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Biomedical subjects

F W Heaton

Publications and source records attributed to F W Heaton.

At least 37 records · Page 2Linked to original sources

Changes in the alkaline phosphatase (EC 3.1.3.1) and inorganic pyrophosphatase (EC 3.6.1.1) activities of rat tissues during magnesium deficiency. The importance of controlling feeding pattern.

1. The adoption of a meal-eating pattern of feeding by rats altered the alkaline phosphatase (EC 3.1.3.1) activity in serum and liver. It was therefore necessary to regulate the feeding pattern of both magnesium-deficient rats and control animals receiving a Mg-adequate diet in order to study the effect of the deficiency. 2. Mg deficiency decreased the activities of alkaline phosphatase and inorganic pyrophosphatase (EC 3.6.1.1) in serum, kidney and tibia, but increased them in spleen. 3. Addition of a standard concentration of exogenous Mg to tissue extracts usually increased the activity of corresponding enzymes from Mg-deficient and control rats by the same proportion, indicating that the main effect of the deficiency was on the amount of enzyme present rather than on the efficiency of its operation. 4. Certain quantitative differences in the response to exogenous Mg and the activity ratio, alkaline phosphatase:inorganic pyrophosphatase were found between tissues from Mg-deficient and control rats. The significance of these are discussed in relation to the association of the two enzymic activities with the same protein molecule, and the possible occurrence of isoenzymes.

Alkaline Phosphatase↗

Changes in cellular composition during magnesium deficiency.

Mg deficiency increased the water content of the liver, kidney, heart and thigh muscle in the rat and decreased the proportion of nitrogen in the dry matter of the same tissues. Changes in the concentration of metals also occurred. 2. Cellular fractional indicated that the Mg and K depleted in liver occurred primarily in the heavy-mitochondrial and microsomal fractions respectively. The calcification of liver and kidney was due to preferential deposition of Ca in the heavy-mitochondrial fraction. 3. The proportion of cellular nitrogen present in the heavy-mitochondrial and microsomal fractions was markedly decreased in the liver and kidney of the Mg-deficient rats, and the proportion in the supernatant fraction increased. 4. Electron microscopy revealed that the cross-sectional areas of liver cells and all their mitochondria were decreased in Mg deficiency. The number of mitochondrial per cell was decreased even more severely and the average area of a mitochondrion was greater in deficient rats than in control animals. 5. The significance of these observations is discussed in relation to the location of the primary metabolic disturbance during Mg deficiency.

Animals↗

Effect of magnesium deficiency and parathyroid hormone on cyclic AMP metabolism in rat renal cortex.

The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex. Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.

Adenylyl Cyclases↗