Effectiveness of selenium supplements in a low-selenium area of China

BACKGROUND: Selenium is an essential micronutrient with a recommended dietary allowance for adults of 55 mug/d. It functions as an essential constituent of selenoproteins. Although there is no evidence of selenium deficiency in the United States, people in many other areas of the world are selenium deficient, with the consequence that they are unable to express their selenoproteins fully. OBJECTIVE: We carried out a supplementation trial in a selenium-deficient population in China to assess the requirement for selenium as selenite and as selenomethionine. DESIGN: One hundred twenty subjects with an average selenium intake of 10 mug/d were randomly assigned and administered tablets containing no selenium or amounts as high as 66 mug Se/d for 20 wk. Plasma was sampled before supplementation and at 4-wk intervals during supplementation and was assayed for the 2 plasma selenoproteins, glutathione peroxidase and selenoprotein P. RESULTS: Full expression of glutathione peroxidase was achieved with 37 mug Se/d as selenomethionine and with 66 mug/d as selenite. Full expression of selenoprotein P was not achieved at the highest doses of either form. CONCLUSIONS: Full expression of selenoprotein P requires a greater selenium intake than does full expression of plasma glutathione peroxidase. This suggests that selenoprotein P is a better indicator of selenium nutritional status than is glutathione peroxidase and that the recommended dietary allowance of selenium, which was set with the use of glutathione peroxidase as the index of selenium status, should be revised. Selenium as selenomethionine had nearly twice the bioavailability of selenium as selenite.     

Bioavailability of selenium to residents in a low-selenium area of China

For 8 wk 5 groups of 10 men each were given 0.5 g/day DL-methionine, 150 micrograms Se/day as sodium selenite with or without methionine or 150 micrograms Se/day as selenomethionine with or without methionine. Twenty subjects received placebo as controls. Initially plasma Se rose more rapidly than RBC Se. Increases in Se levels were significantly greater with selenomethionine than with the selenite supplement. In the placebo and methionine supplemented groups neither plasma nor RBC Se varied significantly over the course of the study. Supplementation with selenium resulted in marked increases in plasma and RBC GSH-Px within 2 and 4 wk, respectively. Plasma and RBC GSH-Px activity did not differ significantly between Se-supplemented groups. These studies suggest that selenomethionine-Se was more effective in raising plasma and RBC Se than was selenite-Se. Methionine supplements may increase the bioavailability of selenium in severely deficient subjects.     

Associations between glutathione peroxidase-1 Pro198Leu polymorphism, selenium status, and DNA damage levels in obese women after consumption of Brazil nuts

Objective

Alterations in selenium (Se) status may result in suboptimal amounts of selenoproteins, which have been associated with increased oxidative stress levels. The Pro198Leu polymorphism at the glutathione peroxidase-1 (GPx1) gene is supposed to be functional. The response of Se status, GPx activity, and levels of DNA damage to a Se supplementation trial between the genotypes related to that polymorphism was investigated.

Methods

A randomized trial was conducted with 37 morbidly obese women. Participants consumed one Brazil nut, which provided approximately 290 μg of Se a day, for 8 wk. Blood Se concentrations, erythrocyte GPx activity, and DNA damage levels were measured at baseline and at 8 wk. The results were compared by genotypes.

Results

The genotype frequencies were 0.487, 0.378, and 0.135 for Pro/Pro (the wild-type genotype), Pro/Leu, and Leu/Leu, respectively. At baseline, 100% of the subjects were Se deficient, and after the supplementation, there was an improvement in plasma Se (P < 0.001 for Pro/Pro and Pro/Leu, P < 0.05 for Leu/Leu), erythrocyte Se (P = 0.00 for Pro/Pro and Pro/Leu, P < 0.05 for Leu/Leu), and GPx activity (P = 0.00 for Pro/Pro, P < 0.00001 for Pro/Leu, P < 0.001 for Leu/Leu). In addition, the Pro/Pro group showed a decrease in DNA damage after Brazil nut consumption compared with baseline (P < 0.005), and those levels were higher in Leu/Leu subjects compared with those with the wild-type genotype (P < 0.05).

Conclusion

Consumption of one unit of Brazil nuts daily effectively increases Se status and increases GPx activity in obese women, regardless of GPx1 Pro198Leu polymorphism. However, the evaluated biomarkers showed distinct results in response to the supplementation when the polymorphism was considered.     

Selenium supplements do not increase plasma total homocysteine concentrations in men and women

Studies in rats indicate that plasma total homocysteine (tHcy) is decreased in selenium deficiency and increases with selenium supplementation. The aim of this study was to determine the effect of selenium supplements on plasma tHcy concentrations in a population that has suboptimal selenium status. Subjects from Dunedin, New Zealand (n = 189) were randomly assigned to receive a supplement containing 200 micro g selenium or placebo for 20 wk. At baseline, 67% (n = 112) of the participants had plasma selenium concentrations < 1.2 micro mol/L, a concentration believed to be that necessary for full glutathione peroxidase (Gpx) activity. At 20 wk, plasma selenium concentration and Gpx activity increased in the selenium group by 1.2 micro mol/L [95% confidence interval (CI): 1.1, 1.3] and 5.1 nkat/g protein (3.7, 6.5), respectively, changes that were significantly greater than the changes in the placebo group (P < 0.001). At 20 wk, mean changes in plasma tHcy concentrations were 0.1 micro mol/L (95% CI: -0.4, 0.5) and -0.2 micro mol/L (-0.7, 0.3) in the supplemented and placebo groups, respectively, compared to baseline. There was no difference in the mean changes in plasma tHcy between the supplemented and placebo groups (P = 0.54). These results suggest that selenium supplementation does not influence plasma tHcy concentrations in healthy populations in developed countries, whose selenium status is characterized by lower plasma selenium concentrations.     

Effects of dietary selenite, selenocystine and selenomethionine on selenocysteine lyase and glutathione peroxidase activities and on selenium levels in rat tissues

Weanling male rats were fed a basal selenium (Se)-deficient diet or this diet plus 2 ppm Se as either selenite, selenocystine (SeCys) or selenomethionine (SeMet) for 9 wk. The rats were killed by decapitation while anesthetized with ether, and tissues were assayed for glutathione peroxidase (GPx) and selenocysteine lyase activities, and for Se content. Dietary Se had no effect upon the activity of tissue selenocysteine lyase. This activity was highest in the liver, followed by kidney, muscle and testis in decreasing order. Although the GPx activity was lower in tissues of the Se-deficient rats, there were no significant differences in its activity between animals given the different chemical forms of dietary Se. Except for the kidney, the tissue Se concentrations were similar in rats fed selenite or SeCys, but the Se content in testis, muscle, pancreas, heart, spleen, whole blood, erythrocytes and plasma was significantly higher in rats fed SeMet than in those fed either selenite or SeCys. The greatest increase due to SeMet compared with the selenite and SeCys treatments was about 10-fold in the muscle compared with 1.3- to 3.6-fold for the other tissues.     

The effect of selenium on thyroid status in a population with marginal selenium and iodine status

The effects of Se on thyroid metabolism in a New Zealand population are investigated, including (a) the relationship between Se and thyroid status, and (b) the effect of Se supplementation on thyroid status. The data used come from two cross-sectional studies of Se, I, thyroid hormones and thyroid volume (studies 1 and 4), and three Se intervention studies in which thyroid hormones, Se and glutathione peroxidase (GPx) activities were measured (studies 2, 3 and 5). There were no significant correlations between Se status and measures of thyroid status after controlling for sex at baseline or after supplementation in any of the studies. When data from study 4 were divided into two groups according to plasma Se, plasma thyroxine (T4) was lower in males with higher plasma Se levels (P=0.009). Se supplementation increased plasma Se and GPx activity, but produced only small changes in plasma T4 and triiodothyronine (T3):T4 ratio. In study 2, there was a significant reduction in plasma T4 (P=0.0045). In studies 3 and 5 there were small decreases in plasma T4 and a small increase in the T3:T4 ratio, which were not significantly different from placebo groups. Lack of significant associations between plasma Se and thyroid status, and only small changes in T4 suggest that Se status in New Zealand is close to adequate for the optimal function of deiodinases. Adequate plasma Se may be approximately 0.82-0.90 micromol/l, compared with 1.00-1.14 micromol/l for maximal GPx activities.     

Selenium deficiency decreases antioxidative capacity and is detrimental to bone microarchitecture in mice

Selenium (Se), an essential mineral, plays a major role in cellular redox status and may have beneficial effects on bone health. The objective of this study was to determine whether Se deficiency affects redox status and bone microarchitecture in a mouse model. Thirty-three male C57BL/6J mice, 18 wk old, were randomly assigned to 3 groups. Mice were fed either a purified, Se-deficient diet (SeDef) containing ～0.9 μg Se/kg diet, or Se-adequate diets containing ～100 μg Se/kg diet from either selenomethionine (SeMet) or pinto beans (SeBean) for 4 mo. The Se concentration, glutathione peroxidase (GPx1) activity, and GPx1 mRNA in liver were lower in the SeDef group than in the SeMet or SeBean group. The femoral trabecular bone volume/total volume and trabecular number were less, whereas trabecular separation was greater, in the SeDef group than in either the SeMet or SeBean group (P < 0.05). Bone structural parameters between the SeMet and SeBean groups did not differ. Furthermore, Serum concentrations of C-reactive protein, tartrate-resistant acid phosphatase, and intact parathyroid hormone were higher in the SeDef group than in the other 2 groups. These findings demonstrate that Se deficiency is detrimental to bone microarchitecture by increasing bone resorption, possibly through decreasing antioxidative potential.     

Effect of intermittent supplementation with selenate on selenium status of rats fed selenium-deficient diet

To examine the selenium (Se) status of rats intermittently supplemented with Se, we measured tissue Se contents and glutathione peroxidase (GPx) activities in rats fed a Se-deficient diet intermittently supplemented with selenate. In experiment 1, four groups of male 4-wk-old Wistar rats were fed a Torula yeast-based Se-deficient diet (Se content, < 0.01 microg/g) for 28 d. During the experimental period, the diet of each group was supplemented with sodium selenate (0.17 microg Se/g) for 0, 1, 2 or 7 d/wk. The tissue Se contents and GPx activities both increased gradually with an increase in frequency of the selenate supplementation, and significant linear regressions were observed between the frequency and these Se indices. In particular, the correlation coefficient in the liver and plasma indices was nearly equal to a value of 1.0. In experiment 2, three groups of rats were fed the Se-deficient basal diet for 28 d. Among these, one group was daily supplemented with sodium selenate to the Se-deficient diet at a level of 0.17 microg Se/g, and another group was intermittently supplemented with the selenate at a level of 1.19 microg Se/g for 1 d/wk. The tissue Se contents and GPx activities both were increased by the selenate supplementation and no significant difference was observed between daily and weekly supplementation in the Se indices except in erythrocyte Se. These results indicate that Se status in the growth period is dependent on total Se intake in this period and that weekly intermittent supplementation with Se can maintain adequate Se status.     

Selenium supplementation, soluble tumor necrosis factor-alpha receptor type 1, and C-reactive protein during psoriasis therapy with narrowband ultraviolet B

OBJECTIVE: We examined the influence of supplementation with selenomethionine on soluble tumor necrosis factor-alpha receptor type 1 (sTNF-R1) and C-reactive protein (CRP) concentrations in patients with psoriasis who were treated with narrowband ultraviolet B. METHODS: Thirty-seven patients had narrowband ultraviolet B therapy five times a week and received 200 mug of selenium daily as selenomethionine (group 1, n = 19) or placebo (group 2, n = 18) for 4 wk. Assessment, performed at baseline, after 2 and 4 wk, and 4 wk after the end of treatment included measurement of the Psoriasis Area and Severity Index (PASI) and serum concentrations of selenium (micrograms per liter), sTNF-R1 (nanograms per milliliter), and CRP (milligrams per liter). Control sera were obtained from 20 healthy volunteers. RESULTS: Baseline PASI was 12.70 +/- 5.48 (13.02 +/- 6.25 in group 1 and 12.37 +/- 4.71 in group 2), selenium concentration was 50.55 +/- 9.54 (49.05 +/- 10.38 and 52.13 +/- 8.61, respectively), sTNF-R1 concentration was 1.91 +/- 0.38 (1.96 +/- 0.37 and 1.87 +/- 0.40, respectively), and CRP concentration was 25.34 +/- 8.27 (26.12 +/- 8.42 and 24.57 +/- 7.72). In controls, selenium concentration was 48.71 +/- 9.39 (P > 0.05 versus patients), sTNF-R1 concentration was 1.48 +/- 0.30 (P < 0.05), CRP concentration was <6. The baseline sTNF-R1 level correlated to PASI value (r = 0.40, P < 0.05) and CRP concentration (r = 0.36, P > 0.05). The treatment resulted in an almost parallel decrease in PASI in both groups. At 4 wk after the end of treatment, selenium concentrations were 83.77 +/- 5.13 in group 1 and 52.12 +/- 7.54 in group 2 (P < 0.05), sTNF-R1 concentrations were 1.72 +/- 0.27 and 1.47 +/- 0.26 (P < 0.05), and CRP concentrations were 7.72 +/- 4.23 and 8.15 +/- 3.32, respectively (P > 0.05). Selenium concentration correlated inversely with CRP in group 1. CONCLUSION: The results confirm that sTNF-R1 and CRP concentrations are increated in active psoriasis and that supplementation with selenomethionine for 4 wk in safe doses is ineffacious as adjuvant therapy in patients with psoriasis.     

Selenium status of term infants fed selenium-supplemented formula in a randomized dose-response trial

BACKGROUND: The optimal form and dose of selenium supplementation required to achieve indicators of selenium status equivalent to those in breastfed infants are unclear. OBJECTIVE: The objective was to evaluate the effect of fortifying infant formula (6 microg Se/L) with 2 concentrations of selenate (7 and 15 microg/L) on biochemical indicators of selenium status and growth at 16 wk in term infants. DESIGN: A randomized dose-response trial was conducted in 3 groups of term infants fed formula with different selenium concentrations [6 microg/L, F+0 (control); 13 microg/L, F+7; and 21 microg/L, F+15] and in a parallel breastfed reference group (BF; 11 +/- 2 microg Se/L). RESULTS: One hundred sixty-one (47% males) infants completed the 16-wk study. Baseline plasma selenium was 0.3 +/- 0.1 micromol/L. At 16 wk, plasma selenium had increased in all groups (P < 0.001) and was greater (P < 0.01) in the F+7 and F+15 groups and lower (P < 0.05) in the F+0 group than in the BF group. Plasma glutathione peroxidase increased in the F+15 group, decreased in the F+0 group, and, at 16 wk, was lower in the F+0 group than in the other groups (all P < 0.05). Erythrocyte selenium and glutathione peroxidase decreased in all groups (P < 0.05), but the magnitude of the change was greater in the F+0 than in the F+15 group (P < 0.05). There was no effect of selenium supplementation on growth. CONCLUSIONS: Selenate fortification of formula resulted in an increase in plasma indicators of selenium status relative to indicators observed in infants fed low-selenium-containing formula. Although the erythrocyte indicators decreased in all groups, the 21-microg/L dose (F+15 group) resulted in a smaller decrease and in higher erythrocyte selenium than did the standard formula. Supplementation of low-selenium formula to provide a net selenium concentration close to that found in the breast milk of US women (18 microg/L) may be justified.     

Brazilian nut consumption improves selenium status and glutathione peroxidase activity and reduces atherogenic risk in obese women

Studies have shown that there are inverse relationships between nut consumption and the reduction of cardiovascular risk. This study tested the hypothesis that daily consumption of Brazilian nuts would have a positive effect upon selenium (Se) status, erythrocyte glutathione peroxidase activity, lipid profile, and atherogenic risk in severely obese women. Thirty-seven severely obese women each consumed 1 Brazilian nut a day (290 μg of Se a day) for 8 weeks. Blood Se concentrations, total erythrocyte glutathione peroxidase activity, lipid profile, and Castelli I and II indexes were evaluated before and after the nuts consumption. All the patients were Se deficient at baseline; this deficiency was remedied by the consumption of the Brazilian nut (P < .0001). The intake of Brazilian nuts promoted a significant increase in high-density lipoprotein cholesterol concentrations (P < .00001), which then resulted in a significant improvement of the Castelli I (P < .0002) and II (P < .0004) indexes. This study shows that obese people who implement daily consumption of Brazilian nuts can improve both Se status and lipid profile, especially high-density lipoprotein cholesterol levels, thereby reducing cardiovascular risks.     

Chemical forms of selenium in rat tissues after administration of selenite or selenomethionine

The chemical forms of selenium (Se) were determined in erythrocyte and liver proteins after injection of 75Se as either sodium selenite or selenomethionine (Se-Met) in male weanling rats. Gel-filtration chromatography (Sephadex G-150) of erythrocyte lysate revealed labeling of four fractions corresponding to void volume proteins, glutathione peroxidase (GPx), hemoglobin (Hb) and low-molecular-weight materials. Acid hydrolysates of erythrocyte protein fractions and whole liver were analyzed by ion-exchange chromatography (Dionex DC6A). Void volume proteins contained principally selenocysteine (75Se-Cys) in [75Se]selenite-injected animals. This material contained both 75Se-Met and 75Se-Cys 1 d postinjection in 75Se-Met-injected animals, but primarily 75Se-Cys at 20 d afterwards. GPx contained 75Se as 75Se-Cys regardless of the selenium compound injected. Hb of 75Se-Met-injected animals contained principally 75Se-Met at both 1 and 20 d postinjection. In [75Se]selenite-injected animals, 75Se was present in hemoglobin as two unidentified forms. In acid hydrolysates of whole liver 75Se was recovered principally as 75Se-Cys from animals injected with [75Se]selenite. For animals injected with 75Se-Met, liver 75Se was present initially as 75Se-Met, but after 5 d the majority of liver 75Se was as Se-Cys. No differences were found in deposition of 75Se in liver, kidney, testes, erythrocytes or plasma in rats injected with labeled selenite or Se-Met, but a significantly greater retention was found in muscle of Se-Met-injected rats as compared to those given selenite.     

Effects of dietary selenium on DMBA-induced carcinogenesis in rats fed a diet high in mixed fats

The effects of selenium intake on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis were examined in rats fed a diet high in mixed fats and representative of that consumed in North America. Six groups of 20 rats were fed an AIN-76 diet modified to contain 20% fat from lard:corn oil (3:1 wt/wt) and various amounts of selenium (0.1, 0.035, 0.1, 1.0, 2.0 or 4.0 mg Se/kg diet). At wk 5, animals in groups 2-6 were dosed with 4.32 mg of DMBA. Serum clinical parameters and the activities of plasma selenium-dependent and total glutathione peroxidase (GSHPx), erythrocyte GSHPx and superoxide dismutase (SOD) were determined every 4 wk for 25 wk. The extent of lipid peroxidation was determined by measuring urinary malondialdehyde during wk 13 and 24, and erythrocyte malondialdehyde at wk 25. Erythrocyte GSHPx was found to be a better indicator of selenium status than plasma activity, while SOD did not vary with dietary selenium. The group of animals fed 4.0 mg Se/kg diet had reduced numbers of tumors (P less than 0.01), but this reduction was associated with evidence of chronic selenium toxicity. Variations in GSHPx activity with dietary selenium did not result in differences in tumor incidence, nor in changes in lipid peroxidation in the other groups. Thus, nontoxic levels of selenium do not appear to offer any protective effect during carcinogenesis in rats fed a casein-based diet similar in fat content to that consumed by North Americans.     

An estimation of selenium requirements for New Zealanders.

BACKGROUND: Current US dietary recommendations for selenium are based on maximization of plasma glutathione peroxidase (GSHPx) activity according to data from one study of Chinese men. OBJECTIVE: The effect of various amounts of supplemental selenium on GSHPx activities in blood of New Zealand adults was investigated to calculate a selenium requirement for New Zealanders. The effect on plasma selenoprotein P and thyroid hormones was also investigated. DESIGN: Fifty-two adults with low blood selenium concentrations ingested a placebo or 10, 20, 30, or 40 microgram Se as L-selenomethionine daily for 20 wk. RESULTS: Plasma and whole-blood GSHPx activities increased in all supplemented groups but reached a plateau only in the group receiving 40 microgram Se, as determined by statistical analysis. Increases in selenoprotein P were greater than those for selenium and GSHPx at all supplement intakes. Thyroxine concentrations decreased in supplemented groups but the decrease was significantly different from that in the control group only for the 10-microgram group and for all supplemented groups combined. CONCLUSIONS: An upper estimated requirement of 90 microgram Se/d was calculated as the intake necessary for maximization of plasma GSHPx activity, as used in the derivation of the US recommended daily allowance. Our lower estimated requirement of 39 microgram Se/d was the intake necessary to reach two-thirds of maximal GSHPx activity, as was used in calculating the World Health Organization normative requirement. The lower estimate is a realistic goal for New Zealand but the upper estimate could be achieved only with regular inclusion of high-selenium foods.     

Brazil nut ingestion increased plasma selenium but had minimal effects on lipids,apolipoproteins, and high-density lipoprotein function in human subjects

The Brazil nut (Bertholletia excelsa) of the Amazon region is consumed worldwide. It is rich in both monounsaturated fatty acids and polyunsaturated fatty acids and is known for its high selenium content. This study tested the hypothesis whether the consumption of this nut could affect the plasma lipids and apolipoproteins and some functional properties of the antiatherogenic high-density lipoprotein (HDL). Fifteen normolipidemic subjects aged 27.3 ± 3.9 years and with body mass index of 23.8 ± 2.8 kg/m² consumed 45 g of Brazil nuts per day during a 15-day period. On days 0 and 15, blood was collected for biochemical analysis, determination of HDL particle size, paraoxonase 1 activity, and lipid transfer from a lipoprotein-like nanoparticle to the HDL fraction. Brazil nut ingestion did not alter HDL, low-density lipoprotein cholesterol, triacylglycerols, apolipoprotein A-I, or apolipoprotein B concentrations. HDL particle diameter and the activity of antioxidative paraoxonase 1, mostly found in the HDL fraction, were also unaffected. Supplementation increased the reception of cholesteryl esters (P < .05) by the HDL yet did not alter the reception of phospholipids, free cholesterol, or triacylglycerols. As expected, plasma selenium was significantly increased. However, the consumption of Brazil nuts for short duration by normolipidemic subjects in comparable amounts to those tested for other nuts did not alter serum lipid profile. The only alteration in HDL function was the increase in cholesteryl ester transfer. This latter finding may be beneficial because it would improve the nonatherogenic reverse cholesterol transport pathway.     

Selenium and vitamin E supplementation: activities of glutathione peroxidase in human tissues

Twenty-seven New Zealand women received daily for 4 wk, 200 micrograms selenium as sodium selenite, 170 mg alpha-tocopherol acetate, or a placebo. Se supplementation raised platelet selenoglutathione peroxidase (Se-GSHPx, p less than 0.001) and also Se and Se-GSHPx in whole blood and plasma. Se concentrations and Se-GSHPx activities in liver biopsies taken after supplementation were greater (p less than 0.05) for the Se group and a good correlation was found between Se and Se-GSHPx in liver and muscle for all subjects. Platelet Se-GSHPx correlated well with Se and Se-GSHPx in liver, indicating its suitability for assessing Se bioavailability. This is the first reported study of relationships between Se and Se-GSHPx in human liver and muscle tissue and platelet Se-GSHPx after Se supplementation. These observations verify in man relationships observe in animal studies, giving support to assumptions made in methods for assessing Se status and bioavailability in man, in particular the use of platelet GSHPx.     

硒掺入缺硒大鼠血小板、肝及血浆的动力学研究

给缺硒大鼠一次大剂量注射含~(75)硒的硒化合物。测定血小板,肝、血浆谷是胱甘肽过氧化物酶活性及~(75)硒含量。结果表明,血小板谷胱甘肽过氧化物酶活性反映一次大剂量硒摄入时的一个良好指标。同时证明血小板GSH-Px变化与肝GSH-Px变化一致。以两种不同形式硒化合物(亚硒酸钠和硒蛋氨酸)给予缺硒大鼠,两组大鼠血小板、肝、血浆中GSH-Px活性是相似的,但~(75)硒含量亚硒酸钠组显著低于硒蛋氨酸组,由此表明,硒蛋氨酸中部分硒没有掺入到血小板的GSH-Px中去,推测在体内硒可能存在其它代谢途径,这是很值得探讨的问题。     

Selenium and zinc status are suboptimal in a sample of older New Zealand women in a community-based study

The importance of selenium and zinc in the immune functioning of the aged is widely recognized. Seniors in New Zealand are at particularly high risk of low selenium status because of the low selenium soil environment. The zinc status of the New Zealand elderly has never been assessed. In this cross-sectional study, the biochemical selenium, zinc and lipid levels, physical functional capacity and dietary intakes of 103 randomly selected free-living New Zealand women (mean age +/- SD, 75 +/- 3 y) were assessed. Among nonusers of selenium supplements (n = 80), 80% [95% confidence interval (CI): 70; 88%] had plasma selenium levels (0.85 +/- 0.23 micromol/L) below 1.00 micromol/L [ approximately 10% below mean plasma selenium necessary for full expression of glutathione peroxidase (GPx) activity in New Zealand subjects]. Plasma selenium was strongly correlated with GPx: r = 0.56; P < 0.0001. For nonusers of zinc supplements (n = 88), serum zinc concentrations were 12.4 +/- 1.4 micromol/L, with 12% (95% CI: 6; 21%) having levels below the cut-off value (10.7 micromol/L). Estimated mean daily selenium and zinc intakes were 34 +/- 10 microg and 8.7 +/- 2.0 mg, respectively. Subjects in the highest tertile of a functional capacity index had higher biochemical zinc and selenium values than those in the lowest tertile (P < 0.05). The correlation between plasma selenium and GPx indicates that selenium intake in these women is still insufficient for full expression of GPx activity. Lower serum zinc levels also appear to be prevalent. Because a suboptimal trace element status may be more common among those with a poor physical functioning, promotion of the consumption of nutrient dense foods or supplements to improve selenium and zinc status of elderly women in New Zealand may be beneficial.