Endotoxin and lipid peroxidation in vivo in selenium- and vitamin E-deficient and -adequate rats.

The effect of Salmonella typhimurium endotoxin injected intraperitoneally (0.5 mg/kg body weight) on lipid peroxidation in vivo was assessed. Peroxidation was monitored by measuring ethane production, an autoxidation product of (n-3) unsaturated fatty acids. Weanling rats were fed a selenium- and vitamin E-deficient basal diet or one supplemented with 0.2 mg Se/kg and/or 200 mg vitamin E/kg. After 11 to 13 wk of feeding, ethane production was tripled in LPS-treated Se- and vitamin E-deficient rats compared to saline-treated deficient rats. In both doubly deficient and adequate rats, LPS increased ethane production, but it did so to a greater extent in Se- and vitamin E-deficient rats. Dietary Se or vitamin E supplementation alone significantly reduced ethane production from LPS-treated rats. Vitamin E was more protective than Se against LPS-induced lipid peroxidation. Escherichia coli and Salmonella minnesota LPS also increased ethane production in Se- and vitamin E-deficient rats. These results show that low doses of LPS stimulate lipid peroxidation in vivo in Se- and vitamin E-deficient rats.

Endotoxin and lipid peroxidation in vitro in selenium- and vitamin E-deficient and -adequate rat tissues.

The effect of Salmonella typhimurium endotoxin injected intraperitoneally into rats (0.5 mg/kg of body weight) on subsequent lipid peroxidation in vitro was assessed. Peroxidation was monitored by measuring ethane production from tissue slices, as well as thiobarbituric acid-reactive substances and conjugated dienes in tissue homogenates. Weanling rats were fed a selenium- and vitamin E-deficient basal diet or one supplemented with 0.2 mg of Se/kg of diet and 200 mg of vitamin E/kg. After 9 to 16 wk, ethane production and thiobarbituric acid-reactive substances in liver and lung generally were increased by LPS treatment of Se- and vitamin E-deficient rats. Conjugated dienes were increased by LPS treatment in liver of Se- and vitamin E-deficient rats, but paradoxically, were higher in Se- and vitamin E-adequate liver tissue. Daily injections of 1 g of hydroxyurea/kg of body weight, a cell proliferation inhibitor, for 2 d prior to LPS injection significantly decreased the LPS-induced ethane production in Se- and vitamin E-deficient rat liver and lung. These results show that low doses of LPS injected into rats stimulated lipid peroxidation in vitro in Se- and vitamin E-deficient rat liver tissue. Hydroxyurea decreased LPS-induced lipid peroxidation in vitro; this suggests that neutrophils or macrophages are involved in LPS-induced lipid peroxidation.

The metabolism of 75Se-selenomethionine in sheep given supplementary copper and molybdenum.

Four groups of three ram lambs were fed, in group pens, the following diets from 4 to 19 wk of age: 1) control (6 mg Cu/kg and 1 mg Mo/kg); 2) control plus 10 mg Cu/kg; 3) control plus 10 mg Mo/kg and 4) control plus 10 mg/kg of both Cu and Mo. Copper and Mo were added to the diet as copper sulfate and sodium molybdate. The main ingredients of the diets were alfalfa hay (20%), oats (20%) and corn (59%). At 19 wk, the animals were allocated randomly to individual metabolism cages and received a single oral dose of 75Se-selenomethionine. Liver Cu concentrations at slaughter (22 wk) were 77, 259, 68 and 316 mg/kg fresh weight for treatments 1 through 4. There was clinical evidence of Cu poisoning in lambs on treatment 2. Sheep given Cu supplements without additional Mo had reduced (P less than .05) levels of 75Se activity in muscle compared with control animals. This decrease in muscle 75Se in Cu-supplemented lambs was associated with a nonsignificant increase in 75Se content of other tissues and a nonsignificant increase in fecal excretion of 75Se. Apparent absorption and net retention of 75Se was 80% and 74%, respectively. Long-term ingestion of moderate levels of Cu influenced the metabolism of Se fed as selenomethionine, possibly through effects of chronic Cu toxicity on liver function.

Effects of copper and molybdenum supplements on the copper and selenium status of pregnant ewes and lambs.

The aim of this work was to investigate whether Cu, alone or in combination with Mo, reduces the Se status of sheep. Thirty-six Hampshire ewes were separated prior to mating into four treatment groups of nine sheep each. The four groups consisted of 1) basal (alfalfa hay or legume-grass low-moisture silage, corn, oats), 2) basal plus 10 mg Cu/kg diet, 3) basal plus 10 mg Mo/kg and 4) basal plus Cu and Mo (each 10 mg/kg). Copper and Mo were added to both ewe and lamb diets. Treatments continued until lambs were weaned at 10 wk postpartum. The basal ewe diet contained, in mg/kg, 5.6 Cu, .05 Se and 1.0 Mo. The basal lamb diet contained, in mg/kg, 6.1 Cu, .07 Se and less than 1.0 Mo. Sulfur concentrations in the ewe and lamb diets were .24% and .20%, respectively. Copper supplements increased, and Mo supplements decreased, the concentration of Cu in the livers of ewes and lambs (P less than .05). Despite this, there were no effects of treatment on Se concentration or glutathione peroxidase activity in blood or tissues. Selenium levels in plasma of all ewes declined throughout pregnancy and lactation, indicating that .05 mg/kg Se was insufficient for the maintenance of Se status during pregnancy in Hampshire ewes. Copper and Se levels (mg/kg fresh weight) in the liver of lambs at weaning for Treatments 1 through 4 were 48 and .13, 158 and .10, 11 and .11, and 136 and .13, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of calcium phosphates and zinc in salt-mineral mixtures on ad libitum salt-mix intake and on zinc and selenium status of sheep.

In two separate experiments, 72 crossbred ewes were fed hay, haylage (50% dry matter) and corn diets with ad libitum salt-mineral mixtures (SMM; Exp. 1) or salt (Exp. 2). Calcium phosphates (Ca X P) and(or) zinc (Zn) were added in a 2 X 2 factorial arrangement to salt + trace minerals for ewes 7 mo prepartum through lactation in Exp. 1 and to salt only for ewes 3 mo prepartum through lactation in Exp. 2. The diets fed were estimated to contain 23 and 28 mg Zn/kg dry diet (ppm), respectively, and .08 and .05 ppm Se. Large variations (up to fivefold) were found in SMM intake per month between replicates and from month-to-month within treatment; thus, monthly variations of up to sevenfold occurred in Zn and Se intakes of supplemented groups. There were no significant treatment effects on SMM intake. Small but significant Zn treatment effects were detected for plasma and wool Zn of ewes and lambs, but all values were in the normal range. There was no significant treatment effect on plasma alkaline phosphatase activity. In Exp. 2, erythrocyte glutathione peroxidase (GSH-Px) activity was significantly lower in all treatment groups compared with a Se-supplemented control group but only rare occurrences of subclinical muscular dystrophy were found. There was no significant treatment effect on GSH-Px activity, whole blood Se in ewes and lambs or plasma creatine phosphokinase activity in lambs. These results indicate large animal and seasonal variability in SMM intake and no significant treatment effects of Ca X P on SMM intake or on Zn and Se status. Zinc addition to SMM had no effect on Se status.

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

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

Ovine coccidiosis: comparison of the effects of monensin and aureomycin on lambs infected with coccidia.

Lambs naturally infected with mixed species of Eimeria were fed monensin (30 mg/kg of feed) and aureomycin (10 mg/kg of feed) separately and in combination. An evaluation was made of the efficacy of the treatments in the suppression of oocyst production. Comparisons were made of the parasitic damage to the intestinal surface. Performance of the lambs was measured by weight gains and feed efficiency. Monensin given separately or in combination with aureomycin produced decreases in oocyst counts that were not significantly different from those in the lambs given only aureomycin. Body weight gains and feed efficiency were best in the aureomycin-treated group, and less so in the monensin-treated and the control groups. Animals fed the monensin-aureomycin combination had the poorest weight gains and feed efficiency. Scanning electron microscopy indicated that the groups fed monensin or aureomycin separately had morphologically normal intestinal surfaces. This was in contrast to the control group and the group fed the monensin-aureomycin combination, wherein there was disrupted intestinal surface morphology.

Selenium: biochemical role as a component of glutathione peroxidase.

When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.