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PubMed2003

Potential therapeutic effect of antioxidants in experimental diabetic retina: a comparison between chronic taurine and vitamin E plus selenium supplementations.

Although good glycaemic control can delay the development and progression of diabetic retinopathy, new therapies are needed to obtain a better control of this diabetic complication. Oxidative stress seems to be a contributing factor in diabetic retinal alterations, therefore, it has been suggested that antioxidants may be beneficial in reducing diabetic retinal changes. However, many questions are still open. In fact, it remains to be ascertained which antioxidants are the most active when they are chronically administered in vivo and their effective dosages. Therefore, we compared the effect of chronic taurine supplementations versus a mixture of vitamin E + selenium on biochemical retinal changes induced by diabetes at different stages of the disease. Briefly, streptozotocin (STZ) diabetic rats were administered for 4 months following the dietary supplements: (a) 2% (w/w) taurine; (b) 5% (w/w) taurine; (c) 200 IU vitamin E + 8 mg selenium/kg diet (d) 500 IU vitamin E + 8 mg selenium/kg diet. In STZ diabetic rat in poor metabolic control (i.e. serum glucose >16.5 mmol/l), at 2, 4, 8, 16 weeks following the onset of diabetes, retinal conjugated dienes (CD) and lipid hydroperoxides (LP) were significantly and progressively increased, while sodium pump activity was gradually and significantly reduced. In taurine and vitamin E + selenium supplemented diabetic rats, glycaemia and body weight were not significantly different from those of non-supplemented diabetic animals. In diabetic rats, 2 and 5% taurine significantly decreased CD. This reduction is long lasting. Regarding CD, both vitamin E + selenium supplementations reduced CD only during the first 4 weeks of diabetes. Two percent taurine supplementation significantly lowered LP for the first 8 weeks of the disease while 5% taurine-induced-reduction lasted for the whole experimental time. A 200 IU vitamin E + 8 mg selenium supplementation did not significantly modify LP, while 500 IU vitamin E + 8 mg selenium significantly lowered them for the whole studied period. Finally, taurine preserved ATPase activity being more effective at 5% than 2%. Two hundred IU vitamin E + 8 mg selenium did not generally modify pump activity, while 500 IU vitamin E + 8 mg selenium partially prevented the decrease in pump activity. We conclude that taurine and vitamin E + selenium supplementations ameliorate biochemical retinal abnormalities caused by diabetes. These effects are dose- and time-dependent Moreover, the effect of taurine on CD is longer lasting than that of vitamin E + selenium. In addition, taurine seems to better preserve ATPase activity in comparison with vitamin E + selenium. Finally, in diabetic animals a negative correlation is found between CD and LP on one side and Na+K+ATPase activity on the other; thus, lipid peroxidation and pump activity seem to be associated. The same inverse correlations are present in vitamin E + selenium supplemented diabetic rats, but are lost in taurine supplemented animals. Therefore, taurine effects may not be simply mediated by its antioxidant activity. Thus, chronical (4 months) taurine and vitamin E + selenium supplementations reduce biochemical retinal alterations in diabetic rat in poor metabolic control.

Animals↗
PubMed1993

Protective effects of selenium on cadmium toxicity in rats: role of altered toxicokinetics and metallothionein.

Selenium prevents the toxicity of the carcinogenic metal cadmium through undefined mechanisms. In this study, we determined the effects of selenium on cadmium toxicokinetics and on the ability of cadmium to induce metallothionein, a metal-binding protein that is thought to confer tolerance to cadmium toxicity. To assess the acute protective effects of selenium, male Wistar (WF/NCr) rats were given selenium (as SeO2; 10 mumol/kg, sc) at -24, 0, and +24 h relative to cadmium (as CdCl2; 45 mumol/kg, sc). Over a 14-d period this dose of cadmium killed 6 out of 10 rats, while 100% of the cadmium-treated rats given concurrent selenium treatments survived. The acute increases in testicular weight that were seen with cadmium, indicative of edematous damage, were also prevented by concurrent selenium treatments. Further studies assessed the distribution and excretion of cadmium and its ability to induce metallothionein in rats given 40 mumol Cd/kg, sc, at time 0 and selenium (10 mumol/kg, sc) at -24 and 0 h. Selenium treatments enhanced cadmium accumulation at 24 h in the liver (23%), testes (145%), and epididymis (35%) but reduced renal accumulation by more than half. Urine samples, collected at 0-3, 3-6, and 6-24 h following cadmium administration, indicated a markedly reduced excretion of cadmium in selenium treated rats during all time periods. The synthesis of metallothionein was stimulated to a much lesser extent by cadmium in selenium-treated rat kidney (41% decrease) but was unaffected in liver. The levels of cadmium-binding proteins within the testes were markedly reduced by cadmium treatment, an effect unmodified by selenium treatments. These results suggest selenium prevents acute cadmium toxicity through a mechanism that does not involve induction of metallothionein and in spite of a markedly enhanced retention of cadmium.

Animals↗
PubMed1984

Dietary selenium levels needed to maintain balance in North American adults consuming self-selected diets.

Dietary selenium intake and selenium balance were measured during 4 1-wk metabolic periods over the course of 12 months in 27 free-living adult volunteers consuming self-selected diets. Men consumed more selenium in their diets than women (90 +/- 4 versus 74 +/- 3 micrograms/day), but plasma selenium levels were similar for both sexes (136 +/- 4 versus 133 +/- 4 ng/ml, respectively). Neither dietary selenium intake nor plasma selenium levels varied seasonally. Regression of selenium balance versus intake indicated that adult men needed 80 micrograms SE/day to stay in balance, whereas women needed only 57 micrograms SE/day. When balance and intake were adjusted for body weight, the sex difference disappeared, and both men and women needed about 1 microgram of dietary selenium per kg of body weight per day to maintain balance. The levels of dietary selenium reported here as necessary to maintain balance in North American adults are considerably higher than those previously reported as needed for balance in adult women from New Zealand, a country where low selenium status is common. Our results indicate that the levels of dietary selenium needed to achieve balance are a function of lean body mass and historical selenium intake.

Adult↗
PubMed2003

Selenium and iodine supplementation of rural Tibetan children affected by Kashin-Beck osteoarthropathy.

BACKGROUND: Kashin-Beck disease is an osteoarthropathy endemic in selenium- and iodine-deficient areas around Lhasa, Tibet. OBJECTIVE: We assessed the efficacy of selenium supplementation on disease progression. DESIGN: A double-blind, randomized controlled trial of selenium supplementation was carried out in 324 children aged 5-15 y who had Kashin-Beck disease. Two hundred eighty children received iodized oil before being randomly assigned to receive selenium or placebo, and a control group of 44 subjects was not supplemented at all. Clinical and radiologic signs, selenium status, urinary iodine, and thyroid function were evaluated at baseline and at 12 mo. RESULTS: The frequencies of joint pain, decreased joint mobility, and radiologic abnormalities were not significantly different between the 3 groups at 12 mo. Height-for-age z scores increased significantly in the subjects who received placebo and iodine or selenium and iodine. In contrast, unsupplemented control subjects did not recover from growth retardation. Serum selenium concentrations at 12 mo were within the reference range and were significantly greater in the selenium-iodine group than in the placebo-iodine group. Serum thyroid hormone concentrations were within the reference ranges after the administration of iodine, and these values were not significantly affected by selenium supplementation. CONCLUSIONS: The results of this study do not rule out the possibility that selenium may help to prevent the occurrence of Kashin-Beck disease. However, selenium supplementation had no effect on established Kashin-Beck disease, growth, or thyroid function once iodine deficiency was corrected. These results suggest that iodine, but not selenium, deficiency should be corrected in Tibetan children with Kashin-Beck disease.

Adolescent↗
PubMed2005

Prostate cancer risk and DNA damage: translational significance of selenium supplementation in a canine model.

Daily supplementation with the essential trace mineral selenium significantly reduced prostate cancer risk in men in the Nutritional Prevention of Cancer Trial. However, the optimal intake of selenium for prostate cancer prevention is unknown. We hypothesized that selenium significantly regulates the extent of genotoxic damage within the aging prostate and that the relationship between dietary selenium intake and DNA damage is non-linear, i.e. more selenium is not necessarily better. To test this hypothesis, we conducted a randomized feeding trial in which 49 elderly beagle dogs (physiologically equivalent to 62-69-year-old men) received nutritionally adequate or supranutritional levels of selenium for 7 months, in order to mimic the range of dietary selenium intake of men in the United States. Our results demonstrate an intriguing U-shaped dose-response relationship between selenium status (toenail selenium concentration) and the extent of DNA damage (alkaline Comet assay) within the prostate. Further, we demonstrate that the concentration of selenium that minimizes DNA damage in the aging dog prostate remarkably parallels the selenium concentration in men that minimizes prostate cancer risk. By studying elderly dogs, the only non-human animal model of spontaneous prostate cancer, we have established a new approach to bridge the gap between laboratory and human studies that can be used to select the appropriate dose of anticancer agents for large-scale human cancer prevention trials. From the U-shaped dose-response, it follows that not all men will necessarily benefit from increasing their selenium intake and that measurement of baseline nutrient status should be required for all individuals in prevention trials to avoid oversupplementation.

Age Factors↗
PubMed1980

The requirement and toxicity of selenium in rainbow trout (Salmo gairdneri).

This study measured the dietary selenium requirement of rainbow trout and their response to excessive levels of dietary selenium. A dietary selenium level of 0.07 microgram/g dry feed with a waterborne selenium level of 0.4 +/- 0.2 microgram/liter and a dietary vitamin E level of 0.4 IU/g dry diet was sufficient to prevent frank selenium deficiency symptoms. Maximal plasma GSH.px activity was obtained at a dietary selenium level between 0.15 and 0.38 microgram/g dry feed which is less than the average selenium concentration of commercial diets. Chronic dietary selenium toxicity occurred at 13 microgram selenium/g dry feed. Major effects of selenium toxicity were reduced growth rate, poor feed efficiency and a high number of mortalities. No histopathological lesions or significant deviation in the investigated blood parameters or liver somatic index were detected in trout raised on diets containing 13 microgram selenium/g dry feed. Tissue selenium analysis indicated that trout can maintain homeostasis with dietary selenium levels up to 1.25 microgram/g dry feed. The selenium uptake and accumulation in tissues of trout reared on diets containing in excess of 3 microgram/g dry feed may ultimately be toxic to trout if maintained over long periods of time.

Animals↗
PubMed1983

Effect of increased dietary carbohydrate on selenium metabolism and toxicity in rainbow trout (Salmo gairdneri).

Juvenile trout were reared on either a high available carbohydrate (HC) or low available carbohydrate (LC) diet supplemented with from 0 to 10 micrograms selenium per gram of diet for 16 weeks, to determine if excess liver glycogen deposition affected the metabolism and toxicity of dietary selenium. Trout reared on the HC diet with 10 micrograms selenium per gram diet first demonstrated signs of selenosis and had significantly higher (P less than 0.05) liver selenium levels than trout reared on the LC diet with 10 micrograms selenium per gram diet after 16 weeks, indicating that excess dietary carbohydrate enhances dietary selenium toxicity in trout. The mechanism of the interaction is unclear since neither selenium elimination rates nor carcass and kidney selenium levels were affected by the dietary carbohydrate level. Trout reared on high dietary selenium diets (10 micrograms/g) had an increased incidence of renal calcinosis. In addition, liver copper levels were significantly affected by both dietary selenium and liver glycogen content indicating a significant copper-selenium and copper-glycogen interaction in trout. The development of renal calcinosis and the copper interactions suggest a variety of toxic effects of selenium on trout that may all be responsible for the observed changes in growth and feed efficiency.

Animal Feed↗
PubMed1989

Maternal and fetal selenium concentrations and their interrelationships in dairy cattle.

Paired dam-fetus serum, whole blood and liver samples were collected from 101 pregnant dairy cattle at slaughter to establish mean values for fetal tissue selenium concentration and to determine relationships between maternal and fetal selenium status. Samples were assayed for selenium concentration in serum, whole blood and liver and for whole blood glutathione peroxidase (GSH-Px) activity. Fetal age was estimated from fetal crown-to-rump length. Mean fetal liver (2.14 micrograms/g dry wt) and serum (21.4 ng/ml) selenium concentrations and whole blood GSH-Px activity (21.6 mu/ml) differed (P less than 0.0001, 0.0001 and 0.01, respectively) from corresponding maternal values (0.95 micrograms/g liver dry wt; 44.0 ng/ml; 16.7 mu/ml, respectively), while no differences were found between whole blood or erythrocyte selenium concentrations. Fetal liver selenium concentration was greater than corresponding maternal liver selenium in 99% (96/97) of the dam-fetal pairs, suggesting efficient placental transfer and fetal concentrating ability. Maternal liver selenium concentration was most highly correlated to all fetal tissue selenium concentrations and used to develop prediction models. These data suggest that selenium efficiently passes the placenta, and based on published values of adequate adult liver selenium concentrations and maternal-fetal relationships, we suggest an adequate liver selenium concentration in the bovine fetus to be greater than 2.2 micrograms/g liver dry wt, and in whole blood, greater than 120 ng/ml.

Animals↗
PubMed2003

Dietary selenium intake modulates thyroid hormone and energy metabolism in men.

Most studies of selenium and thyroid hormone have used sodium selenite in rats. However, rats regulate thyroid hormone differently, and selenite, which has unique pharmacologic activities, does not occur in foods. We hypothesized that selenium in food would have different effects in humans. Healthy men were fed foods naturally high or low in selenium for 120 d while confined to a metabolic research unit. Selenium intake for all subjects was 47 microg/d (595 nmol/d) for the first 21 d, and then changed to either 14 (n = 6) or 297 (n = 5) microg/d (177 nmol/d or 3.8 micromol/d) for the remaining 99 d, causing significant changes in blood selenium and glutathione peroxidase. Serum 3,3',5-triiodothyronine (T3) decreased in the high selenium group, increased in the low selenium group, and was significantly different between groups from d 45 onward. A compensatory increase of thyrotropin occurred in the high selenium group as T3 decreased. The changes in T3 were opposite in direction to those reported in rats, but were consistent with other metabolic changes. By d 64, the high selenium group started to gain weight, whereas the low selenium group began to lose weight, and the weight changes were significantly different between groups from d 92 onward. Decreases of serum T3 and compensatory increases in thyrotropin suggest that a subclinical hypothyroid response was induced in the high selenium group, leading to body weight increases. Increases of serum T3 and serum triacylglycerol accompanied by losses of body fat suggest that a subclinical hyperthyroid response was induced in the low selenium group, leading to body weight decreases.

Body Composition↗
PubMed1998

Glutathione peroxidase is not a functional marker of selenium status in the neonatal period.

BACKGROUND: The antioxidant enzyme glutathione peroxidase is a selenoprotein that, in adults with low selenium intakes, has a strong linear relationship with blood selenium and hence is used as a functional indicator of selenium status. Our aim was to evaluate glutathione peroxidase as a functional marker of selenium status in preterm infants. METHODS: Erythrocyte glutathione peroxidase activity and plasma and erythrocyte selenium were measured between days 1-5 and then weekly until discharge in 63 preterm infants with mean +/- standard error birth weight and gestation of 1572+/-60g and 30.7+/-0.3 weeks. A healthy reference group of term infants (n = 46) was assessed at day 5 and at 6 weeks. RESULTS: In preterm infants, over the first 3 months, the association of glutathione peroxidase activity with erythrocyte selenium was weak and inconsistent and nonexistent with selenium intake or plasma selenium. No correlations between any of these indicators were evident for term infants. In preterm infants, plasma and erythrocyte selenium declined over the first 6 weeks (p < 0.01), while glutathione peroxidase activity increased (p < 0.05). In term infants, plasma selenium increased (p < 0.001), but there was no change in erythrocyte selenium or glutathione peroxidase activity. For preterm infants, glutathione peroxidase activities at weeks 4 and 6 were associated with maximum inspired oxygen concentration, ventilator pressure, and days of ventilation. CONCLUSIONS: This data is consistent with animal and in vitro evidence that glutathione peroxidase may be confounded by oxygen. We conclude that erythrocyte glutathione peroxidase activity is not a reliable functional marker of preterm selenium status in the neonatal period.

Biomarkers↗
PubMed1995

Comparisons of selenite and selenium yeast feed supplements on Se-incorporation, mastitis and leucocyte function in Se-deficient dairy cows.

The dairy cows at the Estonian Agricultural University appeared to have an extremely low selenium status. The selenium level was 5.6 micrograms/l in whole blood and 3.2 micrograms/l in milk, on average. The blood glutathione peroxidase was consequently extremely low. The effects of organic selenium (selenized yeast) and sodium selenite were compared in a feeding experiment on 100 dairy cows. Selenium incorporation, udder health and the in vitro function of blood neutrophils were monitored. Supplementation of the feed either with 0.2 ppm organic selenium or sodium selenite for 8 weeks, increased the blood selenium level (geometric mean) within this period from the back-ground level (about 5.6 micrograms/l) to 167 (Se-yeast) and to 91 micrograms/l (selenite). The respective change in whole blood glutathione peroxidase (GSH-PX) was from 0.22 to 3.0 (Se-yeast) and to 2.3 (selenite) microKat/g Hb. Blood GSH-PX continued to increase up to 10 weeks after the supplementation was stopped. The bioavailability of yeast selenium was superior to selenite: the relative bioavailability (selenite = 1) of yeast selenium was 1.4 if blood GSH-PX, 1.9 if blood selenium, and 2.7 if milk selenium was used as the response criterion. Selenium-supplementation showed a positive effect on udder health. The percentage of quarters harbouring mastitis pathogens dropped from 22.9 to 13.0 in the Se-yeast group and from 18.4 to 7.4 in the selenite group during the supplementation period. The effect of selenium on mastitis was also reflected as a decrease in the output of milk somatic cells and N-acetyl-beta-D-glucosaminidase (NAGase). The time-luminescence profile of zymosan-induced activity of blood neutrophils became skewed to the left in Se-supplemented cows.

Acetylglucosaminidase↗
PubMed1996

Assessment of selenium and vitamin E deficiencies in dairy herds and clinical disease in calves.

Because of the very low concentrations of selenium in the dry matter of grass, grass silage, hay and maize silage Slovenian dairy herds need to be supplemented with selenium. Selenium in the form of mineral and feed mixtures maintained adequate mean (sd) blood serum selenium concentrations of 43.9 (27.6) to 65.3 (18.5) micrograms/litre in lactating cows, but in late lactation and in the dry period when only mineral mixtures were used, about 60 per cent of the cows had marginal serum selenium concentrations, mainly because of the low intake of the mineral supplement. In 18 herds which were either unsupplemented or irregularly supplemented with selenium, the mean (sd) concentrations in blood serum were 13.7 (5.5) micrograms/litre and 17.4 (9.2) micrograms/litre, respectively, for selenium and 2.98 (2.72) mg/litre and 1.62 (1.73) mg/litre for vitamin E, indicating that under extensive farming conditions in Slovenia the lack of both micronutrients may be responsible for nutritional muscular dystrophy in calves. Among 37 clinical cases, cardiorespiratory signs predominated in 25 of the calves and skeletal myopathy was dominant in 12. A very low mean serum selenium concentration [9.7 (7.2) micrograms/litre] and typically high activities of aspartate aminotransferase (AST) [1125 (373) U/litre] and creatine kinase (CK) [9169 (3681) U/litre) were observed for the myocardial form of the disease, and 2797 (550) U/litre and 22,650 (13,500) U/litre were observed for the skeletal form of the disease. A highly significant (P < 0.0001) difference in the selenium concentration of liver dry matter between the regularly supplemented [402 (207) micrograms/kg] and irregularly supplemented [173 (69) micrograms/kg] herds was observed. If a minimum value of 300 micrograms/kg of liver dry matter is accepted as the criterion for the determination of adequate selenium status, 93 per cent of the samples from the irregularly supplemented herds were selenium deficient. A similar proportion was estimated to be selenium deficient when the criterion was taken to be 30 micrograms selenium/litre of blood serum.

Animal Feed↗
PubMed1980

Liver necrosis and lipid peroxidation in the rat as the result of paraquat and diquat administration. Effect of selenium deficiency.

Paraquat and diquat facilitate formation of superoxide anion in biological systems, and lipid peroxidation has been postulated to be their mechanism of toxicity. Paraquat has been shown to be more toxic to selenium-deficient mice than to controls, presumably as the result of decreased activity of the selenoenzyme glutathione peroxidase. The present study was designed to measure lipid peroxidation and to assess toxicity in control and selenium-deficient rats given paraquat and diquat. Lipid peroxidation was measured by determining ethane production rates of intact animals; toxicity was assessed by survival and by histological and serum enzyme evidence of liver and kidney necrosis. Paraquat and diquat were both much more toxic to selenium-deficient rats than to control rats. Diquat (19.5 mumol/kg) caused rapid and massive liver and kidney necrosis and very high ethane production rates in selenium-deficient rats. The effect of paraquat (78 mumol/kg) was similar to that of diquat but was not as severe. Acutely lethal doses of paraquat (390 mumol/kg) and diquat (230 mumol/kg) in control rats caused very little ethane production and no evidence of liver necrosis. These findings suggest that paraquat and diquat exert their acute toxicity largely through lipid peroxidation in selenium-deficient rats. Selenium deficiency had no effect on superoxide dismutase activity in erythrocytes or in 105,000 g supernate of liver or kidney. Glutathione peroxidase, which represents the only well-characterized biochemical function of selenium in animals, was dissociated from the protective effect of selenium against diquat-induced lipid peroxidation and toxicity by a time-course study in which selenium-deficient rats were injected with 50 mug of selenium and later given diquat (19.5 mumol/kg). Within 10 h, the selenium injection provided significant protection against diquat-induced lipid peroxidation and mortality even though this treatment resulted in no rise in glutathione peroxidase activity of liver, kidney, lung, or plasma at 10 h. This suggests that a selenium-dependent factor in addition to glutathione peroxidase exists that protects against lipid peroxidation.

Animals↗
PubMedDate not supplied

Selenium renal homeostasis is impaired in patients receiving long-term total parenteral nutrition.

Selenium deficiency has been reported previously in patients receiving long-term total parenteral nutrition (TPN) without selenium supplementation in their solutions. The recommended dietary allowance for selenium is 0.87 microgram/kg, of which 80% is absorbed. We studied 28 adult long-term TPN patients aged 21 to 79 years (mean, 51.2 +/- 3.0 years) who have received TPN for 8.3 +/- 4.4 years. They receive 40 to 60 micrograms of selenium daily in their TPN solution. Twenty-one (75%) of 28 patients had low serum selenium levels. Of the patients with low serum selenium levels, 15 (73%) had elevated urinary selenium losses. However, no significant correlation between serum or urine selenium levels and glomerular filtration rate (measured by indium-111-diethylenetriamine pentaacetic acid clearance) or renal tubular function was observed. We conclude that the previously described renal homeostatic mechanism for selenium conservation may be significantly impaired in patients receiving long-term TPN. Such patients may require much larger doses of selenium than previously recommended. Therefore, patients receiving long-term TPN should have their serum selenium level monitored even though they receive daily selenium supplementation.

Adult↗
PubMed2004

Selenium substitution has no direct effect on thyroid hormone metabolism in critically ill patients.

BACKGROUND: In severe illness, plasma selenium levels are decreased; a decreased activity of the selenoenzyme 5'-deiodinase has been hypothesized to contribute to low tri-iodothyronine (T3) levels in non-thyroidal illness (NTI) syndrome in these patients. OBJECTIVE: To analyse the influence of selenium substitution on thyroid hormone metabolism in patients with severe sepsis. DESIGN: A prospective, randomized, controlled study at the medical internal intensive care unit of the University of Munich. Results are for 41 consecutive patients with severe sepsis with an APACHE II score >15. Patients received either sodium selenite (500 microg/day for the first 3 days, reducing to 250 and then 125 microg/day every 3 days) or a placebo. RESULTS: At study entry, APACHE II score and demographics were identical in both groups. The mean levels of TSH, free tri-iodithyronine and total T3, as well as plasma selenium and selenium-dependent peroxidase (GSH-Px) activity, were decreased. Plasma selenium and GSH-Px activity were normalized on days 3, 7 and 14 in patients receiving selenium (n=21), but remained below normal in the control patients. Patients receiving selenium had a better clinical outcome and thyroid hormone levels normalized earlier. Thyroid hormone levels increased in patients who showed clinical improvement, independent of selenium levels or selenium substitution. CONCLUSIONS: Selenium substitution in patients with NTI improves morbidity, but has no direct effect on the free and total thyroid hormones. In severely ill patients, decreased deiodinase activity due to low plasma selenium levels seems unlikely. After clinical revival, TSH and then the thyroidal hormones normalize independently of selenium substitution.

APACHE↗
PubMed2004

Selenium deficiency as a model of experimental pre-eclampsia in rats.

Epidemiological studies and in vitro analysis demonstrate correlations between selenium status and human pre-eclampsia (PET). Selenium is an essential component in the anti-oxidant proteins glutathione peroxidase and thioredoxin reductase, which are produced in lower amounts in pre-eclamptic placenta. This study examined the effect of modulating dietary selenium content in pregnant rats. Rats were fed diets containing no selenium, 239 microg/kg selenium or 1000 microg/kg selenium, four weeks prior to and following conception. Significant pregnancy-specific increases in systolic blood pressure (116.4 +/- 5.2 mmHg vs 108 +/- 6.8 mmHg vs 111.4 +/- 4.7 mmHg) and proteinuria (9.68 +/- 2.12 microg/ml vs 5.93 +/- 1.59 microg/ml vs 4.43 +/- 0.96 microg/ml) were demonstrated in animals fed a selenium free-diet when compared with normal or high selenium diets. Placental weight and pup number were not affected by selenium deprivation, however a significant decrease in the pup weight was evident. Selenium deprivation caused dose-dependent decreases in liver glutathione peroxidase (28.55 +/- 3.82 mmoles/min/mg vs 34.68 +/- 8.64 mmoles/min/mg) and thioredoxin reductase (2.37 +/- 1.25 U/mg vs 6.68 +/- 1.82 U/mg) activity, whereas superoxide dismutase activity remained constant. Placental activity of these enzymes also decreased leading to oxidative stress as measured by increased lipid peroxides (17.92 +/- 1.78 micromoles/mg vs 8.30 +/- 5.52 micromoles/mg) and protein carbonyls in tissue extracts from selenium-free animals. These results suggest that selenium deficiency in pregnant rats leads to symptoms similar to those seen in human PET and may provide an experimental model for studying this complex disease.

Animals↗
PubMed1979

Transfer of dietary selenium to milk.

Twenty-five lactating cows were used in groups of five to study the amounts of dietary selenium transferred to milk. Amounts of dietary selenium varied from deficient to five times the adequate concentration and ranged between 41 ppb and 828 ppb. Sodium selenite and brewers grains, a rich naturally occurring source of selenium, supplied supplemental selenium. Selenium in milk and plasma were related to the amount consumed, but the response was nonlinear since 4.8% of the added selenium was transferred to milk with a deficient diet but only .9% of the amount of added selenium was in milk of cows consuming diets adequate in selenium. Nineteen percent of the selenium furnished in brewers grains appeared in the milk when the ration was deficient in selenium. The small amounts of selenite selenium transferred from the diet to milk were too little (5.5 micrograms/kg) to be a potential hazard to human health when a diet containing .1 to .2 ppm of selenium was fed to dairy cows, an amount sufficient to meet the cow's dietary needs.

Animals↗
PubMed1984

Selenium content and glutathione peroxidase activity in tissues of the dairy cow after short-term feeding.

The effect of selenium and vitamin E on concentrations of selenium and selenium-dependent glutathione peroxidase in tissues of dairy cows was studied. Selenium (5 mg/day) and vitamin E (2 g/day) were supplemented for 10 days in a 2 X 2 factorial arrangement. Selenium supplementation increased content of selenium in whole blood, plasma, ovary, and liver and increased activity of selenium-dependent glutathione peroxidase in liver. Activity of selenium-dependent glutathione peroxidase in follicular fluid was closely correlated with selenium-dependent glutathione peroxidase in plasma. Significant activity of selenium-dependent glutathione peroxidase was detected in luteal tissue of the ovary. Relationships were linear between content of selenium and selenium-dependent glutathione peroxidase in ovary, uterus, and adrenal tissues.

Administration, Oral↗