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Biomedical subjects

G H Spray

Publications and source records attributed to G H Spray.

At least 19 recordsLinked to original sources
PubMed1976

The effects of dietary histidine, methionine and homocystine on vitamin B12 and folate levels in rat liver.

1. L-histidine (20 g/kg) added to vitamin B12-deficient and cyanocobalamin-supplemented diets based on soya-bean flour reduced the growth of rats given the vitamin B12-deficient diet but stimulated growth of rats given the cyanocobalamin-supplemented diet. Liver weight (g/kg body-weight)increased, but the protein content of the livers decreased, in rats given histidine supplements. The histidine was associated with significantly higher folate concentrations in the livers of cyanocobalamin-supplemented rats.

Animals↗
PubMed1976

Effect of some anticonvulsant drugs on depletion of folate in rats on a vitamin B12-deficient diet.

Rats fed on vitamin B12-deficient or vitamin B12-supplemented diets and treated with phenobarbitone by intraperitoneal injection for 5 d showed significant increases in the activity of glutamate formiminotransferase in liver. The only significant depletion in liver folate activity was in vitamin B12-supplemented rats that were starved for 48 h. When rats were given the same diets, with phenobarbitone and diphenylhydantoin added, for 12 weeks or more in two separate experiments, significant increases in transferase activity were found only in the livers of animals fed on the deficient diet. However, there was significant depletion of liver folate in animals taking the supplemented diet.

Animals↗
PubMed1971

Metabolic effects of propionate in normal and vitamin B 12 -deficient rats.

1. Administration of propionate caused a twofold increase in the concentrations of lactate and pyruvate in the blood of vitamin B(12)-deficient rats, whereas there was a slight decrease in lactate and a 50% increase in pyruvate in normal rats. 2. Concentrations of total ketone bodies in the blood of normal rats were not significantly altered by propionate administration but the [3-hydroxybutyrate]/[acetoacetate] ratio decreased from 3.0 to 2.0. In the vitamin B(12)-deficient rats there was a 40% decrease in total ketone bodies and a change in the ratio from 3.4 to 1.2. 3. The changes in the concentration of ketone bodies in freeze-clamped liver preparations were similar in pattern to those observed in blood. 4. Propionate administration caused a decrease in the concentration of acetyl-CoA in the livers of both groups of animals, but the absolute decrease was greater in the vitamin B(12)-deficient group. The decrease in the concentration of CoA was similar in both groups. 5. As in blood, there were threefold increases in the concentrations of lactate and pyruvate in the livers of the vitamin B(12)-deficient rats after propionate administration, whereas there was no significant change in the concentrations of these metabolites in the normal rats. 6. There was a 50% inhibition of glucose synthesis in perfused livers from vitamin B(12)-deficient rats when lactate and propionate were substrates as compared with lactate alone. 7. It is concluded that the conversion of lactate into glucose is inhibited in vitamin B(12)-deficient rats after propionate administration, and that this effect is due to inhibition of the pyruvate carboxylase step resulting from a decrease in acetyl-CoA concentration and a postulated increase in methylmalonyl-CoA concentration.

Acetoacetates↗
PubMed1970

Gluconeogenesis from propionate in kidney and liver of the vitamin B12-deficient rat.

1. Kidney-cortex slices and the perfused livers of vitamin B(12)-deficient rats removed propionate from the incubation and perfusion media at 33 and 17% respectively of the rates found with tissues from rats receiving either a normal or a vitamin B(12)-supplemented diet. There was a corresponding fall in the rates of glucose synthesis from propionate in both tissues. 2. The addition of hydroxocobalamin or dimethylbenzimidazolylcobamide coenzyme to kidney-cortex slices from vitamin B(12)-deficient rats in vitro failed to restore the normal capacity for propionate metabolism. 3. Although the vitamin B(12)-deficient rat excretes measurable amounts of methylmalonate, no methylmalonate production could be detected (probably because of the low sensitivity of the method) when kidney-cortex slices or livers from deficient rats were incubated or perfused with propionate. 4. The addition of methylmalonate (5mm) to kidney-cortex slices from rats fed on a normal diet inhibited gluconeogenesis from propionate by 25%. 5. Methylmalonate formation is normally only a small fraction of the flux through methylmalonyl-CoA. This fraction increases in vitamin B(12)-deficient tissues (as shown by the urinary excretion of methylmalonate) presumably because the concentration of methylmalonyl-CoA rises as a result of low activity of methylmalonyl-CoA mutase (EC 5.4.99.2). Slow removal of methylmalonyl-CoA might depress propionate uptake owing to the reversibility of the steps leading to methylmalonyl-CoA formation.

Animals↗
PubMed1969

Estimation of red cell folate activity.

The conditions described by Hoffbrand, Newcombe, and Mollin (1966) for the estimation of red cell folate activity have been confirmed using a different method (Spray, 1964) of micro-biological assay with Lactobacillus casei. In 81 control subjects the levels of folate activity in the red cells were between 80 and 470 mmug/ml (mean 192), and in plasma between 2.1 and 13 mmug/ml (mean 4.9). In 16 patients with megaloblastic anaemia due to folic acid deficiency, the red cell folate level was between 3 and 74 mmug/ml (mean 32). In 15 of these patients the plasma level was between 0.1 and 1.0 mmug/ml; in the other patient it was 3.3 mmug/ml. Subnormal red cell levels were found in only eight out of 29 other patients whose plasma folate level was below 2.0 mmug/ml. In 26 patients with untreated pernicious anaemia, the red cell folate activity was between 44 and 280 mmug/ml (mean 129) and the plasma level was between 1.6 and 19 mmug/ml (mean 7.5).

Anemia, Macrocytic↗