Effect of diet on protein degrading activity in the sheep rumen.
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Biomedical subjects
Publications and source records attributed to R C Siddons.
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1. Glutatione peroxidase activity (EC 1.11.1.9) and erythrocyte stability were measured in Friesian bull calves which were given for 36 weeks semi-purified diets either adequate or low in selenium or vitamin E or both. 2. Dietary Se or vitamin E content had no effect on growth rate and haematlogical values. None of the calves exhibited clinical deficiency symptoms and serum aspartate amino transferase (EC 2.6.1.1) and creatine phosphokinase (EC 2.7.3.2) activities remained normal. Heart and skeletal muscles of all calves appeared macroscopically and microscopically normal ato autopsy. 3. Glutathione peroxidase activity in plasma, blood and other tissues, except the testis, was significantly lower in calves receiving low dietary Se but was independent of dietary vitamin E content. 4. Plasma vitamin E levels decreased rapidly and to very low levels in calves given low vitamin E diets irrespective of the Se content of the diet. 5. A low dietary vitamin E intake increased the susceptibility of erythrocytes to auto- and peroxidative haemolysis whereas a low Se intake in the presence of adequate vitamin E did not. However, erythrocytes from calves receiving low Se and low vitamin E were more susceptible to peroxidative haemolysis than erythrocytes from calves receiving low vitamin E and adequate Se. The effect of dietary vitamin E content on osmotic haemolysis induced by hypotonic saline was variable. 6. The results suggest that measurement of blood glutathione peroxidase activity and the susceptibility of erythrocytes to auto- or peroxidative haemolysis could be used for the differential diagnosis of subclinical Se and vitamin E deficiency in ruminants.
1. Wilted perennial ryegrass (Lolium perenne L. cv. Endura) was ensiled without additive or after addition of a mixture of equal volumes of formic acid (850 g/kg) and formalin (380 g formaldehyde/kg) applied at a rate of 35 g formaldehyde/kg herbage crude protein (nitrogen x 6.25). The digestion of the two silages and the effect of supplemental N as urea or urea plus soya-bean meal on the digestion of the treated silage was studied using sheep fitted with a rumen cannula and re-entrant cannulas in the proximal duodenum and distal ileum. 2. The additive markedly reduced carbohydrate fermentation and protein degradation in the silo. 3. There were no significant differences between diets in rumen pH, dilution rate, volatile fatty acid production and the molar proportions of acetate, propionate and butyrate. However, rumen ammonia levels and the apparent digestibility of organic matter (OM), gross energy (GE) and cellulose in the stomach were significantly depressed (P less than 0.05) by the additive. It also reduced (P less than 0.05) the extent to which the N of the silage was degraded in the rumen and, with the treated silage, more microbial N was synthesized in the rumen than food N degraded, resulting in a net grain of N between mouth and duodenum, as compared to a net loss with the untreated silage. 4. Supplementation of the treated silage with urea or urea plus soya-bean meal significantly increased (P less than 0.05) the amount of food N degraded in the rumen and rumen ammonia levels but had no effect on the apparent digestibility of OM, GE and cellulose in the stomach or on the amount of microbial N reaching the duodenum. 5. The quantity of microbial amino acids entering the small intestine and the apparent digestibility of amino acids in the small intestine were similar for all four diets. However, the quantity of food amino acids reaching the small intestine was significantly higher with the three diets containing the treated silage and consequently the apparent absorption of amino acids from the small intestine was substantially higher with these diets than with the untreated silage.
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The effect of a vitamin B12 and folic acid deficient diet on juvenile and adolescent baboons (Papio cynocephalus anubis) was studied. The baboons developed clinical and hematological signs characteristics of folacin deficiency, although they were less severe in juvenile baboons. The signs disappeared when folic acid was replaced in the diet. The serum vitamin B12 levels increased in all baboons fed the vitamin B12 and folic acid deficient diet. When folic acid was added to the diet, the levels gradually decreased in adolescent baboons, liver vitamin B12 levels decreased to a lesser extent when fed a vitamin B12 and folic acid deficient diet than when fed a vitamin B12 deficient diet. In juvenile baboons fed a vitamin B12 and folic acid deficient diet, for 7 months and a vitamin B12 deficient diet for a further 11 months, liver vitamin B12 levels did not decrease at any time but were similar to those in baboons fed a vitamin B12 and folic acid supplemented diet.
Branched chain fatty acids of the anteiso series and others with methyl substitution nearer to the carboxyl group were found, together with odd numbered, straight chain fatty acids, in very small proportions in baboon liver lipids. The proportions were increased in vitamin B12-depleted animals, especially after administration of a B12 analogue.
1. Measurement of the vitamin B12 content of baboon tissues showed that the liver contained the highest concentration, followed by the pituitary, kidney, heart, spleen and pancreas. 2. The dietary vitamin B12 requirement of the baboon for the maintenance of satisfactory body stores was between 1 and 2 mug/d. 3. Satisfactory liver vitamin B12 stores were invariably associated with serum levels above 125 pg/ml, whereas liver levels were usually low when the serum level was below 50 pg/ml. 4. Increased methylmalonic acid (MMA) excretion after a valine load occurred when the liver vitamin B12 level was less than 0-40 mug/g. L- and DL-valine were approximately equally effective as precursors of MMA, whereas sodium propionate, whether given orally or intraperitoneally, was less effective. 5. The distribution of radioactivity along the wall of the intestinal tract after an oral dose of [57-Co]cyanocobalamin suggested that the distal half of the small intestine was the main site of vitamin B12 absorption. However, the utilization of vitamin B12 put direct into the middle part of the small intestine was much lower than that of an oral dose. 6. The unsaturated vitamin B12-binding capacity of baboon serum was not related to the serum vitamin B12 level. There was a significant difference between the unsaturated vitamin B12-binding capacities of the two subspecies of baboon (Papio cynocephalus cynocephalus and P. cynocephalus anubis) studied.
After the intramuscular administration of the vitamin B12 analogue, 2-methyl-2-aminopropanol-B12, to vitamin B12-depleted baboons (Papio cynocephalus) the effects on vitamin B12 and folate metabolism have been studied. The 'apparent' serum vitamin B12 and the serum folate concentrations increased, the liver folate concentrations decreased, and the liver vitamin B12 concentrations were unchanged. The analogue caused a marked increase in the amount of formiminoglutamic acid excreted after a histidine load whereas the amount of methylmalonic acid excreted after a valine load decreased. The rate of red blood cell regeneration after venesection was normal in baboons treated with the analogue and there was no evidence of megaloblastic haemopoiesis. Two baboons given the analogue developed a partial loss of utilization and lack of co-ordination in the hind limbs.
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A dietary deficiency of vitamin B12 was produced in the baboon by use of an artificial diet. Deficiency was further aggravated by feeding propionate or ampicillin, as judged by serum, liver and brain vitamin B12 levels, and urinary excretion of methyl malonic acid. Reduced glutathione levels in the blood and liver increased during deficiency, while ascorbic acid levels were not affected, Brain and liver nucleic acids did not change significantly. Blood pyruvate and serum lipid factors were affected more in the group fed propionate. These results are compared with the work on vitamin B12 deficient rats and pernicious anaemia in humans.
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