Rapid mitochondrial enlargement in muscle as a response to triamcinolone acetonide and its relationship to the ribosomal defect

Human Zygapophyseal Joint Synovial Folds

“…1965], containing 2 mM of calcium chloride (which virtually eliminates myelin-like figures [linker, 1958;Bullock et al. 1971;Glauerl, 1975).…”

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

“…All preparative procedures, including centrifugation, were done at 4°C. The method used was that described by Bullock et al (1971) except that the medium used as the dense layer during the final centrifugation was medium B in which the KCI concentration was 0.3M. Glycogen-free ribosomes (Peters et al, 1970) were prepared by treating the 2000g supernatant with amylase for 20min at 0°C.…”

“…Ribosomes isolated from the predominantly white hind-limb muscles ofadult male rats have a decreased ability to incorporate amino acids into protein in vitro when the animals have previously been treated with the powerful catabolic agent triamcinolone acetonide (9a-fluoro-1l1l,21-dihydroxy-16ac,17ao-isopropylidenedioxypregna -1,4 -diene -3,20 -dione) (White, 1967;Bullock et al, 1968;Peters et al, 1970;Bullock et al, 1971). Similar results were obtained when rabbits were given cortisone (Bullock et aL, 1968).…”

“…The ribosomal defect develops comparatively rapidly (4-6h) after the administration of Vol. 127 the catabolic agent to rats (Peters et al, 1970) and can be fully or partially reversed by treating the animals with steroids that have an anabolic action (White, 1967;Bullock et al, 1968Bullock et al, , 1971. From this it would appear likely that the dysfunctional state of the ribosomes reflects events in the cell that are primary determinants of steroid-induced muscle catabolism.…”

“…First, studies so far have only involved the use of two catabolic steroids (cortisone and triamcinolone acetonide) and hence no attempt has been made to relate the catabolic effectiveness of a range of steroids with their effect on changes in ribosomal activity. Secondly, mitochondrial function as distinct from morphology (Bullock et al, 1971) has not been taken into account soon after steroid administration and therefore the question of lack of energy as a cause of catabolism has not been ruled out. To meet these omissions, the function of isolated skeletal-muscle mitochondria, skeletal-muscle ribosomes and heart ribosomes were measured at various times after different doses of cortisone, prednisolone (11,B,17oc,21-trihydroxypregna-1,4-diene -3,20dione), triamcinolone (9ac -fluoro -1 1f,160,17a,21 -tetrahydroxypregna-1,4-diene-3,20dione 16a,21-diacetate), betamethasone (9a-fluoro-1,B, 17,B, 21-trihydroxy-16,8-methylpregna-1, 4-diene-3,20-dione dexamethasone (9oc-fluoro-1 1,B,170c,21trihydroxy-16ax-methylpregna-1, 4-diene-3,20-dione) and triamcinolone acetonide, and related to the different degrees of catabolism engendered by these steroids.…”