Yeast-based Diet Research Articles

Effects of Dietary Selenium on UVB-Induced Skin Carcinogenesis and Epidermal Antioxidant Status

Low plasma selenium levels have been linked to increased risk of non-melanoma skin cancer in humans. The present study examined the relationship between selenium level in the diet and development of skin tumors induced by ultraviolet radiation in female Skh:HR-1 hairless mice. Animals were maintained on a torula yeast-based diet containing either 0, 0.1, or 0.5 mg/kg selenium as Na2SeO3. Ultraviolet light at a dose of 90 mJ/cm2, three times weekly for 20 weeks, resulted in skin tumors in all groups. Following cessation of ultraviolet light exposure, tumors continued to increase in selenium-deficient mice and those fed only 0.1 mg/kg, but leveled off for those on 0.5 mg/kg. During the carcinogenesis process, epidermal antioxidant enzymes catalase, superoxide dismutase, and glutathione peroxidase were monitored. Selenium deficiency decreased glutathione peroxidase and resulted in an early increase in superoxide dismutase and catalase in response to ultraviolet light treatment. These results indicate that dietary Se may be an important chemopreventive agent for skin cancer.

Aggregation pheromone ofCarpophilus antiquus (Coleoptera: Nitidulidae) and kairomonal use ofC. lugubris pheromone byC. antiquus

Males ofCarpophilus antiquus Melsheimer (Coleoptera: Nitidulidae) emit an aggregation pheromone that was found to be a novel hydrocarbon, (3E,5E,7E,9E)-6,8-diethyl-4-methyl-3,5,7,9-dodecatetraene. A synthetic scheme and spectra (mass and proton NMR) are given for the compound. Beetles produced the pheromone when feeding on a variety of media, including the brewer's yeast-based artificial diet, fermenting whole-wheat bread dough, corn, and prunes; live baker's yeast was generally added to the food media. Males held individually produced, on average, 25 × more pheromone per beetle than males held in groups of 10 or more. Pheromone was not produced until males were at least 5 days old but was still detected from the oldest beetles tested (47 days). In field tests, the pheromone was attractive to both sexes ofC. antiquus, and it was synergized by food volatiles: A combination of pheromone and fermenting whole wheat dough attracted 2.5× more beetles than pheromone alone, but dough by itself was not significantly more attractive than the control. Semiochemical interactions were studied amongC. antiquus and two other sympatric species for which pheromones are known,C. lugubris Murray andC. freemani Dobson.C. antiquus responded readily to the pheromone ofC. lugubris, but all other interspecific responses to the pheromones were weak. In a sample of naturally infested corn ears, the presence ofC. antiquus was strongly associated with the presence ofC. lugubris, as would be expected if the pheromone ofC. lugubris serves as a kairomone forC. antiquus.

Selenium bioavailability of soy-based diets in rats

Bioavailability of selenium from soy grown with sodium selenite and sodium selenate was evaluated by the use of glutathione peroxidase activity regeneration in rats. Male weanling Sprague-Dawley rats were fed a selenium-deficient Torula yeast-based diet for 4 weeks followed by a 7-week repletion period during which animals were fed one of six experimental selenium repletion diets. Soybeans grown with selenite and selenate were processed into flour and used as the protein source in diets providing 50 and 100 ng/g selenium. Bioavailability was determined by liver and plasma glutathione peroxidase regeneration and tissue selenium repletion in response to Se in soy diets and compared with changes in response to Se in reference diets containing Torula yeast supplemented with sodium selenite. Results indicate that selenium from soy was as bioavailable as sodium selenite from the reference diet. In addition, selenium from soy grown with sodium selenite was as bioavailable to the rat as selenium from soy grown with sodium selenate. These data indicate that soy protein provided a bioavailable source of dietary selenium to rats and that the form of selenium available in plants did not influence selenium bioavailability of the resulting soy-based product.

Enzymological and excretory adaptations of Ceratitis capitata (Diptera: Tephritidae) larvae to high protein and high salt diets

1. 1. Ceralitis capitata (Diptera, Cyclorrhapha, Tephritidae) larvae spend more time in the two first larval instars and attain a smaller weight on pupation if maintained on a high salt, high protein meat diet than on a yeast-based diet without added salts. 2. 2. The Malpighian tubules of larvae reared in the meat diet store carbonates at their distal ends. The amount of stored carbonates depends on the ash content of the diets. 3. 3. Midgut amylase and maltase activities are similar in C. capitata larvae maintained on meat and yeast diets. 4. 4. Trypsin is more active in the midgut contents of larvae fed a meat diet than a yeast diet. After the transference of the larvae from both diets to starch the observed differences increased. 5. 5. Midgut aminopeptidase is found with lower activity in larvae grown in a meat diet and its activity is not increased if the larvae are transferred onto starch gels. 6. 6. The results suggest that C. capitata larval adaptations to a high salt diet include salt storage on the Malpighian tubules. The adaptations to a high protein diet might include an increase in the midgut trypsin, which is thought to lower protein excretion by permitting its removal after digestion from the peritrophic membrane contents, and a decrease in midgut aminopeptidase, which is thought to avoid harmful effects of excess luminal free amino acids.

Comparative Antioxidant Effectiveness of Dietary β-Carotene, Vitamin E, Selenium and Coenzyme Q10 in Rat Erythrocytes and Plasma

Five groups of five weanling rats were each fed a Torula yeast-based diet either unsupplemented or supplemented with 30 mg beta-carotene/kg, 30 IU vitamin E/kg, 1 mg selenium/kg or 30 mg coenzyme Q10/kg. Elevated levels of plasma aspartate aminotransferase and alanine aminotransferase are sensitive indicators of liver damage. The former enzyme was lower (P less than 0.01) in the vitamin E-, selenium- and beta-carotene-supplemented groups than in the unsupplemented control group, and the latter enzyme was lower in the vitamin E- and selenium-supplemented groups, suggesting a relatively equal effectiveness of these three antioxidants against liver damage. Erythrocytes were tested for protection against uninduced oxidative damage or that induced by 1 mmol/L bromotrichloromethane (BrCl3C) by measuring thiobarbituric acid-reactive substances (TBARS), hemoglobin, hemolysis, protein precipitation, alanine release and several enzyme activities. In untreated erythrocytes, selenium, beta-carotene and coenzyme Q10 exhibited protection by lowering (P less than 0.05) TBARS and alanine release, but only vitamin E protected against hemolysis. In BrCl3C-treated erythrocytes, vitamin E, selenium and beta-carotene protected by decreasing (P less than 0.05) protein precipitation, whereas selenium and beta-carotene decreased alanine release. The results of this study suggested that, in a manner analogous to vitamin E and selenium, beta-carotene and coenzyme Q10 function as antioxygenic nutrients.

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Selenium and Immune Cell Functions. II. Effect on Lymphocyte-Mediated Cytotoxicity

Selenium (Se) is an essential nutritional factor with a chemopreventive potential. This study examined the ability of C57BL/6J mice, maintained for 8 weeks on Se-deficient (0.02 ppm Se), normal (0.20 ppm Se), or Se-supplemented (2.00 ppm Se) Torula yeast-based diets, to generate cytotoxic lymphocytes (CTL) and to destroy tumor cells. CTL were generated in vivo by intraperitoneal immunization with P815 cells and in vitro by allogeneic stimulation of cells from animals maintained on a normal diet in media supplemented with 1 x 10(-9) to 1 x 10(-6) M Se (as selenite). Lymphocytes from animals maintained on the Se-supplemented diet had a greater ability to destroy tumor cells than lymphocytes from animals maintained on the normal diet, whereas Se deficiency reduced the cytotoxicity. The effects on cytotoxicity were accompanied by parallel changes in the levels of lymphotoxin produced. The greatest enhancement of tumor cytodestruction occurred with supplementation of 1 x 10(-7) M Se, whereas with 1 x 10(-6) M there was inhibition of the cytotoxic responses. The stimulatory effect of Se occurred during the phase of CTL generation rather than during the lytic phase of cytotoxicity. These results indicated that Se supplementation enhances CTL generation and the ability of a host to destroy malignant cells, whereas Se deficiency has the opposite effect.

Selenium and Immune Cell Functions. I. Effect on Lymphocyte Proliferation and Production of Interleukin 1 and Interleukin 2

The dietary intake of selenium (Se) has been shown to influence the development and expression of various biologic processes. This study examined the immunologic competence of lymphocytes from C57BL/6J mice maintained for 8 weeks on Se-deficient (0.02 ppm Se), normal (0.20 ppm Se, as sodium selenite), or Se-supplemented (2.00 ppm Se) Torula yeast-based diets. The ability of the cells to recognize alloantigens, to proliferate in response to stimuli, and to produce interleukin 2 (IL-2) was determined. Se deficiency significantly inhibited the ability of the lymphocytes to proliferate in response to allogeneic stimulation in the mixed lymphocyte reaction or to mitogen stimulation by phytohemagglutinin, whereas Se supplementation significantly enhanced both responses. In contrast, the amounts of IL-2 and interleukin 1 (IL-1) produced by lymphocytes and macrophages, respectively, removed from Se-deficient or Se-supplemented animals did not differ significantly from the amounts of IL-2 and IL-1 produced by cells removed from animals maintained on the control diet. These results suggest that the mechanism(s) responsible for the observed effects of Se on lymphocyte proliferation are independent of the levels of IL-2 or IL-1.

Comparative Toxicity and Tissue Retention of Selenium in Methionine-Deficient Rats Fed Sodium Selenate or L-Selenomethionine

Selenium (Se) toxicity is known to be affected by level of intake of the mineral, but there are conflicting reports on the relative toxicities of the various chemical forms of Se. We monitored Se toxicity in rats fed Torula yeast-based diets containing 0.1, 0.5 or 2.5 micrograms Se/g of diet as either sodium selenate (Na2SeO4) or L-selenomethionine (SeMet). Half the diets were supplemented to contain adequate dietary methionine (Met). Weights were monitored weekly for 6 (Met-adequate) or 7 (Met-deficient) wk, at which time the rats were killed. There were no significant differences in final weight among Met-adequate rats, regardless of level or form of dietary Se. Methionine-deficient rats all gained significantly less weight than their Met-adequate counterparts. Selenosis was most severe in the Met-deficient rats fed 2.5 micrograms Se/g of diet as Na2SeO4, as indicated by significantly impaired weight gains. Nonetheless, Se retention in serum, heart, brain, bone, testes, colon, skin, lungs and pancreas was greater in rats fed SeMet than in those fed Na2SeO4, and Met deficiency further intensified this trend. The kidney was the only organ in which Se levels were markedly higher in the severely poisoned Met-deficient rats fed Na2SeO4. Further research is needed to determine whether elevated kidney Se levels are related to the greater toxicity observed in the Met-deficient rats fed Na2SeO4.

Fish roe as a major component in start-feed for marine fish larvae

Marine fish larvae, cod ( Gadus morhua L.) and plaice ( Pleuronectes platessa), were start-fed in laboratory tanks using diets containing fish roe as a major component, and compared to larvae start-fed on other types of diets ( Calanus diets, yeast-based diets, microencapsulated diets and several experimental diets from various commercial sources). Although metamorphosis did not occur due to a high mortality rate, It is concluded that roe-based start diets were consumed by the larvae, and gave better growth rates and longer survival time than the other dry feeds. Roe diets were also tested in start-feeding of salmon fry, which showed negligible mortality and, in some cases, a higher growth rate than fry on a commercial salmon diet.

Effect of Selenium Repletion on Glutathione Peroxidase Protein Level in Rat Liver

We have previously reported that liver glutathione peroxidase (GSH-Px, EC 1.11.1.9) protein level and activity decrease exponentially during Se deficiency. To determine the effect of Se repletion on these parameters, Se-deficient rats were repleted with 0.1 or 0.5 mg Se/kg diet as Na2SeO3 in a 30% torula yeast-based diet and were killed 0, 1, 2, 3, 5, 7 or 14 d later. GSH-Px protein was quantitated using anti-GSH-Px antibodies. Dietary repletion with 0.5 mg Se/kg diet increased GSH-Px protein and activity significantly (P less than 0.05) after 1 d. After 5 d for GSH-Px protein and 7 d for activity the rate of increase slowed, and at d 14 neither GSH-Px protein nor activity was significantly different from that of Se-adequate rats. Repletion with 0.1 mg Se/kg diet did not significantly increase GSH-Px protein or activity until 14 d. To examine the short-term effect of Se repletion, Se-deficient rats were injected intravenously with 15 or 60 micrograms Se as Na2SeO3 and killed 1, 3, 6, 12 or 24 h later. Only rats injected with 60 micrograms Se and killed 24 h later had a significant increase in GSH-Px activity along with a marginally significant increase in GSH-Px protein. These response curves indicate that homeostatic processes control the level of GSH-Px. The lack of an increase in GSH-Px until 24 h after Se administration implies that additional metabolic events after a rise in cellular Se may be necessary prior to an increase in GSH-Px synthesis in Se-deficient rats.

Effect of Dietary Methionine on Utilization of Tissue Selenium from Dietary Selenomethionine for Glutathione Peroxidase in the Rat

To study the effect of dietary methionine on the bioavailability of Se from selenomethionine ([Se]Met), weanling rats were first loaded with Se by feeding 0.5 mg Se as [Se]Met per kg diet of a low methionine (0.17% by analysis) torula yeast-based diet for 21 d, and then were fed an Se-deficient diet (less than 0.02 mg Se/kg) supplemented with 0, 0.4 or 0.9% methionine for 28 d. Plasma, liver and muscle Se increased 2.6-, 2.5- and 2.2-fold, respectively, during [Se]Met supplementation, and then the tissue Se declined exponentially during the Se-deficient diet period. Plasma, liver and muscle glutathione peroxidase (GSH-Px) activities decreased 43-50% during the [Se]Met supplementation period in spite of the increase in tissue Se. When these [Se]Met-loaded rats were fed the Se-deficient diet and supplemented with methionine, tissue GSH-Px activities increased significantly within 3 to 7 d, but then decreased for the remainder of the experiment. Calculation of the percentage of tissue Se present as Se in GSH-Px indicated that substantial Se from dietary [Se]Met was stored in tissues in a form different from GSH-Px when a low methionine diet was fed. These results indicate that the dietary methionine level can modulate the availability of Se from dietary [Se]Met and from stored tissue [Se]Met; the inability of stored [Se]Met to provide Se for GSH-Px synthesis over a prolonged period of time suggests that [Se]Met may not be an optimum form for Se supplementation.

Effects of torula and brewer's yeast diets in obese and lean mice

Obese C57BL/6J-OB mice (ob/ob) and their lean littermates (?/+) were fed either torula yeast-based diet (TY) or brewer's yeast-based diet (BY) for a 23-d experimental period. Obese mice fed the BY diet had significantly lower liver weights than did mice fed the TY diet. Likewise, plasma glucose and insulin were significantly lower in obese mice fed the brewer's yeast diet (BY) than the torula yeast diet (TY). Liver weight and plasma glucose and insulin of lean mice were not significantly affected by diet during the experimental period. Despite the low Cr content of both TY and BY diets, bone Cr of the TY and BY groups was significantly higher than concentrations previously reported for the groups fed casein-based diets. The obese mouse may be particularly sensitive to Cr, making it a valuable model for elucidating effects of other dietary components on chromium status.

Modifying effects of supplemental selenium and sulfur on cadmium toxicity in rats.

Interactions among dietary supplements of selenium (Se), cadmium (Cd), and sulfur (S), and their effects on Cd toxicity in the cardiovascular system were explored in rats. Weanling male Sprague-Dawley rats were fed a Torula yeast-based diet in a 23 factorial design, which provided two levels each of supplemental Se (0 and 0.5 ppm-mg/kg diet—as Na2SeO3), and S (0 and 2% as K2SO2). Supplemental Cd (0 and 25 ppm-mg/L as Cd (C2H3O2)2 · 2H2O) was added to drinking water. Supplemental Cd induced cardiac hypertrophy only in rats not supplemented with Se. Selenium supplementation enhanced growth more markedly in Cd-fed rats than in rats not receiving Cd. Renal Cd content was increased by Cd feeding, but there was no significant effect of Cd feeding on hemoglobin or blood pressure. Supplemental Cd did not influence Se-GSH-Px activity in heart or kidney cytosol. Interactions between Se and Cd were not altered by S supplementation. These results suggest 1) that hypertension is not associated with increased kidney accumulation of Cd,per se; 2) a supplement of 0.5 ppm Se as selenite is sufficient to protect against Cd-induced reductions in Se-GSH-Px activity in heart and kidney cytosol; and 3) increased S intake does not compromise Se's protective effect against certain manifestations of Cd toxicity.

The Effect of Progressive Selenium Deficiency on Anti-Glutathione Peroxidase Antibody Reactive Protein in Rat Liver

Liver glutathione peroxidase (GSH-Px, EC 1.11.1.9) activity decreases when weanling rats are fed a Se-deficient diet. To determine the effect of dietary Se deficiency on the concentration of the protein portion of GSH-Px, weanling rats were fed a Se-deficient (< 0.02 ppm Se) or a Se-supplemented (0.2 ppm Se as Na2SeO3) 30% torula yeast-based diet and killed 0, 3, 7, 14, 21 or 28 d later. GSH-Px activity was assayed using H2O2, so only the Se-dependent GSH-Px was measured. Anti-GSH-Px antibodies, produced in a rabbit by three injections of purified rat liver GSH-Px, were used in an enzyme-linked immunosorbent assay for GSH-Px protein. Immunoblotting showed that the antibodies were highly specific for GSH-Px. In Sesupplemented rats, liver GSH-Px activity increased 66% and GSH-Px protein increased 50% over the 28 d. In Se-deficient rats, liver GSH-Px activity decreased exponentially to zero with a half-life of 2.8 d. Liver GSH-Px protein also decreased exponentially, but with a longer half-life of 5.2 d (P < 0.001), and the anti-GSH-Px antibody-reactive protein did not decrease to zero. This experiment shows that both GSH-Px activity and GSH-Px protein decrease exponentially during progressive dietary Se deficiency. The longer half-life of GSH-Px protein compared with GSH-Px activity suggests that an inactive GSH-Px polypeptide is present in rat liver during the early stages of Se deficiency.

The effects of ozone inhalation on the immunological response of selenium- and vitamin E-deprived rats

Deficiencies in vitamin E (E) or Se result in immune alterations, possibly due to reduction of antioxidant activity. Such reductions might greatly compromise the ability of the immune system to deal with additional oxidant stress, as encountered during exposure to air pollutants such as ozone (O3). To study possible interactions of these oxidative stresses on immune function, male Long-Evans hooded rats were maintained 5 weeks on torula yeast-based diets, with or without the addition of E or Se. Each dietary group was subdivided into O3-exposed and nonexposed groups. Two different regimens of O3 exposure were used: continuous (1.0 ppm, 8 hr/day for 7 days) or intermittent (2.0 ppm, 8 hr/day for 4 days, 2-4 days in ambient air followed by 1 day of exposure prior to sacrifice). Exposure to O3 in either regimen resulted in increased numbers of cells recovered by pulmonary lavage. With continuous exposure this increase was due to macrophage influx and, with intermittent exposure, due to influx of both macrophages and neutrophils. Combined deficiency of E and Se led to an enhanced ability of spleen and lung cells to mediate antibody-dependent cell-mediated cytotoxicity (ADCMC). In animals deficient in E, but not Se, O3 exposure depressed spleen cell ADCMC. Deficiencies of either E or Se also depressed lymphocyte response to mitogens. Although intermittent exposure to O3 caused no changes in mitogen response, in animals exposed continuously to O3 there was a significant enhancement of this response.

Rearing of sturgeon ( Acipenser baeri Brandt) larvae : 2. Protein metabolism: Influence of fasting and diet quality

Protein metabolism was analysed in sturgeon larvae fed either on a natural food ( Tubifex — diet 1, control) or on various artificial foods: mixed liver- and yeast-based diet (2), salmon starter diet (3) and casein-gelatin-based diet (4) (experiment I), or starved during 24 h (experiment II). Two pathways of protein metabolism, viz, protein synthesis and arginine oxidation, were measured in whole fish after immersion in a solution containing L- 14C(U)-arginine. During short-term fasting, there was a large decrease in protein synthesis (from 220 to 10% day within 24 h) and only a small increase in arginine oxidation (from 1.9 to 4.7 μmoles of arginine oxidized per g body weight/day). In fish fed on an artificial diet, an improvement in performance (increasing from diet 4 to diet 2), assessed by growth and survival, led to an increase in protein synthesis and in the oxidation of arginine. Thus, the overall amino acid metabolism was stimulated. Fish fed on natural food showed a better efficiency of protein metabolism, associated with a lower rate of protein synthesis and a lower rate of arginine oxidation, than fish fed on artificial food. These changes in whole fish protein synthesis could be linked both to a change in protein deposition rate in muscle and to a change in protein turnover rate of active tissues such as liver, pancreas and digestive tract in response to different feeding conditions (namely feeding frequency and diet composition).

Increased proliferative activity in selenium-deficient mouse liver

Male albino NMRI mice were fed a selenium-deficient (Se-), torula yeast-based diet containing less than 10 ppb Se for at least 2 months (Se-) while a control group received the same diet supplemented (Se+) with 330 ppb Se as Na2SeO3. The Se-(-)animals showed multiple enzyme modulations of liver enzyme activities indicating that they were in a severely Se- state. No significant difference in the basic DNA synthesis rate of Se-(-)animals compared to Se+ controls was measured. However, when liver cell proliferation was induced by either hepatopoietin pretreatment or by partial hepatectomy, an about 3-fold increase in DNA replication rates was found in Se- compared to controls. We conclude that the enhanced proliferative activity in Se- mouse liver is expressed in an emergency situation.

The effects of dietary sulfur on selenium utilization by the rat

The antagonistic effects of S on Se utilization were studied by measurement of tissue Se concentrations and glutathione peroxidase (GSHpx, E.C.1.11.1.9) activities in rats offered Torula yeast-based diets supplemented with sodium sulfate to provide 1.5, 3, or 5 g S/kg diet. Increasing sulfur concentrations in the diet caused small but significant decreases in GSHpx activity of liver, spleen, heart, lung small intestine, and skeletal muscle. Also significantly decreased were Se concentrations in liver and hair. Dietary sulfur content had no significant effect on body weight gain of the rats. With an adequate supply of Se in the diet, there are probably no major deleterious effects of dietary S on Se metabolism in the rat.

Selenium and drug metabolism—III: Relation of glutathione-peroxidase and other hepatic enzyme modulations to dietary supplements

Male mice were fed a torula yeast-based diet containing different amounts of added selenium for a period of 4 months. Liver glutathione peroxidase activity assayed with H 2O 2 showed a logarithmic dependence on dietary selenium with a saturation plateau above 2 ppm Se and an extrapolated zero of 0.02 ppm Se. In contrast, liver selenium content and GSH-Peroxidase activity showed a linear correlation. Glutathione peroxidase activity became undetectable at a liver Se content of about 90 ng Se/g liver wet wt. Thus, about 10% of liver selenium is not related to GSH-Px activity. Five dietary groups were supplemented, respectively, with 0, 0.05, 0.5, 5.0 and 10 ppm Se in the form of Na 2SeO 3. Some changes in drug metabolism enzymes were observed with the high Se diets. An increase occurred in Non-Se-GSH activity as well as in ethacrynic acid-assayed GSH transferase, these are interpreted as early signs of Se toxicity. The diet containing 0.01 ppm Se with no supplementary Se produced the multiple hepatic enzyme modulations which were previously reported. The animals raised on this very low Se diet had normal hepatic contents of glutathione, α-tocopherol, calcium, magnesium, iron, zinc, copper and manganese compared to controls supplemented with 0.5 ppm Se. However, significant changes in the microsomal fatty acid pattern were observed while the total phospholipid content as well as membrane fluidity showed no differences between the two dietary groups.