Effects Of Selenium Deficiency Research Articles

The effect of selenium deficiency on the feed consumption and growth of goats.

The feed consumption of goats was only reduced after considerable Se depletion. The conversion of Se-depleted animals to an Se-rich ration increased feed consumption within one day. An intrauterine Se deficiency (less than 38 micrograms Se/kg DM of the ration) did not induce intrauterine growth depression in kids. Se depletion led to a highly significant postnatal growth depression which increased with advancing Se depletion both during the lactation period and after weaning.

The effect of selenium deficiency on reproduction and milk performance of goats.

Even with a high vitamin E offer, Se deficiency (less than 38 micrograms/kg DM of the ration) led to a 33% lower conception rate (P less than 0.05) in goats and to a greater than 50% lower number of kids on the 91st day of life. The Se deficiency reduced the milk production significantly by 23% during the first 56 days of lactation, the milk fat production by 11% and the milk protein production by 12%.

Vitamin E and immune functions.

Vitamin E, the major lipid-soluble antioxidant present in all cellular membranes, is an important nutrient for optimal immune function. When animals are fed nutritionally complete diets lacking vitamin E, immune responses are adversely affected. Supplementation of these diets with higher than nutritionally adequate levels of vitamin E enhances immune responses. High levels of PUFA are immunosuppressive, and vitamin E can partially overcome this immunosuppression. High levels of vitamin C can protect tissue levels of vitamin E and may indirectly contribute to the immunoenhancement by vitamin E. Severe selenium deficiency is immunosuppressive. Vitamin E can protect some aspects of immune responses from the adverse effects of selenium deficiency. These data clearly indicate that nutrients that affect the overall antioxidant status have important effects on immune functions. In addition, antioxidant nutrient interactions can synergize to overcome the adverse effects of polyunsaturated fatty acids on immune functions (Fig 2).

Some effects of selenium deficiency on enzyme activities and indices of tissue peroxidation in Atlantic salmon parr ( Salmo salar)

Two groups of Atlantic salmon ( Salmo salar), mean weight 6 g, were given diets of differing selenium content (deficient 0.017 mg Se/kg; supplemented 0.944 mg Se/kg) and adequate vitamin E content (40 mg α-tocopheryl acetate/kg) for 28 weeks. The final weight and packed cell volume of salmon given the Se-supplemented diet were significantly greater than those of the Se-deprived fish. Blood vitamin E concentrations, and liver, blood and brain Se concentrations were all significantly lowered in Se-deficient salmon. No gross pathologies were observed but pathology was evident in pancreatic tissue (loss of integrity in endoplasmic reticulum and increased vacuolation) from Se-deficient salmon. Glutathione peroxidase (EC.1.11.1.9) activity was greatly reduced in liver of the Se-deficient salmon although there was no indication of any compensatory non Se-dependent glutathione peroxidase activity. Hepatic glutathione S-transferase (EC.2.5.1.18) activity, plasma pyruvate kinase (EC.2.7.1.40) activity, erythrocyte fragility and kidney reduced glutathione were all increased in Se deficiency.

The effect of selenium deficiency on peroxidative injury in the house fly, Musca domestica: A role for glutathione peroxidase

Selenium-dependent glutathione peroxidase activity is documented for the first time in insects. Reduction in glutathione peroxidase activity in the cytosol of adult house flies by lowering selenium in the diet results in significant increases in peroxidative injury. Catalase activity, while higher in low-selenium flies than in selenium-supplemented flies, does not prevent lipid peroxidation. The discovery of glutathione peroxidase activity in insects eliminates an anomaly which partially limited the usefulness of these animals as models for the study of the antioxidant defense system.

EFFECTS OF SELENIUM DEFICIENCY ON THE MORPHOLOGY AND ULTRASTRUCTURE OF THE COASTAL MARINE DIATOM THALASSIOSIRA PSEUDONANA (BACILLARIOPHYCEAE)1,2

ABSTRACTThe effects of selenium deficiency on the siliceous and nonsiliceous components of the planktonic marine diatom Thalassiosira pseudonana (Hust.) Hasle and Heimdal (clone 3H) are examined using light and electron microscopy. Selenium deficiency induces elongation along the pervalvar axis initially as a result of chain formation caused by the failure of sibling cells to separate and subsequently by cell elongation via the production of hyaline girdle bands. In Se‐deficient cultures cell elongation involves the blockage of both mitotic and cytokinetic components of cell division. Selenium deficiency results in ultrastructural alterations in the reticular membrane system and in mitochondrial and chloroplast membranes. Various types of inclusions are seen in vacuolar areas and the accumulation of lipid reserves is evident in Se‐deficient cells. These results provide indirect evidence for a metabolic Se requirement in this algal species.

EFFECTS OF SELENIUM DEFICIENCY ON THE MORPHOLOGY AND ULTRASTRUCTURE OF THE COASTAL MARINE DIATOM THALASSIOSIRA PSEUDONANA (BACILLARIOPHYCEAE)1,2

ABSTRACTThe effects of selenium deficiency on the siliceous and nonsiliceous components of the planktonic marine diatom Thalassiosira pseudonana (Hust.) Hasle and Heimdal (clone 3H) are examined using light and electron microscopy. Selenium deficiency induces elongation along the pervalvar axis initially as a result of chain formation caused by the failure of sibling cells to separate and subsequently by cell elongation via the production of hyaline girdle bands. In Se‐deficient cultures cell elongation involves the blockage of both mitotic and cytokinetic components of cell division. Selenium deficiency results in ultra‐structural alterations in the reticular membrane system and in mitochondrial and chloroplast membranes. Various types of inclusions are seen in vacuolar areas and the accumulation of lipid reserves is evident in Se‐deficient cells. These results provide indirect evidence for a metabolic Se requirement in this algal species.

Effect of Selenium Deficiency on the Chronic Toxicity of Adriamycin in Rats ,

The effect of selenium deficiency on the chronic toxicity of adriamycin was examined in rats fed diets adequate in vitamin E. Selenium-deficient and selenium-supplemented diets were fed to rats for 10 wk, after which groups of 10 rats fed each diet were given weekly intravenous injections of adriamycin in saline at doses of 0, 0.5 or 1.0 mg/kg body weight for 12 wk. All rats were killed at 24 wk. Even though the cardiac glutathione peroxidase activity in the selenium-deficient group was less than 1% of that of the selenium-supplemented group, the severity of the adriamycin-induced cardiomyopathy was similar in both groups. However, the selenium-deficient rats were more sensitive to the growth-inhibiting effect of the higher dose of adriamycin than the selenium-supplemented rats. Moreover, the lower dose of adriamycin caused a mild nephropathy in 70% of the deficient rats but affected only 10% of the supplemented rats. Selenium status may have to be considered when adriamycin is used as a chemotherapeutic agent.

Effect of selenium deficiency on hydroperoxide-stimulated release of glutathione from isolated perfused liver of rainbow trout (Salmo gairdneri).

1. Duplicate groups of rainbow trout (Salmo gairdneri) were each given partially purified diets which were either adequate or depleted in selenium for 40 weeks. 2. Although there was no significant difference in weight gain, liver Se concentration was significantly lower in fish given the deficient diet. 3. Glutathione (GSH) peroxidase (EC 1.11.1.9) activity was significantly reduced in liver of Se-deficient fish but a differential assay did not indicate the presence of a non-Se-dependent GSH peroxidase activity, although liver GSH S-transferase (EC 2.5.1.18) was significantly increased. 4. Perfusion of livers from trout given Se-adequate diets with t-butyl hydroperoxide (BuOOH) or hydrogen peroxide caused an increase in the rate of release of glutathione disulphide (GSSG) into the perfusate. 5. Perfusion of livers from Se-deficient trout with BuOOH or H2O2 did not result in any change in rate of release of GSSG into the perfusate. 6. These findings confirm the absence of any compensatory non-Se-dependent peroxidase activity in Se-depleted trout.

The Response of Selenium-Deficient Mice to Candida albicans Infection

The effects of selenium deficiency on the responses to Candida albicans infection were examined in mice. When selenium-deficient and selenium-supplemented mice were given i.v. injections of 0.1 ml suspensions of 1 × 105 or 5 × 104C. albicans in 0.9% sterile saline, deaths in the selenium-deficient animals started after 2.5–3.5 d compared with 7–8.5 d in the selenium-supplemented animals. Further studies demonstrated that 3 d after an i.v. injection of 1 × 105C. albicans, significantly more of the microorganisms were found in the kidneys (P < 0.001), livers (P < 0.025) and spleens (P < 0.01) of the selenium-deficient mice compared with the same organs of selenium-supplemented animals. Selenium deficiency was also demonstrated to impair the ability of mouse neutrophils to kill C. albicans in in vitro tests. The possible relationships of this defect in function to decreased resistance to C. albicans infection is discussed.

The effect of selenium deficiency in goats on lymphocyte production of leukocyte migration inhibitory factor

The effect of dietary selenium on caprine leukocyte migration inhibitory factor (LMIF) production was examined in vitro using lymphocytes from goats fed a diet deficient in selenium. Selenium deficiency was determined by decreased plasma glutathione peroxidase (GSH-Px). The ability of peripheral blood lymphocytes to produce LMIF induced by concanavalin A (Con A) was significantly (P < 0.05) inhibited when cells from selenium-deficient and selenium-adequate goats were compared. In contrast, no significant (P > 0.05) differences were found between lymphocytes from selenium-deficient and selenium-adequate goats for Interleukin-2 (IL-2) production and blastogenesis induced by Con A. These data suggest that selenium deficiency may selectively impair LMIF production and hence the ability of lymphocytes to modulate neutrophil migration.

Relationships between in vitro selenium supply, glutathione peroxidase activity, and phagocytic function in the HL-60 human myeloid cell line.

Utilizing the HL-60 human promyelocytic leukemia cell line cultured in defined medium, we examined the quantitative and temporal relationships between Se supply and the activity of the selenoenzyme glutathione peroxidase, as well as the effects of selenium deficiency on phagocytic function. Glutathione peroxidase activity depended on the medium Se concentration up to 2.6 X 10(-8) M (sodium selenate, 5 ng/ml), above which a plateau occurred. HL-60 cells grown in medium without Se supplementation became GSH peroxidase deficient, with activity 1-3% that of Se-replete cells. Replenishment of the medium with sodium selenate returned enzyme activity to 23% that of replete cells by 24 h and to 85% by 7 days, a process blocked by cycloheximide. Se-deficient HL-60 cells induced to granulocytic differentiation by dimethylformamide showed decreased hexose monophosphate shunt activity in response to phorbol myristate acetate and to an exogenous enzymatic H2O2-generating system. However, Se-deficient and -replete cells showed equal responses to methylene blue, which stimulates the shunt independently from the glutathione cycle. Se-deficient mature HL-60 cells stimulated with phorbol myristate acetate released 2.3-fold more H2O2 than Se-replete cells and only slightly (not significantly) less O2. Se-deficient and -replete differentiated HL-60 cells did not differ significantly in their capacities for cell motility or for ingestion of serum-opsonized bacteria. Differences between the findings of the present study and previous in vivo rat studies may reflect both the defined in vitro environment of the cell line and the inverse ratios of catalase and glutathione peroxidase activities in human and rat granulocytes.

Effect of Selenium Deficiency on Hydroperoxide-Induced Glutathione Release from the Isolated Perfused Rat Heart

Selenium deficiency has been implicated as a cause of the cardiomyopathy known as Keshan disease in China. Selenium is an essential constituent of glutathione peroxidase, an enzyme that destroys hydroperoxides by using the reducing equivalents of reduced glutathione (GSH). We studied glutathione-dependent hydroperoxide metabolism in isolated perfused rat hearts. Hearts from selenium-deficient rats contained 5% of the glutathione peroxidase activity found in control hearts. Glutathione reductase activity and glutathione content were not affected by selenium deficiency. Infusion of t-butylhydroperoxide into control hearts caused an increase in heart glutathione disulfide (GSSG) concentration proportional to the rate of hydroperoxide infusion up to 200 nmol/(g heart · min). GSSG was released into the perfusate in proportion to the hydroperoxide infusion rate up to 150 nmol/(g heart · min), but GSSG release did not increase further with higher infusion rates. Thus, GSSG release by the heart is saturable. It had a maximum rate of about 14 nmol GSH equivalents/(g heart · min) when stimulated by t-butylhydroperoxide infusion. This indicates that GSSG release by the heart is carrier-mediated and is not due to passive diffusion. Infusion of hydroperoxide into selenium-deficient hearts failed to cause increases in heart GSSG concentration and in GSSG release. This indicates that selenium-deficient heart cannot metabolize hydroperoxides through glutathione-dependent pathways. We suggest that selenium deficiency might predispose the heart to injury from oxidant stress.

Effect of selenium deficiency on cuticle integrity in the Cladocera (Crustacea).

Daphnia pulex de Geer and Daphnia magna Straus populations cannot be maintained in defined (sensu stricto) media containing less than 0.1 part per billion (ppb) of selenium. A concentration of 1 ppb is sufficient to satisfy minimal needs in otherwise sufficient media. In the first generation with no selenium added to the medium or detected in it, media deficiency is shown by a premature cuticle deterioration visually similar to senescence, by progressive loss of distal segments of second antennae (primary swimming appendages), and by a shortened lifespan. No progeny attain reproductive maturity in the second generation. Although experimental animals in prime condition exhibit a shortened lifespan in the first generation maintained at 0.5 ppb selenium, culture lines can be maintained at 0.5 ppb for indefinite numbers of generations if established as young orthoclones . Tests in organic-rich media indicate a significant sparing effect of organic additions. This selenium requirement is reminiscent of that for the stability of feathers in domestic fowl.

The effect of selenium-deficiency on rat fat-cell glucose oxidation

When rats are fed a selenium-deficient diet, the glutathione peroxidase activity of epididymal fat-cells decreases to 5-9% of that of control rats fed the same diet supplemented with 0.5 p.p.m. of selenium as sodium selenite. [1-14C]Glucose oxidation in fat-cells from rats fed a selenium-deficient diet is unresponsive to the action of t-butyl hydroperoxide, which stimulates 14CO2 formation from [1-14C]glucose 4-fold in control rats. Insulin enhances [1-14C]glucose oxidation and incorporation into lipids in fat-cells from both groups of rats; however, the response elicited is reduced in fat-cells prepared from selenium-deficient animals. The 'C-1/C-6 ratio' (ratio of glucose C-1 to glucose C-6 oxidized) is enhanced by insulin to a similar degree in fat-cells from both groups of animals. The stimulatory action of Zn2+ and dithiothreitol on [1-14C]glucose oxidation observed in fat-cells from selenium-supplemented rats is greatly reduced in fat-cells from selenium-deficient rats. [1-14C]Glucose oxidation in fat-cells from both groups of animals is highly sensitive to the stimulatory action of adenosine. It is concluded that the enhanced formation and glutathione-linked destruction of H2O2 plays, at the most, only a minor role in the stimulation of the flux of glucose through the pentose phosphate pathway elicited by insulin, although elimination of glutathione peroxidase activity may influence the action of insulin on glucose oxidation. Production and subsequent destruction of H2O2 may play an important role in the stimulatory action of Zn2+ and dithiothreitol on fat-cell [1-14C]glucose oxidation.

Interaction of selenium deficiency and fat intake in the regulation of enzymes associated with peroxide metabolism

The present study was designed to examine the effect of selenium deficiency on the activities of heme hydroperoxidase and glutathione peroxidases in the liver of male rats maintained on either a 5% or a 25% corn oil diet and treated with phenobarbital. Our results showed that although the basal levels of cytochrome P-450 and heme hydroperoxidase were unaffected by selenium deficiency, the magnitude of phenobarbital induction was impaired because of the depletion of this trace element. This effect was accentuated especially in rats with a high-fat intake. Selenium deprivation resulted in a virtual disappearance of glutathione peroxidase activity when assayed with hydrogen peroxide, because of depletion of the selenium-dependent enzyme. In contrast, only a 60% reduction in glutathione peroxidase activity was observed when assayed with cumene hydroperoxide. Phenobarbital administration was found to increase the activity of the latter only. Unlike the situation with the hemoprotein, dietary fat had no influence on either the basal or stimulated glutathione peroxidase activities, regardless of the selenium status of the animals.

Effect of selenium deficiency on liver and blood glutathione peroxidase activity in the black bullhead

AbstractMale black bullheads, approximately 4 gm, were fed a selenium‐deficient torula yeast‐based diet for 18 weeks, and the activity of glutathione peroxidase was studied in liver and blood using H2O2 as a substrate. Controls were on the same diet, but received weekly intraperitoneal injections of Na2SeO3. At 12 and 18 weeks significant decreases in blood and liver glutathione peroxidase activity were observed in the experimental animals. Liver showed an even greater decrease than blood in glutathione peroxidase activity in the selenium‐deficient animals. Females (4 gm) kept on the diet for 15 weeks showed similar results. Liver activities were not decreased nearly as much when cumene hydroperoxide was used as the substrate instead of H2O2. This indicates that at least two glutathione peroxidase activities are present in fish liver. One is selenium dependent; its activity, as measured with H2O2 as substrate, becomes almost undetectable in selenium‐deficient fish. This situation is very similar to that found in mammalian species.

Effects of selenium deficiency on the shape and arrangement of rodent sperm mitochondria

AbstractSelenium‐deficient male mice were obtained by feeding a selenium‐deficient diet for three successive generations to Swiss‐Webster mice. Examination of epididymal sperm by transmission electron microscopy revealed progressively increasing alterations in the shape and arrangement of mitochondria within the midpiece. Other midpiece anomalies included acute bends, disorientation of the axoneme and dense fibers, and cytoplasmic masses at atypical locations. Some cross sections showed both the principal piece and midpiece within the same plasma membrane. Negatively stained whole mounts of mitochondrial ghosts prepared from epididymal sperm of normal and first‐generation selenium‐deficient mice and rats indicated that the selenium‐deficient ghosts were smaller, less curved, and more fragile than those of normal sperm mitochondria. Thus, selenium appears to be required for the normal development or stabilization of mitochondria1 shape during spermiogenesis in these rodents.

6.3 The Development and Effects of Selenium Deficiency

Deficiencies of selenium (Se) and vitamin E can result in myopathies in cattle and sheep but the mechanics have not been clearly described. Both Se, as a component of the enzyme glutathione peroxidase, and vitamin E as a radicle scavenger, are involved in the protection of cells against the toxic effects of oxygen. In young calves, Se/vitamin E deficiency can result in the death of the animals due to a focal myopathy occurring in heart muscle; focal lesions are also found in skeletal muscle. In older calves, a more diffuse myopathy is usually confined to skeletal muscle and usually occurs when cattle are turned out from winter housing to spring pasture. However, low Se/vitamin E status will not invariably result in clinical symptoms of myopathy and other factors may be involved. This report describes some of the biochemical changes which can occur during the onset of clinical myopathy in Se/vitamin E-deficient cattle.

Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes.

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.