Effects of selenium on RNA synthesis and content in rat pancreas.

In order to investigate the effect of selenium supplementation on RNA in the rat pancreas, the rate of in vitro incorporation of [3H]uridine into RNA by pancreas slices derived from two groups of rats fed either a low-selenium diet or a diet supplemented with 0.25 mg/kg selenium as selenite was examined. The RNA and lipid peroxide contents and glutathione peroxidase activity in homogenates from the pancreas were also determined. After feeding for 12-14 weeks, the rates of [3H]uridine incorporation were significantly higher in the pancreatic tissue from the selenium-supplemented diet group. Concomitantly, an increase in glutathione peroxidase activities and RNA content, and a reduction of lipid peroxides, were also found in the pancreatic tissue of the selenium-supplemented group. The results suggest that selenium supplementation at a level of 0.25 mg/kg selenium could promote RNA synthesis with an increase in glutathione peroxidase activity and a decrease of lipid peroxides.     

Distribution of Selenium in Bovine Milk and Selenium Deficiency in Rats Fed Casein-based Diets,Monitored by Lipid Peroxide Level and Glutathione Peroxidase Activity

A major proportion of selenium in bovine milk was found in fluorometric analysis to be associated with the casein fraction, largely in alkali-labile form, and the rest with the whey fraction mostly in free selenite form. This uneven distribution of milk selenium seems to provide an explanation for selenium deficiency in purified caseins. The activity of glutathione peroxidase, a selenoprotein, in the liver of growing male rats fed ad libitum low-selenium diets containing either vitamin-free casein or Torula yeast 0.065 ± 0.012 or 0.015 ± 0.004 μ g Se/g diet, respectively) for 3 weeks decreased to 4 to 6% of that of the control rats fed a commercial stock diet (0.185 ± 0.092 μ g Se/g diet). Selenium status was evaluated by three different parameters for the rats assigned under pair-feeding regimen to those vitamin-free casein-based diets which were supplemented with graded levels of selenium as sodium selenite. The hepatic levels of the thiobarbituric acid-reactive substance, an indication of lipid peroxidation, decreased to control level with selenium supplementation per g diet of 0.1 μ g and over. The hepatic glutathione peroxidase activity reached a plateau above a 0.1 μ g/g diet of selenium supplementation, whereas the erythrocyte enzyme activity increased with increasing levels of supplementary selenium. These results support the notion that semi-purified diets containing vitamin-free casein as a prime protein source would not satisfy the selenium requirement of growing animals unless deliberately supplemented with additional selenium.     

Selenium and Glutathione Peroxidase Levels in Lambs Receiving Feed Supplemented with Sodium Selenite or Selenomethionine

Twenty-one 6 months old female lambs were divided into 7 groups and fed a basal diet containing 0.13 mg Se/kg. The basal diet was further supplemented with 0, 0.1, 0.5 or 1.0 mg Se/kg either as sodium selenite or as selenomethionine, and was fed for 10 weeks. Both feed additives produced an increase in the selenium concentration in the tissues analysed. Significant correlations were found between the concentrations of selenomethionine or sodium selenite added to the feed and the subsequent tissue levels. However, the selenium levels seemed to plateau at approximately 0.5 mg Se/kg of supplemented sodium selenite. The total glutathione peroxidase (GSH-Px) activity of the tissues increased when the selenium supplementation increased from 0 to 0.1 mg/kg for both selenium compounds. With further increase in selenium supplementation the GSH-Px activity in the tissues plateaued except in the blood where the activity continued to rise with increasing selenomethionine supplementation. The selenium dependent GSH-Px activity in the liver rose with increasing selenomethionine supplementation, but approached a plateau when 0.1 mg Se/kg as sodium selenite was added to the feed. The selenium concentration in whole blood responded more rapidly to the selenium supplementation than did GSH-Px activity. The experiment indicates that the optimal selenium concentration in the feed is considerably higher than 0.1 mg Se/kg, and that selenium levels of 1.0 mg/kg in the feed do not result in any risk for the animals or the consumers of the products.     

Parameters of dietary selenium and vitamin E deficiency in growing rabbits.

4 x 5 growing female rabbits (New Zealand White) with an initial live weight of 610 +/- 62 g were fed a torula yeast based semisynthetic diet low in selenium (<0.03 mg/kg diet) and containing <2 mg alpha-tocopherol per kg (group I). Group II received a vitamin E supplementation of 150 mg alpha-tocopherylacetate per kg diet, whereas for group III 0.40 mg Se as Na-selenite and for group IV both supplements were added. Selenium status and parameters of tissue damage were analyzed after 10 weeks on experiment (live weight 2,355 +/- 145 g). Selenium depletion of the Se deficient rabbits (groups I and II) was indicated by a significantly lower plasma Se content (group I: 38.3 +/- 6.23 microg Se/mL plasma, group II: 42.6 +/- 9.77, group III: 149 +/- 33.4, group IV: 126 +/- 6.45) and a significantly lower liver Se content (group I: 89.4 +/- 18.2 microg/kg fresh matter, group II: 111 +/- 26.2) as compared to the Se supplemented groups III (983 +/- 204) and IV (926 +/- 73.9). After 5 weeks on the experimental diets differences in the development of plasma glutathione peroxidase were observed. As compared to the initial status group (45.2 +/- 4.50) pGPx activity in mU/mg protein was decreased in group I (19.1 +/- 7.08), remained almost stable in the vitamin E supplemented group II (46.3 +/- 11.2) whereas an elevated enzyme activity was measured in the Se supplemented groups III (62.4 +/- 23.9) and IV (106 +/- 19.9). In the rabbit organs investigated 10 weeks of Se deficiency caused a significant loss of Se dependent cellular glutathione peroxidase activity (GPx1) of 94% (liver), 80% (kidney), 50% (heart muscle) and 60% (musculus longissimus dorsi) in comparison to Se supplemented control animals. Damage of cellular lipids and proteins in the liver was due to either Se or vitamin E deficiency. However damage was most severe under conditions of a combined Se and vitamin E deficiency. It can be concluded that the activity of plasma glutathione peroxidase is a sensitive indicator of Se deficiency in rabbits. The loss of GPx1 activity indicates the selenium depletion in various rabbit organs. Both selenium and vitamin E are essential and highly efficient antioxidants which protect rabbits against lipid and protein oxidation.     

Barium Selenate as a Slow-Release Selenium Preparation to Pigs

Pregnant sows were injected subcutaneously (s.c.) or intramuscularly (i.m.) with a barium selenate suspension (0.5–1.0 mg Se/kg body weight (b.w.)) and together with control animals fed a commercial diet. No response to the injection was seen either in blood selenium levels or in glutathione peroxidase (GSH-Px) activity in the sows. There was, however, a significant difference in these parameters between piglets born from treated dams and control animals. This status was maintained during the nursing period. In another experiment pigs (20 kg b.w.) on a Se-deficient diet were injected s.c. and i.m. with barium selenate (2.5 mg Se/kg b.w.). The treated groups maintained their blood levels of selenium and GSH-Px activity, although the selenium values in the group treated intramuscularly started to decline after 4 weeks. Organ samples from both groups were equal with regard to selenium at the time of slaughter while the control group showed a rapid decline both in blood selenium levels and GHS-Px activity.     

Effects of selenium deficiency on Ca transport function of sarcoplasmic reticulum and lipid peroxidation in rat myocardium

Two groups of weanling Sprague-Dawley rats were fed a low-selenium basal diet (Se 0.009 mg/kg) and the same diet supplemented with sodium selenite (Se 0.25 mg/kg), respectively, for 1, 2, and 3 months. At each feeding time, the Ca²⁺-ATPase activity, Ca²⁺ uptake rate and the capacity of Ca²⁺ uptake in isolated cardiac sacroplasmic reticulum from the Se-deficient rats were decreased significantly compared to those from the Se-supplemented rats, the contents of lipid peroxide in postmitochondrial supernatant and isolated sarcoplasmic reticulum from the Se-deficient rats were significantly higher than that from Se-supplemented rats. Compared to the Se-supplemented rats, the cytosolic glutathione peroxidase activity in Se-deficient rats decreased significantly. In addition, significant linear negative correlations of lipid peroxide in postmitochondrial supernatant to sarcoplasmic reticular Ca²⁺-ATPase activity, Ca²⁺ uptake rate and to whole blood selenium concentration were observed. The results suggest that the enhancement of lipid peroxidation via the depressed glutathione peroxidase activity might be responsible for the decrease of Ca²⁺-ATPase and Ca²⁺ uptake activities in sarcoplasmic reticulum in Se-deficient animals.     

Effects of dietary selenium and vitamin E concentrations on phospholipid hydroperoxide glutathione peroxidase expression in reproductive tissues of pubertal maturing male rats

Phospholipid hydroperoxide glutathione peroxidase (PHGPX) is the second intracellular selenium (Se)-dependent glutathione peroxidase (GSH-Px) identified in mammals. Our objectives were to determine the effect of dietary vitamin E and Se levels on PHGPX activity expression in testis, epididymis, and seminal vesicles of pubertal maturing rats, and the relationship of PHGPX expression with testicular development and sperm quality. Forty Sprague-Dawley male weanling rats (21-d old), were initially fed for 3 wk a torula yeast basal diet (containing 0.05 mg Se/kg) supplemented with marginal levels of Se (0.1 mg/kg as Na₂SeO₃) and vitamin E (25 IU/kg as all-rac-α-tocopheryl acetate). Then, rats were fed the basal diets supplemented with 0 or 0.2 mg Se/kg and 0 or 100 IU vitamin E/kg diet during the 3-wk period of pubertal maturing. Compared with the Se-supplemented rats, those fed the Se-deficient diets retained 31, 88, 67, and 50% of Se-dependent GSH-Px activities in liver, testis, epididymis, and seminal vesicles, respectively. Testes and seminal vesicles had substantially higher (5-to 20-fold) PHGPX activity than liver. Dietary Se deficiency did not affect PHGPX activities in the reproductive tissues, but reduced PHGPX activity in liver by 28% (P < 0.0001). Dietary vitamin E supplementation did not affect PHGPX activity in liver, whereas it raised PHGPX activity in seminal vesicles by 43% (P < 0.005). Neither dietary vitamin E nor Se levels affected body weight gains, reproductive organ weights, or sperm counts and morphology. In conclusion, expression of PHGPX activity in testis and seminal vesicles was high and regulated by dietary Se and vitamin E differently from that in liver.     

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat

The aim of this study was to evaluate the influence of arsenic and bromine exposure with or without iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A - standard diet, group B - iodine rich diet (10 mg I/kg food), group C - selenium rich diet (1 mg Se/kg) and group D - iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO(2) ip (6.5 mg.kg(-1) twice a week for two weeks and 3.25 mg.kg(-1) for six weeks) or KBr in drinking water (58.8 mg.l(-1)) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland ( approximately 18 ppm of As, approximately 90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to approximately 50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.     

The influence of dietary selenium and vitamin E on glutathione peroxidase and glutathione in the rat

The effect of dietary selenium (Se) and vitamin E supplementation on tissue reduced glutathione (GSH) and glutathione peroxidase activity has been studied in the rat. Increasing Se intake by 0.4 ppm gave significantly higher enzyme levels in all tissues studied, an effect not influenced by vitamin E intake. Further increasing Se to 4 ppm gave higher enzyme levels in red blood cells only, while in liver was there was a significant decrease in enzyme activity probably reflecting Se hepatotoxicity. In the absence of Se supplements increasing dietary vitamin E to 100 mg/kg diet significantly increased enzyme activity but this effect was modified by simultaneous Se supplementation.Se intake had no effect on GSH levels. Rats on high vitamin E intake 500 mg/kg had a significantly higher tissue GSH level. Dietary Se had a sparing effect on vitamin E, rats supplemented with Se having significantly raised plasma vitamin E levels.These results confirm the role of selenium in glutathione peroxidase and also show that vitamin E influences the activity of the enzyme.     

Effect of selenium status on mRNA levels for glutathione peroxidase in rat liver

To determine the effect of Se status on the level of mRNA for Se-dependent glutathione peroxidase (EC 1.11.1.9), rats were fed either a Se-deficient torula yeast diet (less than 0.02 mg Se/kg diet) or a Se-adequate diet (+0.2 mg Se/kg as Na2SeO3) for greater than 135 d. Liver glutathione peroxidase activity was 0.025 for Se-deficient versus 0.615 EU/mg protein for Se-adequate rats. Total liver RNA and polyadenylated RNA were isolated and subjected to Northern blot analysis using a 700 bp DNA probe from cloned murine glutathione peroxidase. Autoradiography showed that Se-deficient liver had 7-17% of the mRNA for glutathione peroxidase present in Se-adequate liver, suggesting that Se status may regulate the level of mRNA for this selenoenzyme.     

Evaluation of Nutritional Availability and Anti-Tumor Activity of Selenium Contained in Selenium-Enriched Kaiware Radish Sprouts

We estimated the nutritional availability of selenium (Se) in Se-enriched Kaiware radish sprouts (SeRS) by the tissue Se deposition and glutathione peroxidase (GPX) activity of rats administered the sprouts, and examined the effect of SeRS on the formation of aberrant crypt foci (ACF) in the colon of mice administered 1,2-dimethylhydrazine (DMH) to evaluate anti-tumor activity. Male weanling Wistar rats were divided into seven groups and fed a Se-deficient basal diet or the basal diet supplemented with 0.05, 0.10, or 0.15 μg/g of Se as sodium selenite or SeRS for 28 d. Supplementation with Se dose-dependently increased serum and liver Se concentrations and GPX activities, and the selenite-supplemented groups showed a higher increase than the SeRS-supplemented groups. The nutritional availability of Se in SeRS was estimated to be 33 or 64% by slope ratio analysis. Male 4-week-old A/J mice were divided into seven groups and fed a low Se basal diet or the basal diet supplemented with selenite, SeRS, or selenite + non-Se-enriched radish sprouts (NonSeRS) at a level of 0.1 or 2.0 μg Se/g for 9 weeks. After 1 week of feeding, all mice were given six subcutaneous injections of DMH (20 mg/kg) at 1-week intervals. The average number of ACF formed in the colon of mice fed the basal diet was 4.3. At a supplementation level of 0.1 μg Se/g, only SeRS significantly inhibited ACF formation. At a supplementation level of 2.0 μg Se/g, both selenite and SeRS significantly inhibited ACF formation. The addition of NonSeRS to the selenite-supplemented diets tended to inhibit ACF formation, but this was not statistically significant. These results indicate that SeRS shows lower nutritional availability but higher anti-tumor activity than selenite.     

Evaluation of nutritional availability and anti-tumor activity of selenium contained in selenium-enriched Kaiware radish sprouts

We estimated the nutritional availability of selenium (Se) in Se-enriched Kaiware radish sprouts (SeRS) by the tissue Se deposition and glutathione peroxidase (GPX) activity of rats administered the sprouts, and examined the effect of SeRS on the formation of aberrant crypt foci (ACF) in the colon of mice administered 1,2-dimethylhydrazine (DMH) to evaluate anti-tumor activity. Male weanling Wistar rats were divided into seven groups and fed a Se-deficient basal diet or the basal diet supplemented with 0.05, 0.10, or 0.15 microg/g of Se as sodium selenite or SeRS for 28 d. Supplementation with Se dose-dependently increased serum and liver Se concentrations and GPX activities, and the selenite-supplemented groups showed a higher increase than the SeRS-supplemented groups. The nutritional availability of Se in SeRS was estimated to be 33 or 64% by slope ratio analysis. Male 4-week-old A/J mice were divided into seven groups and fed a low Se basal diet or the basal diet supplemented with selenite, SeRS, or selenite + non-Se-enriched radish sprouts (NonSeRS) at a level of 0.1 or 2.0 microg Se/g for 9 weeks. After 1 week of feeding, all mice were given six subcutaneous injections of DMH (20 mg/kg) at 1-week intervals. The average number of ACF formed in the colon of mice fed the basal diet was 4.3. At a supplementation level of 0.1 mug Se/g, only SeRS significantly inhibited ACF formation. At a supplementation level of 2.0 microg Se/g, both selenite and SeRS significantly inhibited ACF formation. The addition of NonSeRS to the selenite-supplemented diets tended to inhibit ACF formation, but this was not statistically significant. These results indicate that SeRS shows lower nutritional availability but higher anti-tumor activity than selenite.     

The effect of selenium on the hepatic drug metabolism and inducibility in rat

1. Rats were fed either a normal or selenium-deficient diet for 4 weeks. The subgroup on selenium deficient diet had selenium supplementation as 3 ppm Se in the drinking water. Benzo(a)pyrene was given intraperitoneally as an inducer. 2. Se deficiency decreased glutathione peroxidase and cytochrome c-reductase activities while other activities were unchanged as compared to normal diet. 3. Selenium deficiency was a prerequisite for the induction of glutathione peroxidase, S-reductase and S-transferase enzymes. 4. Benzo(a)pyrene increased hepatic microsomal cytochrome P-450 content in rats on normal and selenium supplemented diet but not in the selenium deficient group. 5. The 7-ethoxyresorufin and 7-ethoxycoumarin deethylase, aryl hydrocarbon hydroxylase and cytochrome c-reductase activities were increased by benzo(a)pyrene in all the dietary groups. 6. The UDP-glucuronosyltransferase activity was also increased by benzo(a)pyrene in all the experimental groups and this was true with p-nitrophenol and phenolphthalein as aglycons.     

The effects of in vitro lipid peroxidation on the activity of rat liver microsomal glutathione S-transferase from rats supplemented or deficient in antioxidants

Glutathione S-transferases are a group of multifunctional isozymes that play a central role in the detoxification of hydrophobic xenobiotics with electrophilic centers (1). In this study we investigated the effects of in vitro lipid peroxidation on the activity of liver microsomal glutathione S-transferases from rats either supplemented or deficient in both vitamin E and selenium. Increased formation of malondialdehyde (MDA), a by-product of lipid peroxidation, was associated with a decreased activity of rat liver microsomal glutathione S-transferase. The inhibition of glutathione S-transferase occurred rapidly in microsomes from rats fed a diet deficient in both vitamin E and selenium (the B diet) but was delayed for 15 minutes in microsomes from rats fed the same diet but supplemented with these micro-nutrients (B+E+Se diet). Lipid peroxidation inhibits microsomal glutathione S-transferase and this inhibition is modulated by dietary antioxidants.     

Selenium deficiency-induced alterations in the vascular system of the rat

To enunciate the mechanisms whereby Se protects against cardiovascular diseases, weanling male Wistar rats were fed deficient (0.022 mg/kg diet) and adequate (0.159 mg/kg diet) Se diets for 14 and/or 39 wk. As the Se content and glutathione peroxidase activity were decreased and the lipid peroxide level was increased, the plasma 6-keto-PGF_1α concentration of the Se-deficient group was markedly decreased in blood and tissues of the Se-deficient rats, as compared with the Se-adequate animals. Furthermore, the Se-deficient group had significantly lower plasma nitric oxide content and vascular nitric oxide synthase activity, higher erythrocyte sedimentation equation K value and aggregation index, and lower erythrocyte deformability than the Se-adequate group. Experimental Se deficiency also resulted in significant increases in serum total cholesterol and low-density lipoprotein cholesterol levels and a significant decrease in serum high-density lipoprotein cholesterol level. These results give some experimental supports to the hypothesis that low Se status and lipid peroxidation are involved in the etiology of cardiovascular diseases.     

Microencapsulated sodium selenite supplementation in dairy cows: effects on selenium status

The objective of this study was to compare the efficiency of transfer of selenium (Se) to plasma and milk from inorganic sodium selenite, either free or microencapsulated, and from selenized yeast in dairy cows. The study consisted of an in situ-nylon bags incubation, and in an in vivo experiment to compare the Se status of cows supplemented with either sodium selenite, microencapsulated sodium selenite, or Se yeast. Thirty dairy cows, divided in five groups, were fed the following diets: the control group (CTR) received a total mixed ration supplemented with sodium selenite in order to have 0.3 mg/kg DM of total Se; 0.3M and 0.5M groups received the same control diet supplemented with lipid microencapsulated sodium selenite to provide 0.3 and 0.5 mg/kg DM of total Se, respectively; 0.3Y and 0.5Y groups received selenized yeast to provide 0.3 and 0.5 mg/kg of total Se, respectively. Cows were fed the supplements for 56 days during which milk, blood, and fecal samples were collected weekly to conduct analysis of Se and glutathione peroxidase (GSH-px) activity. Se concentration in the nylon bags was assessed to 72%, 64%, and 40% of the initial value (time 0) after 4, 8, and 24 h of incubation, respectively. In vivo, cows supplemented with 0.3 mg/kg of microencapsulated Se had higher milk Se concentration compared to CTR. The increment was more pronounced at the highest inclusion rate (0.5 mg/kg, 0.5M group). GSH-px activity was not significantly affected by treatments. The results indicate that lipid microencapsulation has the potential to protect nutrients from complete rumen reduction and that Se from microencapsulated selenite is incorporated in milk more efficiently than the free form. Microencapsulated sodium selenite was shown to be comparable to Se-yeast in terms of availability and incorporation in milk when fed at 0.3 mg/kg DM, whereas the inclusion in the diet at 0.5 mg/kg DM resulted in higher plasma and milk concentrations than selenized yeast.     

Influence of selenium deficiency on vital functions in rats

To clarify the relationship between selenium (Se) deficiency and functional disorders, the authors determined the Se concentration, anti-oxidant enzyme activity, and other parameters in rats fed a Se-deficient diet. Rats fed the Se-deficient diet showed a decrease in Se concentration and glutathione peroxidase (GSH-Px) activity in plasma, erythrocytes, heart, liver, and skeletal muscle from the first week after the initiation of the diet, an increase in heart lipid peroxide concentration from the second week, and an increase in liver glutathione S-transferase activity from the fourth week. From the twelfth week, a decrease in the growth rate in the rats fed the Se-deficient diet was observed. In spite of this growth impairment, no changes in electrocardiogram, muscle tone, degree of hemolysis, plasma biochemistry, or hematological values were detected. In summary, the authors found that a reduction of body Se is easily induced, but that the appearance of functional disorders following Se deficiency is difficult to detect in rats.     

Glutathione Peroxidase Activity and Erythrocyte Lipid Peroxidation as Indices of Selenium and Vitamin E Status in Young Pigs

A randomized, blocked 23 factorial experiment was conducted with 48 pigs from sows fed a diet low in selenium and vitamin E. From 3 to 12 weeks of age the piglets were kept in single pens and fed a basic diet consisting mostly of barley, dried skim milk, soybean meal and dried yeast, and containing 55 µg selenium and 3 mg vitamin E per kg. The treatment factors — i.e. feed supplements — were 2 levels of Se (nil, 60 µg/kg), 2 levels of vitamin E (nil, 50 mg/kg), and 2 levels of the feed antioxidant ethoxyquin (nil, 150 mg/kg). Blood samples, collected at termination of the experiment, were examined for glutathione peroxidase activity (GSH-Px) and resistance against erythrocyte lipid peroxidation (ELP) to evaluate Se and vitamin E status, respectively. Analysis of variance showed the GSH-Px activity to be litter-dependent (P < 0.001) and influenced by selenium supplementation (P < 0.001) but not by the other supplements or by interactions between supplements. Resistance against ELP was influenced only by vitamin E supplementation (P < 0.001). GSH-Px and ELP thus seem to be valuable and simple methods for evaluating, respectively, Se status and vitamin E status in growing pigs.     

Effect of selenium supplementation on some blood biochemical parameters in male rats

The long-term effect of selenium supplementation on blood glutathione peroxidase (GSH-Px) activity and plasma TBARS’ production (as an index of peroxidation) was evaluated in 15-mo-old male rats fed a diet supplemented with 0.25 or 0.50 ppm selenium, for 12 mo. A group of nonsupplemented age-matched rats was the control. In addition, triglycerides, phospholipids, total and free cholesterol, HDL-cholesterol, and HDL-phospholipid levels were measured in plasma. Plasma testosterone levels were also determined in order to control the aging process in these animals. The GSH-Px activity and the peroxidation level were unchanged in all the groups. However, concerning the lipid parameters, a decrease in triglycerides concentration was observed in both treated groups (p<0.05). Therefore, in these experimental conditions, despite no observed changes in parameters related to lipid peroxidation, selenium seems to be involved with triglycerides metabolism, eventually improving the triglycerides status of aged animals.     

Effects of long-term selenium yeast supplementation on selenium status studied in the rat

To investigate the selenium status during long-term dietary supply of selenium yeast, 30-day-old male rats were fed for 379 days a methionine-adequate low-selenium diet supplemented with 0.2 mg Se/kg (selenium-adequate diet) or 1.5 mg Se/kg (high-selenium diet) in the form of selenium yeast that contained 60% of the element as l-selenomethionine. Their selenium load was determined at several intervals by neutron activation analysis of the selenium concentrations in the main selenium body pools, skeletal muscle and liver. After 64 days the tissue selenium concentrations plateaued in both groups and then stayed at that level. Compared with the selenium-adequate group, elevated tissue selenium concentrations were found in the high-selenium group, but the increase by a factor of 3.5 in the muscle and by a factor of 2.3 in the liver was smaller than the 7.5-fold increase in the selenium intake. In the selenium-adequate group about 50% of the muscle selenium and 30% of the liver selenium and in the high-selenium group about 85% of the muscle selenium and 70% of the liver selenium were estimated to be present in non-selenoprotein forms. During selenium depletion the liver glutathione peroxidase activity in the high-selenium group remained unaffected for 4 weeks and then decreased more slowly than that in the selenium-adequate group. From these results it can be concluded that selenium incorporated from the selenium yeast diet into non-selenoprotein forms can serve as an endogenous selenium source to maintain selenoprotein levels in periods of insufficient selenium supply.