Metabolism in rats of selenium from intrinsically and extrinsically labeled isolated soy protein

Absorption, retention and tissue accumulation by rats of 75Se from intrinsically labeled isolated soy protein were compared with utilization of 75Se from the extrinsic sources of [75Se]selenite, [75Se]selenate or [75Se]selenomethionine. Extrinsic sources of selenium were given by gavage or mixed with isolated soy protein. There were no differences in absorption and retention of 75Se from intrinsically labeled soy diet compared to the three extrinsically labeled soy diets. Of the three extrinsic sources tested, 75Se from selenate was better absorbed than from selenite or selenomethionine when incorporated into a soy diet. Absorption of 75Se was significantly lower when given to animals in gavage solution than when mixed with soy diets. After a 14-d test period, retention of 75Se was the same for all four soy diet groups. In gavaged groups, 75Se from selenomethionine was retained to a greater extent than 75Se from selenite. The liver, testes and kidney accumulated more 75Se from the test meal than did the blood and lungs. In the testes more 75Se from selenite and selenate was accumulated than from selenomethionine-labeled diets. Selenium absorption from the soy isolate source was very high (86-96%), indicating that, although soy does not normally contain high levels of selenium, the selenium present is well absorbed from this plant source.     

Comparative studies of selenium-75 (selenite and selenomethionine) absorption from various milk diets in suckling rats

Selenium (Se) absorption was studied in human milk, bovine milk and infant formula (Similac) using suckling rats as a model. The effect of age on Se absorption from the three milk diets extrinsically labeled with 75Se, either as selenite or selenomethionine, was also investigated. Milk diets were fed by gastric intubation and the radioactivity in the carcass, gastrointestinal tract and the liver were measured 3 h after feeding. There was no difference in [75Se]selenite absorption from the three milk diets between 8-20 d of age. However, significantly higher quantity of 75Se was absorbed from all three milk diets by 20-d-old rats than by the younger rats (46 vs. 32%). This increase in [75Se]selenite absorption with advancing age is opposite to what has been found for most other trace elements. When rats were fed milk diets labeled with [75Se]selenomethionine, the absorption of 75Se was approximately twofold higher in all age groups compared with 75Se absorption from selenite. No difference in [75Se]selenomethionine absorption existed among the three milk diets in 8- or 10-d-old suckling rats. However, at 15 d of age [75Se]selenomethionine absorption from human milk was higher (82%) than from either bovine milk (72%) or infant formula (72%). Between 8 and 20 d of age, absorption of [75Se]selenomethionine from the three milk diets decreased with advancing age. Adding sodium selenate to increase the total nonradioactive Se of human milk, bovine milk (endogenous plus the added selenium) did not affect the absorption of either [75Se]selenomethionine or [75Se]selenite.     

The retention and distribution by healthy young men of stable isotopes of selenium consumed as selenite, selenate or hydroponically-grown broccoli are dependent on the isotopic form

Twenty-seven healthy young men were randomly assigned to diets that supplied low (32.6 microg/d) or high (226.5 microg/d) levels of selenium for a 105-d study. After consuming the diets for 85 d, subjects were fed a test meal that contained 74Se in the form of selenite or selenate and 82Se incorporated into hydroponically-raised broccoli. Urine, fecal and blood samples were collected daily. Isotope absorption was not different (P > 0.05) for selenate and Se in broccoli; Se absorption from selenite was highly variable and was not included in statistical analyses. Significantly more isotope was absorbed by subjects fed the high Se diet (P = 0. 015). Urinary isotope excretion was greater when selenate was fed than when broccoli was fed (P = 0.0001), and consequently more Se from broccoli (as compared to selenate) was retained (59.2 +/- 2.4 and 36.4 +/- 4.6% for Se in broccoli and selenate, respectively; P = 0.0001). Despite the higher retention, less isotope from broccoli than from selenate was present in the plasma. Plasma proteins separated by gel permeation chromatography showed that most of the isotopes were distributed between two medium molecular weight peaks. Less isotope was found in plasma proteins of subjects fed the high Se diet, but the form of Se had no effect on isotope distribution. These results show that dietary Se intake alters the retention of stable isotopes of Se and that humans retain and distribute Se from broccoli in a different manner than Se from inorganic salts.     

Dose-response relations in urinary excretion of trimethylselenonium in the rat

75Se-labeled selenite was administered to fasting rats by orogastric intubation (1.5-3000 micrograms/kg body wt). Urine was collected and characterized for total radioactivity as well as for radiolabeled trimethylselenonium (TMSe). At lower doses of selenite (up to 500 micrograms/kg body wt), 30% of the administered dose was excreted. At higher doses of selenite, fractional urine excretion decreased as a function of the dose. The observed decrease in fractional urine excretion was not caused by changes in the absorption of the administered radiolabel. There was a direct relationship between the amount of the administered dose of selenite (up to 1500 micrograms/kg body wt) and the proportion of urinary [75Se] excreted as TMSe. Pretreatment with seleno compounds (10 or 100 micrograms Se/kg body wt as selenite, or selenomethionine) for 35 d before a challenge dose of [75Se]selenite did not influence the excretion of total [75Se] or of [75Se]TMSe in urine. Ingestion of a choline-deficient diet, which should deplete the availability of methyl groups, did not have any effect on excretion of total [75Se] or of [75Se]TMSe in urine after a challenge dose of [75Se]selenite (500 micrograms/kg body wt). The data presented here permit the following conclusions: 1) Production of TMSe is dose dependent, 2) production of TMSe from a single acute dose does not depend on the history of selenium intake and 3) rats fed a methyl-deficient diet are able to eliminate Se via formation of TMSe.     

亚硒酸钠和硒蛋氨酸的毒性比较

目的　比较亚硒酸钠和硒蛋氨酸毒性差异以及探讨硒中毒的指标。方法　将断乳Wistar大鼠随机分为 7组 ,每组 14只 ,雌雄各半。其中一组为对照组 ,另外六组分别给予含硒 3、6、10mg kg的亚硒酸钠或硒蛋氨酸饲料 ,于第 12周将其处死。结果　当饲料硒水平达到 3mg kg时 ,动物肝脏出现病理变化 ,在Se6mg kg时 ,体重才出现下降。饲料硒水平为 6、10mg kg时 ,同一饲料硒水平的亚硒酸钠组大鼠体重小于硒蛋氨酸组。饲料硒水平为 3、6mg kg时 ,硒蛋氨酸组大鼠的肝脏病理改变轻于亚硒酸钠组 ,雄性大鼠轻于雌性。亚硒酸钠组较硒蛋氨酸组或雌性大鼠较雄性大鼠在肝脏体重比方面变化更为明显。除雌性大鼠肝脏谷胱甘肽过氧化物酶 (GPX)活性随硒水平升高而降低外 ,其它补硒各组肝、红细胞、血浆GPX活性具有随硒水平的升高而升高的趋势。结论　大鼠硒中毒的剂量为Se 3mg kg,硒蛋氨酸的毒性小于亚硒酸钠 ,雌性大鼠对硒毒性更为敏感     

Effect of selenite, vitamin E and N,N'-diphenyl-p-phenylenediamine on liver organic solvent-soluble lipofuscin pigments in mice

The present experiment was designed to investigate the effect of selenium (Se) supplementation, as sodium selenite, on organic solvent-soluble lipofuscin pigment (OLP) accumulation and glutathione peroxidase (GSH-Px) activity in the livers of mice fed varying levels of vitamin E or N,N'-diphenyl-p-phenylenediamine (DPPD). Four groups of 16 female, weanling mice each were fed either a vitamin E-deficient diet, a diet supplemented with 30 mg/kg or 300 mg/kg vitamin E (as RRR-alpha-tocopheryl acetate), or a diet supplemented with 30 mg/kg DPPD. Each diet contained 0.05 ppm Se. At 5 months of age, eight animals from each dietary group were supplemented with an additional 0.1 ppm Se, as sodium selenite, in their drinking water. The remaining animals were fed their original diets through the 9-month experimental period. Selenite supplementation resulted in a significant increase in OLP concentration and GSH-Px activity in the liver of mice fed vitamin E- or DPPD-supplemented diets. Normal levels of vitamin E and DPPD (30 mg/kg) were not sufficient to protect against the oxidative effects of selenite; however, 10 times the normal level of vitamin E (300 mg/kg) markedly suppressed this oxidative effect.     

Type I iodothyronine deiodinase activity after high selenium intake, and relations between selenium and iodine metabolism in rats.

Type I iodothyronine deiodinase (I-D), which catalyzes the production of the thyroid hormone 3,3',5-triiodothyronine from thyroxine, has recently been identified as a selenoenzyme. It is therefore of interest to investigate the relationships between selenium and iodine metabolism. In the livers of Se-deficient rats I-D activity was inhibited; the production of 3,3',5-triiodothyronine and 3,3'-diiodothyronine from added thyroxine was decreased by greater than 95% relative to Se-adequate controls. The hepatic I-D activity was also reduced in rats fed a diet with a low iodine concentration. Unaltered glutathione peroxidase activities in liver and plasma of these rats suggest, however, that with normal Se intake this metabolic pathway of Se is not affected by iodine depletion. When rats were administered 75Se-labeled selenium at levels equal to the amounts ingested from diets with Se concentrations of 0.3 or 2 mg Se/kg, greater Se concentrations were found in the thyroid and liver of the animals receiving the higher dosage. The thyroidal 3,3',5-triiodothyronine and thyroxine concentrations, however, were comparable in rats fed diets with 0.3 mg Se/kg diet as selenite and 2 mg Se/kg as selenite or L-selenomethionine. The measurement of the hepatic I-D and glutathione peroxidase activities in these animals showed that excessive Se supply does not elevate the activities of the two enzymes but might even have the opposite effect. At high Se intake tissue Se concentration cannot therefore be used as indicator of the selenoenzyme activities.     

4种富硒植物预防MNNG诱发大鼠胃癌效果研究 二、不同源硒预防大鼠胃癌的安全性对比研究

目的对比研究长期摄入高剂量不同源硒的安全性。方法以亚硒酸钠为对照硒材料,采用N-甲基-N′-硝基-N-亚硝基胍(MNNG)诱发大鼠胃癌模型,连续灌以4种不同富硒植物(高剂量硒)17周,测定肝脏谷胱甘肽硫转移酶(GST)、血清谷草转氨酶(AST)和血清谷丙转氨酶(ALT)活性,并观察肝脏和肾脏的病理变化。结果各组大鼠肝GST活性均无显著性差异;75μg/kg bw(以Se计,下同)亚硒酸钠低剂量组大鼠血清AST和ALT活性不仅显著高于空白对照和MNNG组,而且显著高于150μg/kg bw和300μg/kg bw植物硒处理组(P<0.05)。病理分析发现75μg/kg bw亚硒酸钠低剂量组胆管周围有棕黄色颗粒,窦内枯否氏细胞轻度肥大、增生;其余各组未发现有意义的病变。结论亚硒酸钠毒性至少是实验用其它富硒植物的4倍。     

硒营养状况对大鼠感染肺炎支原体发病率的影响

本研究以大鼠为动物模型，观察了缺硒或适硒大鼠感染肺炎支原体（ＭＰ）间质性肺炎的发病率，以及感染后灌喂亚硒酸钠对发病率的影响。选择３周龄断乳Ｗｉｓｔａｒ大鼠１５０只，在喂饲各自实验饲料４周后，用乙醚麻醉Ｂ、Ｃ、Ｄ、Ｅ组动物，滴鼻感染肺炎支原体（ＭＰ）菌液，Ｃ组在感染的同时，开始灌喂亚硒酸钠溶液（２Ｓｅμｇ／ｍｌ，每天灌喂剂量为１．５～２ｍｌ），持续１８天；Ｄ组在感染后第１１天灌喂亚硒酸钠溶液，持续７天；Ｂ组和Ｅ组自感染之日起，灌喂生理盐水１８天，Ａ组无感染。结果证明，适硒感染组支原体肺炎发病率低，适硒感染组和低硒感染同时补硒组严重肺炎例数和心肌损害例数均少于缺硒感染组。提示良好的硒营养状况可减少大鼠ＭＰ肺炎发病率，对感染时的心肌有保护作用；补硒可减轻病情和加速病变恢复     

Bioavailability of selenium from raw and cooked ground beef assessed in selenium-deficient Fischer rats.

The literature on the bioavailability of selenium (Se) from meats, especially beef, is meager, and that which existed when this research began suggested that Se was not highly bioavailable. In addition, much of the analytical values for Se in beef predated the Food and Drug Administration's 1973 approval of Se as an additive to feeds and mineral premixes of livestock.

One hundred and thirty-six weanling female Fischer 344 rats were divided into two dietary groups: the selenium deficient group in which animals were fed a torula yeast (TY) basal diet which contained 0.008 mg/kg Se and the control group in which animals were fed the TY diet to which was added 0.10 mg/kg Se as sodium selenite.

After 6 weeks of dietary treatment liver glutathione peroxidase (GSHPx) activity had fallen in the Se-deficient rats to 2.4% of that of control rats. At this time (week 6) rats from the Se-deficient TY diet were refed diets containing 0.10 mg/kg Se as selenite, selenate, raw or cooked ground beef that had been freeze-dried. During the Se-repletion period rats were sacrificed at weeks 1, 3, 5 and 8. Liver GSHPx activity and total Se levels in liver and muscle tissue were the criteria of Se bioavailability. After 8 weeks of Se resupplementation the recovery of liver GSHPx activity compared to the control animals (set at 100%) were selenite (98%, p > 0.05), selenate (117%, p < 0.05), raw beef (127%, p < 0.05) and cooked ground beef (139%, p < 0.05). Total Se in both liver and muscle tissue reflected the liver GSHPx activity with the total Se concentration in tissues being highest for cooked beef.

The data suggest that bioavailability of Se from ground beef is greater than that from either selenite or selenate.     

Selenium from selenium-rich Spirulina is less bioavailable than selenium from sodium selenite and selenomethionine in selenium-deficient rats

The bioavailabilty of selenium (Se) from selenium-rich Spirulina (SeSp) was assessed in Se-deficient rats by measuring tissue Se accumulation and glutathione peroxidase (GSH-Px) activity. For 42 d, rats were subjected to dietary Se depletion by consumption of a Torula yeast (TY)-based diet with no Se; controls were fed the same diet supplemented with 75 microg Se/kg diet as sodium selenite. Se-deficient rats were then repleted with Se (75 microg/kg) by the addition of sodium selenite, selenomethionine (SeMet) or SeSp to the TY basal diet. Selenium speciation in SeSp emphasized the quasi-absence of selenite (2% of total Se); organic Se comprised SeMet (approximately 18%), with the majority present in the form of two selenoproteins (20-30 kDa and 80 kDa). Gross absorption of Se from SeSp was significantly lower than from free SeMet and sodium selenite. SeMet was less effective than sodium selenite in restoring Se concentration in the liver but not in kidney. SeSp was always much less effective. Similarly, Se from SeSp was less effective than the other forms of Se in restoring GSH-Px activity, except in plasma and red blood cells where no differences were noted among the three sources. This was confirmed by measuring the bioavailability of Se by slope-ratio analysis using selenite as the reference form of Se. Although Se from SeSp did not replenish Se concentration and GSH-Px activity in most tissues to the same degree as the other forms of Se, we conclude that it is biologically useful and differently metabolized due to its chemical form.     

An evaluation of the bioavailability of selenium in high-selenium yeast.

The bioavailability of selenium (Se) in high-Se yeast (SeY) was evaluated by measuring tissue Se accumulation and glutathione peroxidase (GSHPx) activity. For 4 weeks, 4-week-old male Wistar rats were fed a Torula yeast-based Se-deficient diet (basal diet) or a diet supplemented with a graded level (0.04, 0.08, 0.16, and 0.32 microgram/g) of Se as either sodium selenite or SeY, which was obtained from two different sources. Se supplementation did not influence growth, hematological values, or serum biochemical tests. Se contents and GSHPx activities in the liver, serum, and erythrocytes increased gradually with increases of the supplemented Se. At lower Se levels (0.04 and 0.08 microgram/g), selenite produced higher Se deposition and higher GSHPx activities than SeY did, but at a higher Se level (0.32 microgram/g), SeY showed higher measures. Strong correlations were detected between the supplementary Se levels and the tissue Se contents or GSHPX activities when the regression was fitted to this equation: R-Rb = m log X + k, where R represented tissue Se content or GSHPx activity in rats fed the diet supplemented with Se at X level, Rb corresponding mean value in rats fed the basal diet, m slope, and k constant. The bioavailability of Se in SeY, as assessed by slope ratio analysis using selenite as a reference Se, was 135% to 165% in the tissue Se content and 105% to 197% in the GSHPx activities. These results indicate that Se in SeY is more bioavailable than selenite Se, and therefore it is the preferred form for supplementation.     

克山病病区粮对大鼠全血谷胱甘肽过氧化物酶活力及体内抗氧化能力的影响

1.比较了病区和非病区玉米、大米饲料及动物房常备饲料喂养的大鼠全血GSH-Px活力。结果表明:常备组高于非病区组,后者又高于病区组。同时测定的体外用维生素C氧化血红蛋白生成的高铁血红蛋白、胆绿蛋白和Heinz小体的百分率。各组雌鼠之间无显著差异,而雄鼠的结果与GSH-Px活力呈反相关。 2.喂以病区玉米饲料三个月造成乏硒的大鼠补充硒(Na_2SeO_3)50天后,血硒和红细胞GSH—Px活力均升到接近常备饲料组大鼠的水平。     

Effects of vitamin B-6 deficiency on selenium metabolism in the rat

Rats were fed for 23 d diets adequate or deficient in vitamin B-6 and containing selenium as either sodium selenite, selenocysteine (SeCys) or selenomethionine (SeMet). They were then injected with 75Se of the same chemical form and killed 2 d later. Tissue deposition of stable and radiotracer selenium and the activity of glutathione peroxidase (GSHPx) were used to assess selenium utilization. Erythrocyte levels of selenium and GSHPx were lower in vitamin B-6--deficient animals for all forms of selenium; however, 75Se deposition in erythrocytes was not affected by vitamin B-6 status. The activities of cystathionine lyase, aspartate aminotransferase and selenocysteine lyase were lower in livers of vitamin B-6--deficient rats than in vitamin B-6--supplemented rats. The proportion of liver and kidney 75Se soluble in 5% trichloroacetic acid and 0.1 M 2-mercaptoethanol was consistently lower in vitamin B-6--deficient animals, but cation-exchange chromatography of tissue extracts did not identify a specific low-molecular-weight species. Tissue retention of 75Se provided as SeMet was increased in vitamin B-6--deficient animals, but the proportion of 75Se retained in muscle and liver as SeCys was significantly reduced. These findings suggest that the conversion of SeMet to a form available for GSHPx synthesis is reduced by vitamin B-6 deficiency.     

Organ and subcellular distribution of selenium in rats exposed to cadmium,mercury, and selenium

Three groups of rats were given sodium selenite (Se), sodium selenite and cadmium chloride (Se + Cd), or sodium selenite, cadmium chloride, and mercuric chloride (Se + Cd + Hg), respectively. All animals received subcutaneous doses of ¹¹⁵CdCl₂ (0.3 mg Cd/kg) every other day for a fortnight. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day and Na₂⁷⁵SeO₃ intragastrically at doses of 0.1 mg Se/kg every other day for 2 weeks. The whole-body retention of selenium was slightly elevated by cadmium and increased threefold by cadmium with mercury (mainly blood, liver, and kidneys). Cadmium did not affect subcellular levels of selenium in the kidneys and slightly increased the selenium content in the soluble fraction of the liver. On the other hand, combined administration of mercury and cadmium induced a significant elevation of the selenium content in all subcellular fraction of the kidneys and in the nuclear and mitochondrial fractions of the liver. In all animal groups selenium was bound in the soluble fractions of both the liver and kidneys by high-molecular-weight proteins.     

Absorption and retention of selenium from intrinsically labeled egg and selenite as determined by stable isotope studies in humans

A study was carried out with four healthy young adult men, consuming a self-selected diet, to investigate quantitative aspects of the gastrointestinal absorption, urinary excretion, and body retention of egg selenium in comparison with selenite. The approach involved simultaneous consumption of egg biologically labeled (intrinsic) with the stable isotope 74Se and a dose of selenite labeled with 76Se (extrinsic label). Four labeled test diets, given on days 6, 16, 26, and 36 of the study were employed, each differing in their protein source: test diet I, 74Se-labeled egg white; diet II, 74Se-labeled egg yolk (high labeling dose) plus balanced L-amino acid mixture; diet III, 74Se-labeled egg yolk (low labeling dose) plus balanced amino acid mixture; and diet IV, balanced amino acid mixture extrinsically labeled with both 74SeO32- and 76SeO32-. The latter diet was included to assess the magnitude of any cross-isotope methodological bias. Fractional absorption (means +/- SEM) for Diet IV was 0.771 +/- 0.010 for the 74SeO32- and 0.656 +/- 0.021 for the 76SeO32- (ratio: 0.851 +/- 0.020); reflecting a small overall cross-isotope bias. Accepting the measurements made with 74SeO32- as the more accurate, experimentally determined values of absorption for the extrinsic tag were adjusted accordingly. The corrected absorption for these diets (% of dose) was (mean +/- SEM; first value for intrinsic label, second value for extrinsic label): diet I, 54.1 +/- 0.7 and 55.4 +/- 2.2; diet II, 76.7 +/- 0.8 and 83.0 +/- 1.8; diet III, 79.0 +/- 1.5 and 85.2 +/- 4.0.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of stock or purified diet on rat liver enzymes involved in the synthesis of dimethyl selenide.

Rats fed either a stock deit or a purified diet based on casein were tested for their ability to convert 75Se-sodium selenite to volatile selenium (dimethyl selenide) in vivo. This conversion was also studied in liver and kidney in vitro. When injected with a subacute dose of selenite (2 mg Se/kg), rats previously fed stock diet volatilized more than twice as much of the dose compared to rats fed the purified diet, confirming earlier findings. Parallel dietary effects were also observed in vitro using subcellular fractions incubated with 75Se-selenite, glutathione, TPNH, and S-adenosylmethionine. The 9-000 X g supernate prepared from rats fed stock diet synthesized dimethyl selenide at approximately twice the rate of that prepared from rats fed purified diet. A fourfold higher activity was observed with liver microsomal fractions from rats fed the stock diet, whereas cytosol was slightly more active in rats fed the purified diet. Kidney fractions showed analogous changes with diet, although the activity of kidney microsomal fraction was very low. Only minor differences in the levels of glutathione reductase, nonspecific disulfide reducatse, and non-protein thiols were observed in liver and kidney from rats fed the two diets. Considering the effects of diet on the various enzymes known from our previous studies to be involved in dimethyl selenide synthesis, it was concluded that the enhanced ability of rats fed stock diet to synthesize dimethyl selenide results from the induction of a liver microsomal enzyme, apparently a Se-methyltransferase, caused by unknown substances in the stock diet.     

Effects of various dietary levels of selenium as selenite or selenomethionine on tissue selenium levels and glutathione peroxidase activity in rats

Weanling rats were fed a basal diet or this diet plus 0.2, 1.0, 2.0 or 4.0 mg/kg selenium (Se) as either selenite or selenomethionine (SeM). Except at the 0.2 mg/kg Se level, Se accumulated in all tissues at higher levels when SeM was fed than when selenite was given, and the magnitude of difference became more pronounced with increasing levels of dietary Se. This was particularly true for muscle and brain. Se levels in whole blood, testes, kidney and lungs were not significantly different between rats fed 0.2 mg/kg Se as selenite or as SeM, but the Se levels in liver, muscle and brain were higher in rats fed SeM. Although the tissue Se concentrations differed markedly, there were no differences in the glutathione peroxidase (GPX) activity in tissues of rats fed SeM rather than selenite. The percentage of Se associated with GPX was lower in all tissues from rats fed SeM than in those from rats fed selenite. These results indicate that the chemical forms of dietary Se can have a marked influence on biological responses, including bioavailability of dietary Se.     

The effect of sulphur on 75Se absorption and retention in sheep.

Four Border-Leicester X Merino wethers were used in a 4 X 4 Latin square experiment to study the effects of dietary sulphur on selenium absorption and retention. The basal diet contained 0.05% S and sodium sulphate was added to give additional treatment levels of 0.11, 0.17 and 0.24% total sulphur. Sodium selenate was added to all diets to bring the dietary selenium level to a constant 0.25 mg/kg. One hundred muCi 75Se as sodium selenate (specific activity 50 muCi/mg Se) was administered to the rumen per fistulam after a 10-day period of adjustment on each diet. Radioactivity in blood, urine, faeces and rumen digesta was measured at intervals over the succeeding 7 days. Twenty percent of the total activity in the rumen fluid was in the TCA supernatant fraction after 3 hours, and this proportion tended to increase slightly as sulphur intake increased. Fecal excretion of selenium accounted for between 44 and 51% of the dose after 7 days, the high levels being associated with increasing sulphur intake. However, these differences were not significant. Urinary excretion of selenium accounted for between 12% (0.05% S) and 22% (0.24% S) of the dose after 7 days, with treatment differences being significant. Levels of radioactivity in blood were significantly higher in sheep fed the 0.05% S diet compared with those fed the higher levels. The results show that sulphur affects apparent selenium excretion and suggest that the metabolism of these two elements is intimately related.     

Chronic toxicity and retention of dietary selenium fed to rats as D- or L-selenomethionine,selenite, or selenate

Groups of 8 male weanling Sprague-Dawley rats were fed for 6 weeks Torula yeast-based purified diets containing 2.5, 5.0, or 10.0 μg Se/g added as D-selenomethionine (D-SeMet), L-selenomethionine (L-SeMet), sodium selenite, or sodium selenate. All rats consuming diets containing 10.0 μg Se/g experienced severe growth depression and diet within 29 days, regardless of the form of Se fed, whereas rats fed 2.5 μg Se/g diet gave no evidence of depressed growth and survived the entire experimental period. Selenium fed as D-SeMet was retained in the tissues as strongly as L-SeMet. Skeletal muscle and heart Se concentrations were markedly greater when D- or L-SeMet were consumed than when selenite or selenate were consumed. Lesser differences due to the form of dietary Se fed were seen in the retention of Se in red blood cells, plasma, or liver. The increased deposition of Se in muscle tissues was not reflected by proportionate increases in either plasma or RBC Se, so monitoring plasma or whole blood Se may not indicate the degree of increased total Se body burden.