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Biomedical subjects

A M White

Publications and source records attributed to A M White.

At least 73 records · Page 4Linked to original sources
PubMed1972

Relative changes in the function of muscle ribosomes and mitochondria during the early phase of steroid-induced catabolism.

1. Five glucocorticoids, when administered daily to rats for 5-7 days at a dosage of 5mg/kg, were in the following order of effectiveness with respect to their ability to decrease the weight gain of whole animals and the vastus lateralis, vastus medialis and gluteus medius muscles: corticosterone<prednisolone<triamcinolone <betamethasone<dexamethasone<triamcinolone acetonide. 2. The low catabolic potencies of corticosterone and prednisolone were reflected in the high doses (20mg/kg) required to decrease significantly the incorporating activity in vitro of ribosomes isolated from the muscles 6h later. However, triamcinolone was as effective as triamcinolone acetonide in causing a significant effect at 0.05mg/kg, although it had a far lower catabolic potency than the acetonide. 3. The relationship between decrease in ribosomal activity in vitro and weight loss was better understood by considering the duration of the effect after single doses of steroids. Ribosomes returned to normal function between 6 and 12h after the administration of corticosterone (20mg/kg), but still had decreased activity 12h after a similar dose of prednisolone. Normal ribosomal function was renewed between 12 and 18h after the administration of triamcinolone and betamethasone at 5mg/kg, but decreased activity persisted for more than 48h after similar doses of dexamethasone or triamcinolone acetonide. 4. There was no difference in the rate of incorporation of amino acids into nascent protein on polyribosomes from muscle of control animals and animals treated 6h previously with triamcinolone acetonide or dexamethasone. 5. The rate of weight gain of the heart was not affected by any of the steroids tested and heart ribosomes maintained normal activity although concentrations of steroids in this organ 5min after administration were 2-3 times that in skeletal muscle. 6. Mitochondria, isolated from the muscle of animals that had received triamcinolone acetonide (20mg/kg) 12h previously, were shown, by using a Coulter counter, to be enlarged. Nevertheless oxidation was only slightly uncoupled 12h after drug administration and they had normal function 6h later. Similar results with respect to mitochondrial function were obtained after the administration of dexamethasone (20mg/kg) and betamethasone (20mg/kg). 7. From these results it is concluded that the mitochondria are not functionally involved in the early phase of steroid-induced muscle catabolism. The observed decrease in the incorporating ability of muscle ribosomes in vitro appears to be much more closely linked to the initial catabolic event.

Amino Acids↗
PubMed1971

Intracellular enzymes and protein synthesis in rabbit skin after thermal injury.

1. The concentrations of several intracellular enzymes in rabbit skin have been measured 5 min, 2, 6 and 24 h after thermal injury.2. At 5 min and 2 h after a burn (60 degrees C for 1 min) there was a significant fall in the enzyme activities whereas at 6 h their activities were higher than control.3. It appears that the increase in enzyme concentrations in the lymph during the first few hours after thermal injury is associated with a fall in the enzyme concentrations in the tissues and therefore might be the result of leakage of enzyme from storage sites in the injured cells.4. The second increase in enzyme concentrations in the lymph which has been observed 6-18 h after thermal injury occurs at a time when there is also an increase in the enzyme concentrations in the tissue.5. It seems unlikely that these increased activities are due to new synthesis since there was no apparent correlation between tissue enzyme concentrations and protein synthetic activity, and the changes still occurred after administration of cycloheximide.6. There was a change in the LDH isoenzyme pattern after injury towards a predominance of LDH-1. This change did not occur immediately after the burn, but was present at 2 and 6 h, and returned to normal 24 h later.

Acid Phosphatase↗
PubMed1970

Some biochemical effects of triamcinolone acetonide on rat liver and muscle.

1. The powerful anti-inflammatory glucocorticoid triamcinolone acetonide, administered to rats at 20 and 2.5mg/kg, leads to a decrease in the incorporation in vivo of [(3)H]uridine and [(32)P]orthophosphate into hind-limb skeletal muscle. 2. At the higher dose, this decrease in the rate of incorporation of precursors into RNA precedes a decrease in the incorporating ability of muscle ribosomes, which commences about 4-5h after drug administration, but is unaccompanied by any changes in the concentration of tissue ATP or free amino acids. 3. The ribosomal dysfunction extends to polyribosomes, which can only be successfully isolated from the muscle of triamcinolone-treated animals after the addition of alpha-amylase to the tissue homogenate to remove glycogen. 4. The specific radioactivity of muscle protein labelled in vivo with (14)C-labelled amino acids does not decrease progressively after triamcinolone administration. After 2h there is an apparent stimulation of incorporation which leads to an overall discrepancy between measurements of protein-synthetic activity made in vivo and in vitro. 5. There is a significant increase in muscle-glycogen concentration between 8 and 12h after the administration of triamcinolone acetonide (20mg/kg), although a significant decrease occurs after 4h. The fall in glycogen concentration may be due to a decrease in the rate of synthesis of protein essential for glucose uptake into the tissues. 6. As judged by (a) incorporation of (14)C-labelled amino acids into protein, (b) [(3)H]uridine and [(32)P]-orthophosphate incorporation into RNA, (c) the rate of induction of tryptophan pyrrolase and (d) changes in the pool sizes of taurine and tryptophan, the responses in liver followed the same time-course as those in muscle after administration of the drug.

Adenosine Triphosphate↗