Effect of selenium and protein deficiency on selenium and glutathione peroxidase in rats

Twenty-four weanling male Wistar rats were divided into four groups fed diets containing adequate or deficient levels of selenium (0.5 ppm [+ Se] or <0.02 ppm [−Se] and protein (15% [+Pro] or 5% [−Pro]), but adequate levels of all other nutrients for 4 wk to determine the effects of Se deficiency and protein deficiency on tissue Se and glutathione peroxidase (GSHPx) activity in rats. Plasma, heart, liver, and kidney Se and GSHPx were significantly lower in Se-deficient groups in relation to Se-sufficient groups. In Se-deficient groups, Se and GSHPx were significantly higher in −Se−Pro rats in heart, liver, and kidney. Data analysis showed that there were significant interaction effects between dietary Se and protein on Se and GSHPx of rats. It is assumed that under the condition of Se deficiency. a low level of protein may decrease Se and GSHPx utilization, increase GSHPx synthesis, and result in Se redistribution. This could account for high levels of Se and GSHPx in the −Se−Pro rats compared to −Se+Pro rats.     

Comparison of the selenium level with GSH-Px activity in the liver of mice treated with 7,12 DMBA

In this study, the relationship between selenium (Se) and glutathione peroxidase (GSHPx) levels was investigated in 7,12-dimethylbenz(a)anthracene (7,12-DMBA)-treated mouse liver. The potential mammary carcinogen 7,12-DMBA, was injected intraperitoneally (20 mg kg(-1) day(-1)) into 10-12 month old female mice. After 21 days of application the mice were sacrificed and GSHPx and Se levels of liver homogenates were measured. Se and GSHPx levels in 7,12-DMBA-treated mice were significantly lower than those of controls (p < 0.05). The control group exhibited 0.9 +/- 0.066 U mg(-1) protein and 0.86 +/- 0.058 p.p.m. levels of GSHPx and Se respectively. The 7,12-DMBA-treated group had significantly (p < 0.05) decreased GSHPx and Se levels (0.42 +/- 0.062 U mg(-1) protein and 0.69 +/- 0.034 p.p.m. respectively). The results show a direct relationship between Se and GSHPx activity and a negative correlation between antioxidant capacity and existence of a carcinogen in metabolism.     

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.     

The Effect of Different Levels of Selenium in Mineral Mixtures and Salt Licks on Selenium Status in Sheep

This paper describes 3 experiments comparing the effect of 10, 25 and 40 mg Se/kg, as sodium selenite, in mineral mixtures and salt licks fed to sheep. The supplement was given during the indoor season from October to May to 7 different flocks, each consisting of 50 to 100 sheep, in areas with selenium deficiency problems. The average selenium level in the basic diets did not exceed 0.05 mg/kg. Selenium status was monitored in the blood of ewes and lambs, and in milk. Blood selenium in lambs correlated well with blood selenium in their dams (r = 0.85). Selenium levels in milk on day 1 (colostrum) correlated well with selenium levels in dams (r = 0.92) and in offspring (r = 0.87). Statistically significant differences were found between the different flocks. In areas with extreme selenium deficiency, 10 mg Se/kg in mineral mixtures and salt licks proved insufficient. A content of 25 mg Se/kg, providing a daily intake of about 0.4 mg selenium, resulted in selenium levels in ewes’ blood, ewes’ milk and in the offspring that should prevent selenium deficiency disease without causing any toxic effects.     

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.     

Differential effects of dietary selenium (Se) and folate on methyl metabolism in liver and colon of rats

A previous study compared the effects of folate on methyl metabolism in colon and liver of rats fed a selenium-deficient die (<3 μg Se/kg) to those of rats fed a diet containing supranutritional Se (2 mg selenite/kg). The purpose of this study was to investigate the effects of folate and adequate Se (0.2 mg/kg) on methyl metabolism in colon and liver. Weanling, Fischer-344 rats (n=8/diet) were fed diets containing 0 or 0.2 mg selenium (as selenite)/kg and 0 or 2 mg folic acid/kg in a 2×2 design. After 70 d, plasma homocysteine was increased (p<0.0001) by folate deficiency; this increase was markedly, attenuated (p<0.0001) in rats fed the selenium-deficient diet compared to those fed 0.2 mg Se/kg. The activity of hepatic glycine N-methyltransferase (GNMT), an enzyme involved in the regulation of tissue S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), was increased by folate deficiency (p<0.006) and decreased by selenium deprivation, (p<0.0003). Colon and liver SAH were highest (p<0.006) in rats fed deficient folate and adequate selenium. Although folate deficiency decreased liver SAM (p<0.001), it had no effect on colon SAM. Global DNA methylation was decreased (p<0.04) by selenium deficiency in colon but not liver; folate had no effect. Selenium, deficiency did not affect DNA methyltransferase (Dnmt) activity in liver but tended to decrease (p<0.06) the activity of the enzyme in the colon. Dietary folate did not affect liver or colon Dnmt. These results in rats fed adequate selenium are similar to previous results found in rats fed supranutritional selenium. This suggests that selenium deficiency appears to be a more important modifier of methyl metabolism than either adequate or supplemental selenium. The U.S. Department of Agriculture, Agriculture Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination.     

Effect of magnesium deficiency on enterocyte Ca, Fe, Cu, Zn, Mn and Se content

In previous studies based on indirect procedures, we reported that Mg deficit increased the bioavailability of a number of elements such as calcium, zinc, iron, copper, manganese and decreased selenium absorption. The present study was designed to verify these findings by direct methods. We investigated the effect of dietary magnesium deficiency on enterocyte Ca, Fe, Zn, Cu, Mn and Se concentrations. Male Wistar rats were fed a Mg-deficient diet (129 mg Mg/kg food) for 70 days. Whole enterocytes from the upper jejunum were isolated and Ca, Fe, Zn, Cu, Mn and Se were determined. The results were compared with findings in a control group that was pair-fed with an identical diet except that it covered this species's nutritional requirements for Mg (480 mg Mg/kg food). The Mg-deficient diet significantly increased enterocyte content of Ca, Fe, Zn, Cu and Mn; however, we found no significant changes in the Se content of these cells. These data support the results obtained by indirect methods.     

Selenium Deposition in Tissues and Eggs of Laying Hens Given Surplus of Selenium as Selenomethionine

Forty-eight Norwegian bred White Leghorn chickens were divided into 6 groups and fed a basal diet containing 0.30 mig Se/kg supplemented with 0, 0.1, 0.5, 1.0, 3.0 or 6.0 mg Se/ kg in the form of selenomethionine for 18 weeks. A supplement of only 0.1 mg Se/kg induced significantly higher selenium concentrations in breast muscle and eggs, particularly in the egg white. The increase of selenium in the tissue and egg was proportional to the amounts of selenomethionine added to the feed. In the group given 6.0 mg Se/kg, the selenium concentrations in all tissues and eggs analysed ranged from 4.8 to 7.3 μg Se/g. No signs of toxic effects were observed even at the highest intake of selenium. Excess supply of selenium as selenomethionine to chickens was shown to be more potent than sodium selenite in raising the selenium concentration in tissues and eggs. A supplementation up to 10 times the requirement did not increase the levels of selenium in poultry products to such a degree that they could be considered as a potential risk for human consumption.     

The effects of dietary selenium on the biotransformation of 7,21-dimethylbenz[a]anthracene

The influence of dietary selenium on the mutagenic activation of 7,12-dimethylbenz[a]anthracene (DMBA) by rat liver S9 was studied using the Ames test. Rats received supplemental selenium, as sodium selenite, in the drinking water or in the diet. All rats additionally received 0, 20, 50, 100, or 500 mg Aroclor 1254 per kg body weight. Revertant counts decreased 72 and 31% at the 20- and 100-mg/kg induction levels, respectively, with S9 preparations from rats given selenium supplementation, compared to controls. No significant effects of selenium on S9 preparations was observed in rats treated with 500 mg/kg Aroclor. Preparations of S9 from rats receiving 2.5 ppm Se in their diet produced 46, 84 and 70% less revertants than controls at the 20-, 50- and 100-mg/kg induction levels. Increasing the selenium concentration in the diet to 5 ppm reduced the revertant counts by 71, 68 and 65%, at the 20-, 50- and 100-mg/kg induction level of Aroclor, respectively. Dietary selenium supplementation was shown to decrease the mutagenic activation of DMBA by liver microsomes. These studies indicate that in vivo selenium supplementation may reduce susceptibility to the action of various carcinogens.     

Influence of selenium deficiency on the acute cardiotoxicity of adriamycin in rats

The influence of selenium (Se) deficiency on the acute cardiotoxicity induced by the anticancer drug adriamycin (ADR) has been studied in rats by electrocardiography. Two categories were formed by feeding groups of rats a Se-supplemented and a Se-deficient diet. The supplemented animals were taken as normals. The two categories were treated with iv injections of saline solution containing ADR at doses of 0, 7.5, and 15 mg/kg body wt. The cardiac Se concentration and glutathione peroxidase (GSH-Px) activity in the Se-deficient groups were <2% lower than in the normals. The normal groups showed significant widening of the SaT and QaT durations when given 15 mg/kg ADR. The Se-deficient groups exhibited a dose-dependent widening of the SaT and QaT duration at 7.5 and 15 mg/kg and narrowing of the PQ duration at 15 mg/kg ADR. No heart rate or QRS duration changes were detected in both categories. Our results suggest that an imbalance of the antioxidant system is associated with Se deficiency and that Se plays a role in preventing the cardiac functional disorder attributable to oxygen free radical formation induced by ADR.     

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.     

The effect of long-term enrichment of diet with selenium, vitamin E and B15 on the activity of certain enzymes in rat brain

The aim of this study was tracing of changes in the activity of glutathione peroxidase (GSHPx), glutathione transferase (GSH S-Tr), aspartate aminotransferase (AspAT) and alanine aminotransferase (A1AT) in the brain as a result of diet enrichment with antioxidants: selenium (Se), vitamin E and vitamin B15 (pangamic acid). The experiment was carried out on Wistar rats with initial body weight 150 g. Following prolonged enrichment of diet with Se (0.1 ppm of sodium selenite), vitamin E (6 mg/100 g of diet) and vitamin B15 (2.5 mg/100 g of diet) the following results were obtained. The activity of GSHPx in brain microsomes was not changed after one year of vitamin E administration when it was measured against hydrogen hydroxide and against cumene hydrochloride; vitamin E administration increased the activity of GSH S-Tr in the cytoplasmic fraction of brain cells. Diet enrichment with selenium increased after 12 and 18 months the activity of GSHPx measured against both substrates, and GSH S-Tr activity increased considerably. Presence of vitamin B15 in diet reduced GSHPx activity after one-year or longer administration, after 18 months the activity of GSH S-Tr was reduced also. No changes were noted in the activity of AspAT and A1AT.     

Investigation of lipid peroxide and glutathione redox status of chicken concerning on high dietary selenium intake

This study was designed to investigate the effects of excess (24.5 mg Se/kg feed) inorganic and organic dietary selenium supplementation on 3-week-old broilers. The experiments lasted 4 days. Intensity of lipid peroxidation processes (malondialdehyde, MDA) and the amount (reduced glutathione, GSH) and activity (glutathione peroxidase activity, GSHPx) of gluathione redox system were measured in blood plasma, red blood cell hemolysate and liver. Voluntary feed intake in the selenium-treated groups reduced remarkably. Elevated GSH concentration and GSHPx activity were measured in plasma and liver of both selenium-treated groups compared to the untreated control and the 'pair-fed' controls. The lipid peroxidation processes in the liver showed higher intensity than the control due to both selenium treatment. The applied dose of selenite and selenomethionine does not inhibit, but even improves the activity of glutathione redox system in the liver during the early period of selenium exposure.     

Modulation of β-amyloid precursor protein trafficking and processing by the low density lipoprotein receptor family

Selenium is an essential micronutrient that function through selenoproteins. Selenium deficiency results in lower concentrations of selenium and selenoproteins. The brain maintains it's selenium better than other tissues under low-selenium conditions. Recently, the selenium-containing protein selenoprotein P (Sepp) has been identified as a possible transporter of selenium. The targeted disruption of the selenoprotein P gene (Sepp1) results in decreased brain selenium concentration and neurological dysfunction, unless selenium intake is excessive However, the effect of selenoprotein P deficiency on the processes of memory formation and synaptic plasticity is unknown. In the present studies Sepp1(-/-) mice and wild type littermate controls (Sepp1(+/+)) fed a high-selenium diet (1 mg Se/kg) were used to characterize activity, motor coordination, and anxiety as well as hippocampus-dependent learning and memory. Normal associative learning, but disrupted spatial learning was observed in Sepp1(-/-) mice. In addition, severe alterations were observed in synaptic transmission, short-term plasticity and long-term potentiation in hippocampus area CA1 synapses of Sepp1(-/-) mice on a 1 mg Se/kg diet and Sepp1(+/+) mice fed a selenium-deficient (0 mg Se/kg) diet. Taken together, these data suggest that selenoprotein P is required for normal synaptic function, either through presence of the protein or delivery of required selenium to the CNS.     

Supplemented Organic and Inorganic Selenium Affects Milk Performance and Selenium Concentration in Milk and Tissues in the Guanzhong Dairy Goat

Trace amounts of selenium (Se) are essential for several organisms, and deficiencies therein have adverse effects on growth, development, and reproduction; this is particularly significant in animals raised for milk and livestock production. To study the effect of Se on Guanzhong dairy goats, their diets were supplemented with different sources (inorganic or organic) and Se concentrations (0.2 or 0.4 mg Se/kg). A non-Se-fortified basal diet served as a negative control, and a sixth treatment group received both inorganic and organic Se sources (0.2 mg Se/kg diet each). Dietary Se supplementation increased milk production, with organic Se being more effective than inorganic Se. Selenium supplementation also increased Se concentration and glutathione peroxidase activity in whole blood, with organic Se more effective than inorganic Se at the same Se concentration. With increasing Se in diets, the Se content in milk increased markedly, reaching a plateau value at day 30 in all groups, and organic Se (0.4 mg/kg diet) had the best effect. In addition, dietary Se sources and concentrations markedly affected Se concentrations in different tissues and organs. Thus, organic Se supplementation of a basal diet at 0.4 mg/kg is practically applicable for Se-enriched milk and meat production in Guanzhong dairy goats.     

Oxidative DNA base damage, antioxidant enzyme activities and selenium status in highly iodine-deficient goitrous children

The objective of this study was to investigate oxidative DNA damage, and the levels of antioxidant enzymes (AOE) and selenium (Se) in relation to iodine deficiency and/or goiter in children. The study was performed in a group of goitrous high school children (15-18 years of age) ( n =14) with severe or moderate iodine deficiency. Thyroid hormones (TSH, FT 4 , TT 4 , FT 3 , TT 3 ), urinary iodine (UI) and plasma Se levels, and erythrocyte glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were determined and compared with those of a control group consisting of non-goitrous high school children ( n =14) with normal UI levels or mild iodine deficiency. In the goitrous group, concentrations of FT 4 , TT 4 , plasma Se and UI, and activities of GSHPx and SOD were found to be significantly lower. Six typical hydroxyl radical-induced base lesions in genomic DNA of peripheral blood were identified and quantified by gas chromatography/isotope-dilution mass spectrometry (GC/IDMS), and higher levels of DNA base lesions were observed in the goitrous group. The results suggest that highly iodine-deficient goitrous children may be under oxidative stress, which may lead to greater level of oxidative damage to DNA. This study supports the evidence for the reported relationship between iodine deficiency and the increased incidence of thyroid malignancies.     

Cardioprotective Effect of Selenium Against Cyclophosphamide-Induced Cardiotoxicity in Rats

The objective of this study is to evaluate the possible protective effects of selenium (Se) against cyclophosphamide (CP)-induced acute cardiotoxicity in rats. A total of 42 male Spraque-Dawley rats were divided into six groups (n = 7). Rats in the first group were served as control. Rats in the second group received CP (150 mg/kg) at the sixth day of experiment. Animals in the third and fourth groups were treated with only 0.5 and 1 mg/kg Se respectively for six consecutive days. Rats in the fifth and sixth groups received respective Se doses (0.5 or 1 mg/kg) for 6 days and then a single dose of CP administered on the sixth day. On day 7, the animals were sacrificed; blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and ischemia-modified albumin (IMA) levels. Heart tissues were processed routinely and tissue sections were stained with H + E for light microscopic examination. In the CP-treated rats MDA, LDH, CK-MB, and IMA serum levels increased, while GSH levels decreased. Microscopic evaluation showed that tissue damage was conspicuously lower in CP plus Se groups. Moreover, 1 mg/kg Se was more protective than 0.5 mg/kg Se as indicated by histopathological and biochemical values. In conclusion, Se is suggested to be a potential candidate to ameliorate CP-induced cardiotoxicity which may be related to its antioxidant activity.     

Alterations in plasma total and high density lipoprotein cholesterol levels in hyperlipidemic rats fed diets with varied content of selenium and vitamin E

The effect of dietary selenium and vitamin E on plasma total (TC) and high density lipoprotein cholesterol (HDLC) was evaluated in 54 Sprague Dawley rats fed cholesterol/cholic acid enriched diets. Diets 1, 2, and 3 had no added selenium (low Se) and 0 (low), 60 (adequate), and 600 (high) mg/kg dL alpha tocopheryl acetate added respectively. Sodium selenite at 0.2 mg/kg (adequate Se) was added to diets 4, 5, and 6 and at 4.0 mg/kg (toxic Se) to diet 7, 8, and 9 with the same pattern of vitamin E added to the diet as described above. TC and HDLC were measured using the Kodak Ectachem system. Rats in the low and adequate Se groups fed high vitamin E had lower TC values than rats fed lower vitamin E levels but differences were not significant. In the toxic Se groups, rats fed high vitamin E had significantly (p<0.05) higher plasma TC values than did lower Vitamin E groups. Rats on the high vitamin E diets with low or adequate Se had significantly (p<0.05) higher mean plasma HDLC values when compared to rats fed low or adequate vitamin E diets. HDLC values for animals on Se toxic diets were significantly (p<0.05) lower in rats fed a low vitamin E diet. In rats fed Se deficient and adequate diets, a high vitamin E intake resulted in a decrease in TC and an increase in HDLC. In Se toxic rats, TC was elevated by a high dietary intake of vitamin E as was HDLC with both values being significantly higher than values found in the vitamin E deficient rats. Vitamin E deficiency resulted in a plasma lipid pattern that has been associated with greater cardiovascular disease risk.     

Effects of Selenium- and Chromium-Enriched Diets on Growth Performance,Lipid Profile,and Mineral Concentration in Different Tissues of Growing Rabbits

The aim of this study was to investigate the effect of dietary supplementation with different sources of selenium and/or organic chromium on the growth performance, digestibility, lipid profile, and mineral content of hair, liver, and fore and hind limb of growing rabbits. A total of 150 weanling New Zealand White (NZW) male rabbits were randomly allotted to six dietary treatment groups: (1) basal diet (control group), (2) basal diet + 0.6 mg sodium selenite/kg diet, (3) basal diet + 0.6 mg selenium yeast/kg diet, (4) basal diet + 0.3 mg sodium selenite/kg diet + 0.3 mg selenium yeast/kg diet, (5) basal diet + 0.6 mg chromium yeast/kg diet + 0.6 mg selenium yeast/kg diet, (6) basal diet + 0.6 mg chromium yeast/kg diet. Only the combination between inorganic and organic selenium led to significant improvement in body weight, body weight gain, and feed conversion ratio. Carcass traits were not different in all groups. Selenium (Se) and chromium (Cr) were deposited in the tissues of rabbits fed diets supplemented with Se and Cr, respectively. Blood serum in both of selenium- and chromium-supplemented groups showed declined total cholesterol, triglycerides, and low-density lipoprotein (LDL). Group supplemented with organic chromium showed higher high-density lipoprotein (HDL) than the other groups. It could be concluded that using a mixture of inorganic and organic Se has a positive effect on the growth performance of growing rabbits. Both Se and Cr have hypocholesterolemic effect. Both of Se and Cr can be deposited in the meat and other tissues of rabbits and that improves meat quality which positively reflects on human acceptance. The combination between inorganic (0.3 mg sodium selenite/kg diet) and organic selenium (0.6 mg selenium yeast/kg diet) improved growth performance traits of growing rabbits.

     

Effects of selenium deficiency on fatty acid metabolism in rats fed fish oil-enriched diets.

The hepatic fatty acid metabolism was investigated in rats stressed by selenium deficiency and enhanced fish oil intake. Changes in the composition of lipids, peroxides, and fatty acids were studied in the liver of rats fed either a Sedeficient (8 microg Se/kg) or a Se-adequate (300 microg Se/kg) diet, both rich in n-3 fatty acid-containing fish oil (100 g/kg diet) and vitamin E (146 mg alpha-tocopherol/kg diet). The two diets were identical except for their Se content. Se deficiency led to a decrease in hair coat density and quality as well as to changes in liver lipids, individual lipid fractions and phospholipid fatty acid composition of the liver. The low Se status did reduce total and reduced glutathione in the liver but did not affect the hepatic malondialdehyde level. In liver phospholipids (PL), Se deficiency significantly reduced levels of palmitic acid [16:0], fatty acids of the n-3 series such as DHA [22:6 n-3], and other long-chain polyunsaturates C-20-C-22, but increased n-6 fatty acids such as linoleic acid (LA) [18:2 n-6]. Thus, the conversion of LA to arachidonic acid was reduced and the ratio of n-6/n-3 fatty acids was increased. As in liver PL, an increase in the n-6/n-3 ratio was also observed in the mucosal total fatty acids of the small intestine. These results suggest that in rats with adequate vitamin E and enhanced fish oil intake, Se deficiency affects the lipid concentration and fatty acid composition in the liver. The changes may be related to the decreased levels of selenoenzymes with antioxidative functions. Possible effects of Se on absorption, storage and desaturation of fatty acids were also discussed.