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PubMed1982

Selenium intakes and status of human milk and formula fed infants.

Selenium status was assessed in 28 infants receiving either human milk (n = 8) or a proprietary formula (n = 20) as their sole nutritional source from birth to 3 months. Infants' selenium intakes were determined from dietary records, "test weighings," and direct analysis of human milk and formula. Fore milk samples (n = 72) collected from group I mothers had a mean selenium concentration (ng/ml) of 16.3 +/- 4.9, whereas the selenium content of proprietary formula was 8.6 +/- 0.9. The selenium concentration of hind milk was significantly greater (p less than 0.05) than that of fore milk. At 3-months selenium intakes as well as serum selenium concentrations for human milk fed infants were significantly greater than those for formula fed infants. A significant positive correlation (r = 0.42; p less than 0.05) was found between infants' selenium intakes and their serum selenium concentrations. The results indicate that feeding practice directly affects selenium status during infancy.

Animals↗
PubMed1983

Quantitative and qualitative aspects of selenium utilization in pregnant and nonpregnant women: an application of stable isotope methodology.

Selenium utilization of women in early and late pregnancy was compared to that of nonpregnant controls. A defined diet providing about 150 micrograms Se/day was fed for 20 days, and selenium balance was measured during the last 12 days. Net selenium retentions of the women in early and late pregnancy were 10 and 23 micrograms/day, respectively, but probably are inflated estimates of the increased selenium requirement during pregnancy. Apparent absorption of selenium was 80% for all three groups. Pregnant women tended to conserve selenium by decreasing urinary selenium excretion. Those observations were corroborated by monitoring the urinary and fecal excretion of 40 micrograms of a stable isotope of selenium (76Se) from intrinsically labeled egg. The isotope data also indicated that recent selenium intake was incorporated into a long-term selenium pool. Mean glutathione peroxidase activity was lower in plasma and higher in platelets in the pregnant women as compared to controls, but the physiological significance of those observations is unknown.

Adult↗
PubMed1996

The enzymatic antioxidant system in blood and glutathione status in human immunodeficiency virus (HIV)-infected patients: effects of supplementation with selenium or beta-carotene.

To investigate the effects of selenium or beta-carotene supplementation in human immunodeficiency virus (HIV)-infected patients, who are known to have deficiencies of selenium and vitamin A, we evaluated the blood enzymatic antioxidant system, including superoxide dismutase (SOD), selenodependent glutathione peroxidase (GPX), and catalase (Cat); glutathione (GSH) status; and plasma selenium concentration. The placebo group consisted of 18 HIV-infected patients with no supplementation, the selenium group was composed of 14 patients receiving oral selenium treatment, and the beta-carotene group comprised 13 patients receiving oral beta-carotene supplementation. All groups were studied for 1 y. At the beginning of the study, a significantly higher SOD activity (P < 0.001) was observed in all HIV-infected patients compared with uninfected control subjects, and GPX activity at baseline was higher in the placebo (P < 0.004) and selenium (P < 0.014) groups than in the control subjects. These higher enzyme activities could be related to an increased synthesis of these enzymes in erythrocyte precursors under oxidative stress. Moreover, we observed significantly lower GSH values in all HIV-infected patients than in control subjects at the beginning of the study (P < 0.001). After selenium or beta-carotene supplementation, no significant difference was observed for SOD activity compared with baseline. On the contrary, GPX activity increased significantly after selenium treatment (P < 0.04 between 3 and 6 mo), whereas a slight increase was found after beta-carotene treatment. Similarly, a significant increase in GSH values was observed at 12 mo compared with baseline both after selenium supplementation (P < 0.001) and beta-carotene supplementation (P < 0.01). Because GPX and GSH play an important role in the natural enzymatic defense system in detoxifying hydrogen peroxide in water, selenium supplementation could be of great interest in protecting cells against oxidative stress. The lower efficiency of beta-carotene could be attributed to the seriousness of the pathology at the time of recruitment into the beta-carotene group.

Acquired Immunodeficiency Syndrome↗
PubMed2007

Serum selenium and risk of prostate cancer-a nested case-control study.

BACKGROUND: Selenium is a potential chemopreventive agent against prostate cancer, whose chemoprotective effects are possibly mediated through the antioxidative properties of selenoenzymes. Interrelations with other antioxidative agents and oxidative stressors, such as smoking, are poorly understood. OBJECTIVES: The aims were to investigate the association between serum selenium and prostate cancer risk and to examine interactions with other antioxidants and tobacco use. DESIGN: A nested case-control study was performed within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Serum selenium in prospectively collected samples was compared between 724 incident prostate cancer case subjects and 879 control subjects, frequency-matched for age, time since initial screen, and year of blood draw. The men were followed for up to 8 y. RESULTS: Overall, serum selenium was not associated with prostate cancer risk (P for trend = 0.70); however, higher serum selenium was associated with lower risks in men reporting a high (more than the median: 28.0 IU/d) vitamin E intake [odds ratio (OR) for the highest compared with the lowest quartile of selenium: 0.58; 95% CI: 0.37, 0.91; P for trend = 0.05; P for interaction = 0.01] and in multivitamin users (OR for highest compared with the lowest quartile of selenium: 0.61; 95% CI: 0.36, 1.04; P for trend = 0.06; P for interaction = 0.05). Furthermore, among smokers, high serum selenium concentrations were related to reduced prostate cancer risk (OR for the highest compared with the lowest quartile of selenium: 0.65; 95% CI: 0.44, 0.97; P for trend = 0.09; P for interaction = 0.007). CONCLUSION: Greater prediagnostic serum selenium concentrations were not associated with prostate cancer risk in this large cohort, although greater concentrations were associated with reduced prostate cancer risks in men who reported a high intake of vitamin E, in multivitamin users, and in smokers.

Aged↗
PubMed1984

Selective distribution of selenium in colon parallels its antitumor activity.

Results of epidemiologic and experimental studies suggest that selenium can inhibit the development of tumors. In rats, the administration of selenium decreases the incidence of carcinogen-induced colon tumors; the inhibition is greater in the proximal colon that in the distal colon. We investigated the distribution of selenium in the different segments of rat colon and determined the uptake of selenium in the mucosa and in the muscle layers of each segment. The colon was perfused before removal of the segments to ensure complete removal of blood-borne selenium. We found that the concentration of selenium was greater in the proximal colon than in the distal colon and that within each segment the uptake was higher in mucosa than in muscle. In addition, we determined the level of selenium in blood, serum, and liver at different times after the administration of various doses of selenium. Though the mechanism by which selenium prevents tumor development is unknown, the data indicate a correlation between the uptake of selenium in different segments of colon and inhibition of tumorigenesis.

Animals↗
PubMed1994

Enhancement of endothelium dependent relaxation in the rat aortic ring by selenium supplement.

OBJECTIVE: The aim was to examine the effect of selenium supplement on endothelium dependent relaxation in rat aortic rings. METHODS: Rats were supplemented with selenium for 3 d (intraperitoneal injection of 4.33 mumol sodium selenite-kg1 body weight.d-1). Saline injections served as controls. Rat aortic ring was precontracted with phenylephrine and endothelium dependent relaxation was produced by the addition of acetylcholine. RESULTS: Acetylcholine-induced endothelium dependent relaxation was enhanced in aortic rings from rats after receiving selenium supplement as compared to control rats. For comparison, endothelium independent vasodilators (sodium nitroprusside and cromakalim) were investigated. Selenium supplement did not affect the relaxation produced by these vasodilators. N-nitro-L-arginine methyl ester (L-NAME) abolished acetylcholine induced relaxation in aortic rings from animals with selenium supplement while indomethacin had no effect on the relaxation. Direct addition of selenium or glutathione peroxidase and glutathione into the organ bath had no effect on acetylcholine induced endothelium dependent relaxation. CONCLUSIONS: The enhanced relaxation after selenium supplement was due to an increase in the release of nitric oxide since L-NAME was effective in blocking the relaxation. The lack of an effect by indomethacin indicated little role for cyclooxygenase products in this system. Our results suggest that the effect of selenium supplement on endothelium dependent relaxation is mediated by cellular changes that cannot be mimicked by the direct addition of selenium or the selenium dependent enzyme glutathione peroxidase.

Acetylcholine↗
PubMed1982

Some metabolic interrelationships between toxic levels of cadmium and nontoxic levels of selenium fed to rats.

Male rats were fed vitamin E-adequate, Torula yeast-based diets for 30 days to assess the influence of dietary selenium (0, 0.1, or 1.0 ppm) on the toxicity of dietary cadmium (0, 30, or 60 ppm). At all selenium levels, increased cadmium intake depressed feed consumption, reduced feed efficiency and lowered body weight gain. In liver, concentrations of cadmium and zinc increased, and iron concentration decreased with increased intake of cadmium. Dietary selenium did not affect concentrations of cadmium, zinc, iron or copper in liver. Blood hemoglobin level declined and relative heart weight (g/100 g body wt) increased with increased intake of cadmium. Increased selenium intake partially alleviated the cadmium-induced depression in blood hemoglobin levels in rats fed diets that contained 30 ppm cadmium, and partially ameliorated the cadmium-induced increase in heart size in rats fed either 30 or 60 ppm cadmium. Hepatic and renal glutathione peroxidase (GSH-Px) activity increased with increased selenium intake. Increased cadmium intake did not affect renal GSH-Px activity. Hepatic GSH-Px activity in rats fed diets that contained 0.1 ppm selenium decreased with increased cadmium intake; however, hepatic GSH-Px activity was not affected by dietary cadmium in rats fed diets that contained 1.0 ppm selenium. Interactions between nontoxic levels of dietary selenium and relatively high levels of dietary cadmium apparently resulted in an antagonism of selenium metabolism by cadmium in some systems, and partial amelioration of cadmium toxicity by selenium in other systems

Animals↗
PubMed1986

Selenium content and glutathione peroxidase activity in the testis of the maturing rat.

In rats fed a diet with 0.25 mg Se/kg the testis selenium content rose during maturation. The value in 4-mo-old animals (7.0 mg Se/kg dry mass; 0.9 mg Se/kg wet mass) was six times higher than that in 20-d-old weanling rats. By comparison, the selenium content in the main selenium pools, muscle and liver, remained unchanged and rose by half, respectively. Due to the increased selenium requirement of the testis during its pubertal maturation the amount of selenium taken up by the male gonads was 50% of the amount deposited in muscle and liver, whereas before and after that period it was about 10%. Feeding animals a low vitamin E diet had no effect on the rise in testis selenium. Glutathione peroxidase activity was twice as high in 4-mo-old animals as in weanling rats. Because only a small percentage of the element in the male gonads was bound to the enzyme, the rise in testis selenium must have been due to other selenium compounds. The selenium content of the spermatozoa was about 21 mg Se/kg dry mass, which by far exceeded the level of this element in other compartments of the rat. The increase in testis selenium content coincided with the beginning of spermatogenesis, and it may therefore ensure the supply of adequate amounts of the element for the spermatozoa.

Animals↗
PubMed2002

Selenium deficiency in Fisher-344 rats decreases plasma and tissue homocysteine concentrations and alters plasma homocysteine and cysteine redox status.

The purpose of the present study was to determine the effect of graded amounts of dietary selenium on plasma and tissue parameters of methionine metabolism including homocysteine. Male weanling Fisher-344 rats (n = 7-8/group) were fed a selenium-deficient, torula yeast-based diet, supplemented with 0 (selenium deficient), 0.02, 0.05 or 0.1 microg (adequate) selenium (as selenite)/g diet. After 61 d, plasma total homocysteine and cysteine were decreased (P < 0.0001) and glutathione increased (P < 0.0001) by selenium deficiency. The concentrations of homocysteine in kidney and heart were decreased (P = 0.02) by selenium deficiency. The activities of liver betaine homocysteine methyltransferase, methionine synthase, S-adenosylmethionine synthase, cystathionine synthase and cystathionase were determined; selenium deficiency affected only betaine homocysteine methyltransferase, which was decreased (P < 0.0001). The ratios of plasma free reduced homocysteine (or cysteine) to free oxidized homocysteine (or cysteine) or to total homocysteine (or cysteine) were increased by selenium deficiency, suggesting that selenium status affects the normally tightly controlled redox status of these thiols. Most differences due to dietary selenium were between rats fed 0 or 0.02 microg selenium/g diet and those fed 0.05 or 0.1 microg selenium/g diet. The metabolic consequences of a marked decrease in plasma homocysteine and smaller but significant decreases in tissue homocysteine are not known.

Animals↗
PubMed1993

A prospective cohort study on toenail selenium levels and risk of gastrointestinal cancer.

BACKGROUND: Various animal studies and ecologic studies suggest an inverse association between low dietary selenium intake and risk of various types of cancer. PURPOSE: The goal of this prospective cohort study was to investigate the association between toenail selenium levels and risks of stomach cancer and colorectal cancer. METHODS: Our cohort study on diet and cancer started in The Netherlands in 1986 with enrollment of 120,852 subjects aged 55-69 years. Of this number, 58,279 were men and 62,573 were women. Following the case-cohort approach for analysis of the data, we randomly selected from the cohort a subcohort of 3500 subjects (1688 men and 1812 women). After 3.3 years of follow-up, 155 incident cases of microscopically confirmed stomach cancer, 313 cases of colon cancer, and 166 cases of rectal cancer had been detected in the cohort. Toenail selenium data were available for 104 patients with stomach cancer, 234 with colon cancer, and 113 with rectal cancer and for 2459 subjects from the subcohort. RESULTS: In a multivariate analysis, the relative rates (RRs) of stomach cancer for subjects in increasing quintiles of toenail selenium level were 1.00, 0.44, 0.59, 0.84, and 0.64 (trend, P = .491). For men, there was some evidence for an inverse association between toenail selenium levels and stomach cancer: The RR for those in the highest compared with the lowest quintile of toenail selenium was 0.40 (95% confidence interval = 0.17-0.96), but the trend was not statistically significant (P = .136). For stomach cancer in women, there was no negative association with toenail selenium levels. Toenail selenium level was not associated with the risk of colon or rectal cancer. After exclusion of cases diagnosed in the 1st year of follow-up, the RRs of colon cancer for increasing quintiles of toenail selenium were 1.00, 1.27, 1.17, 0.75, and 1.07 (trend, P = .544); for rectal cancer, RR estimates were 1.00, 1.73, 0.83, 1.58, and 1.12 (trend, P = .890). CONCLUSIONS: These data support a suggestive but inconsistent inverse association between selenium levels and risk of stomach cancer. Our findings, like those of other studies, do not suggest an inverse association with risk of colorectal cancer.

Aged↗
PubMed2000

Prospective study of serum selenium levels and incident esophageal and gastric cancers.

BACKGROUND: From March 1986 through May 1991, we conducted a randomized nutritional intervention trial, the General Population Trial, in Linxian, China, a region with epidemic rates of squamous esophageal and adenomatous gastric cardia cancers. We found that participants who received selenium, beta-carotene, and vitamin E had significantly lower cancer mortality rates than those who did not. In the current study, we examined the relationship between selenium levels measured in pretrial (1985) sera from participants and the subsequent risk of developing squamous esophageal, gastric cardia, and gastric non-cardia cancers during the trial. METHODS: This study was designed and analyzed in accord with a stratified case-cohort sampling scheme, with the six strata defined by sex and three age categories. We measured serum selenium levels in 590 case subjects with esophageal cancer, 402 with gastric cardia cancers, and 87 with gastric non-cardia cancers as well as in 1062 control subjects. Relative risks (RRs), absolute risks, and population attributable risk for cancers were estimated on the basis of the Cox proportional hazards models. All statistical tests are two-sided. RESULTS: We found highly significant inverse associations of serum selenium levels with the incidence of esophageal (P: for trend <10(-4)) and gastric cardia (P: for trend <10(-6)) cancers. The RR and 95% confidence interval (CI) for comparison of highest to lowest quartile of serum selenium was 0.56 (95% CI = 0.44-0.71) for esophageal cancer and 0.47 (95% CI = 0.33-0.65) for gastric cardia cancer. The population proportion of these cancers that is attributable to low selenium levels was 26.4% (95% CI = 14.45-38.36). We found no evidence for a gradient of serum selenium associated with incidence of gastric non-cardia cancer (P: for trend =.96), with an RR of 1.07 (95% CI = 0.55-2.08) for the highest to lowest quartile of serum selenium. CONCLUSIONS: Our study supports findings from previous prospective studies and randomized trials that variations in selenium levels affect the incidence of certain cancers. In the United States, where intervention trials of selenium are in the planning stages, consideration should be given to including populations at high risk for squamous esophageal and gastric cardia cancers.

Adult↗
PubMed1987

Diminished blood selenium levels in renal failure patients on dialysis: correlations with nutritional status.

Selenium deficiency has been implicated as contributing to the development of cardiovascular disease, skeletal muscle myopathy, anemia, increased cancer risk, and deranged immune function. Since these problems may also be associated with renal failure, and the kidney plays an important role in selenium homeostasis, we measured selenium and compared it with nutritional status in 24 stable hemodialysis patients, 12 chronic intermittent peritoneal dialysis patients, and 29 healthy controls. Whole blood and plasma selenium was determined by a spectrofluorometric method. For whole blood the mean (+/- SD) selenium levels were 0.11 +/- 0.02 micrograms/ml in controls vs. 0.071 +/- 0.01 micrograms/ml in hemodialysis cases and 0.052 +/- 0.006 micrograms/ml in peritoneal dialysis (p less than 0.005). Significant decreases were seen also for plasma and red blood cell selenium in all groups respectively. Pre- and postdialysis plasma and whole blood selenium levels showed no significant changes in both dialysis groups. However, predialysis residual peritoneal fluid did contain selenium (0.029 +/- 0.005 micrograms/ml). Some evidence of protein-energy undernutrition was noted in both dialysis groups compared with controls. However, no significant differences in nutritional parameters were noted between hemodialysis and peritoneal dialysis patients. When all groups were combined, significant correlations were found between whole blood selenium and serum albumin (r = 0.61; p less than 0.001), triceps skin fold in females (r = 0.62; p less than 0.001), and midarm muscle circumference in males (r = 0.71; p less than 0.001). We conclude that low blood selenium is present in renal failure patients undergoing hemodialysis. This abnormality is even greater in peritoneal dialysis cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2007

Plasma selenium over time and cognitive decline in the elderly.

BACKGROUND: Because brain oxidative stress is a cause of cognitive impairment, selenium, which is an antioxidant, may protect against cognitive decline. The aim of the study was to examine whether declining selenium levels over time are associated with cognitive decline in a cohort of community-dwelling French elderly. METHODS: During 1991-1993, 1389 subjects (age 60-71 years) were recruited into a 9-year longitudinal study with 6 waves of follow-up. Cognitive functions were evaluated by neuropsychologic tests. To take into account the entire set of cognitive measurements and the within-subject correlations between measures, we analyzed mixed linear and logistic models to study associations between selenium change and cognitive decline. RESULTS: After controlling for potential confounders, cognitive decline was associated with decreases of plasma selenium over time. Among subjects who had a decrease in their plasma selenium levels, the greater the decrease in plasma selenium, the higher the probability of cognitive decline. Among subjects who had an increase in their plasma selenium levels, cognitive decline was greater in subjects with the smallest selenium increase. There was no association between short-term (2-year) selenium change and cognitive changes. CONCLUSION: Selenium status decreases with age and may contribute to declines in neuropsychologic functions among aging people.

Age Factors↗
PubMed2003

Prostatic and peripheral blood selenium levels after oral supplementation.

PURPOSE: The dietary trace element selenium has been proposed to be a potential chemopreventive agent for prostate cancer. Epidemiological studies have suggested an inverse association between blood selenium and prostate cancer incidence. However, to our knowledge no study to date has examined selenium absorption by the prostate. Therefore, we determine whether oral selenium supplementation alters selenium levels within the prostate and/or peripheral blood. MATERIALS AND METHODS: In this prospective trial 51 men undergoing transurethral resection of the prostate for benign prostatic hyperplasia were randomly assigned to serve as controls or receive 200 microg selenium daily orally for 1 month. Sample size was calculated to detect a difference of 30 ng/gm in prostate tissue with a power of 80%. Peripheral blood was obtained at enrollment and subsequently at surgery, when prostate tissue was also sampled. Selenium levels were determined using inductively coupled plasma mass spectrometry. RESULTS: Baseline erythrocyte selenium was within the standard reference range. Supplementation increased erythrocyte (initial median 173 and final median 209 ng/ml, p = 0.008) and prostate (supplement median 241 and control median 196 ng/gm, p = 0.016) levels. Erythrocyte levels at surgery correlated poorly with prostate levels in the control (r = 0.18) and supplement (r = 0.07) groups. CONCLUSIONS: Oral selenium supplementation increases prostatic and peripheral blood levels in men in a nonselenium deficient population. Blood and prostate levels correlated poorly, suggesting that peripheral blood measurements are a poor indicator of prostatic selenium content.

Aged↗
PubMed2006

Possible involvement of selenium in Staphylococcus aureus inhibition in cow's whey.

Previous investigations have shown that selenium supplementation inhibits growth of mastitis pathogens in cow's milk. The present study was performed to clarify the role of selenium in defence mechanisms of mammary gland. We have examined the effects of selenium supplementation on Staphylococcus aureus growth inhibiting activity in whey. Six selenium-supplemented and six non-supplemented Estonian dairy cows were used for this study. Selenium-supplemented cows received 4 mg organic selenium in the form of selenium yeast in their daily diet for 8-week period. Cows from non-supplemented group received the same amount of yeast free of selenium in their diet. All cows had initially low blood glutathione peroxidase (GPx) activity (<or=1.02 microkat/g Hb). During the 8-week experiment these cows had low somatic cell count (<300,000 cells/ml) and negative bacteriological findings in their quarter milk samples. Bacterial growth inhibitory activity in specific whey fractions was clearly evident in 3 out of 6 cows supplemented with selenium. The inhibitory effect was more profound if the cow's blood GPx activity exceeded 4 microkat/g Hb, whereas in non-supplemented cows the inhibition of S. aureus growth was not observed. This study confirms the presence of selenium-dependent antibacterial activity in cow's milk.

Animals↗
PubMedDate not supplied

Effects of oral administration of toxic levels of lead and selenium upon concentration of different elements in the liver of broiler chicks.

Broiler chicks fed lead or selenium for varying periods were later intoxicated with two levels of either of these elements. In this way different groups of chicks were exposed to lead or selenium alone or a combination of these two. Lead caused increased liver concentrations of lead and iron. Selenium administration increased liver selenium and iron levels while liver copper decreased. Concurrent administration of lead and selenium greatly enhanced the accumulation of both elements in the liver and increased the liver iron. Lead partially counteracted the depression of liver copper caused by selenium. Mortality due to concurrent exposure to lead and selenium was lower when vitamin E was added to the feed. Body weights were markedly suppressed by selenium. The concurrent administration of lead partially alleviated the growth depression caused by selenium. Selenium fed birds had increased relative weights of liver and heart but this increase was of lesser degree in birds given both elements.

Animals↗
PubMed1999

Association of reduced selenium status in the aetiology of recurrent miscarriage.

OBJECTIVE: To determine whether recurrent miscarriage is associated with reduced selenium status. DESIGN: Case-control study. SETTING: Department of Obstetrics and Gynaecology, Glasgow Royal Infirmary and Glasgow Royal Maternity Hospital. POPULATION: Twenty nonpregnant women with a history of unexplained recurrent miscarriage, and 47 nonpregnant parous women with a history of at least one successful pregnancy and no more than one miscarriage. METHODS: A 7 mL blood sample from each woman was collected into lithium heparin 'vacutainer' tubes. Samples were centrifuged at 3000 g for 15 minutes, and plasma was extracted and stored at -20 degrees C. Selenium concentrations were measured using a fluorescence spectrophotometer. The selenium concentrations in the two groups were compared and the differences examined using the Student's t test. MAIN OUTCOME MEASURES: Plasma selenium concentration (microg/L). RESULTS: The mean selenium concentration for women with a history of unexplained recurrent miscarriage was 67.7 microg/L (SD 16.4). The selenium level for the women with no history of recurrent miscarriage was 70.3 microg/L (SD 12.7). There was no difference in selenium concentrations between the two groups (P = 0.53). CONCLUSIONS: In this study there is no association between unexplained recurrent miscarriage and reduced selenium status, implying that reduced selenium status is not a factor in the pathogenesis of recurrent miscarriage. We can find no rationale for a trial of selenium therapy in women with a history of recurrent miscarriage.

Abortion, Habitual↗
PubMed1978

Blood glutathione peroxidase activity in horses in relation to muscular dystrophy and selenium nutrition.

The activity of glutathione peroxidase, a selenium containing enzyme, was measured in the blood of horses to determine its usefulness as an indicator of selenium status. In 15 horses the enzyme activity was positively related to the blood selenium concentration (P less than .001, r-0.98) over the range of enzyme activities of 8.2 to 140 units (mumoles NADP-oxidised/min/gHb) and selenium concentrations of 0.24 to 2.74 mumol/l. In a group of 8 horses which 2 foals had died with lesions of muscular dystrophy the enzyme activity increased from a mean of 11.8 units before treatment with selenium to 34.5 units after 2 intravenous injections of sodium selenite given one month apart. Another group of 8 horses grazing paddocks adjacent to this affected group did not receive any selenium treatment and had a mean enzyme activity of 11.9 units. Blood glutathione peroxidase activity was measured in 50 pasture-fed horses and 180 stall-fed horses. The range of activities found (7 to 158 units) indicated that selenium intake in horses varied widely between localities. All pasture-fed horses grazing areas where muscular dystrophy had occurred in foals had low activities (less than 20 units). In stall-fed horses the enzyme activity was influenced by selenium treatment, and horses which had been treated usually had higher activities than horses in the same stable with no history of selenium treatment. It was concluded that blood glutathione peroxidase is a suitable indicator of selenium status in horses.

Animals↗