasma, which reflects short term rather than long term selenium content. These findings are consistent with the hypothesis that low selenium concentrations may have a role in the pathogenesis of asthma in New Zealand.

Adolescent↗
PubMed1996

Pulmonary effects of short term selenium deficiency.

BACKGROUND: Selenium dependent glutathione peroxidase (GPx) reduces hydrogen peroxide (H2O2) and organic hydrogen peroxides in both normal and pathological states. Chronic dietary deficiency of selenium results in a gradual decrease in GPx and altered response to environmental stress. However, glutathione-S-transferase (GST) isozymes may increase and compensate for chronic GPx deficiency. The pattern of antioxidant enzyme activity and immunolocalisation of various enzymes in rat lung has not been described in short term (< 3 weeks) acute selenium deficiency. METHODS: The time course of GPx depletion from rat lung (measured every five days in subgroups of rats) during acute dietary selenium deficiency was evaluated. After 20 days of depletion, enzyme activity of lung GPx, catalase, superoxide dismutase (SOD), glutathione reductase (GR), glucose-6-phosphodiesterase (G-6-PD), and GST were determined. Immunohistochemical localisation of GPx and SOD was also performed. The response to lethal hyperoxia (> 95%) in control and selenium deficient rats was then established. RESULTS: At 20 days, lung GPx activity in the rats fed a selenium deficient diet was one third less than in control animals who received a normal diet, while changes in blood enzymes between control and deficient animals were similar. Other lung enzyme activities remained normal with the exception of cyanide inhibited SOD activity measured in selenium deficient rat lungs which declined to approximately 50% of normal. Immunohistochemical localisation of GPx showed a generalised loss of the enzyme throughout the lung parenchyma with some possible sparing of activity in epithelial cells of the bronchioles. When exposed to lethal hyperoxia, selenium deficient animals were more susceptible than control rats. CONCLUSIONS: This is the earliest time at which dietary selenium deficiency has been shown to produce moderate loss of GPx activity. This change in activity was associated with increased susceptibility to pulmonary oxidant stress. However, the role of decreased SOD activity (presumed to represent copper, zinc SOD), although unexpected, may have been a major contributor to increased damage from hyperoxia. These results emphasise the complex potential interaction of elemental deficiency with the natural antioxidant response to lethal hyperoxia.

Animals↗