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Depletion of [3H]methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy.
. 1985 Feb; 178(2):215-21.

Abstract

The present study was undertaken to determine cytosol binding properties of [3H]methyltrienolone, a synthetic androgen, in comparison with [3H]dexamethasone, a synthetic glucocorticoid, under conditions of glucocorticoid excess in skeletal muscle. Male hypophysectomized rats received either seven daily subcutaneous injections of cortisone acetate (CA) (100 mg X kg-1 body wt) or the vehicle, 1% carboxymethyl cellulose. Following treatment, both [3H]dexamethasone and [3H]methyltrienolone-receptor concentrations were decreased from those in vehicle-treated rats by more than 90 and 80%, respectively, in CA-treated animals. Scatchard analysis of [3H]methyltrienolone binding in muscles of vehicle-treated animals became nonlinear at high concentrations of labeled ligand and were reanalyzed by a two-component binding model. The lower affinity, higher capacity component, which was attributed to binding of methyltrienolone to a "dexamethasone" component, disappeared in muscles of CA-treated rats and Scatchard plots were linear. Receptor concentrations of the higher affinity lower capacity "methyltrienolone" component were similar in muscles of vehicle-treated and CA-treated groups. From competition studies, the high relative specificities of glucocorticoids for [3H]methyltrienolone binding in muscles of vehicle-treated animals were markedly reduced by CA treatment. In addition, the binding specificity data also showed strong competition by progesterone and methyltrienolone for [3H]dexamethasone binding and estradiol-17 beta for [3H]methyltrienolone binding. These results demonstrate that most of the [3H]methyltrienolone binding is eliminated under in vivo conditions of glucocorticoid excess. Furthermore, the competitiveness of various steroids for receptor binding suggests that rat muscle may not contain classic (ligand-specific) glucocorticoid and androgen receptors.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3871528

Citation

Kurowski, T T., et al. "Depletion of [3H]methyltrienolone Cytosol Binding in Glucocorticoid-induced Muscle Atrophy." Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), vol. 178, no. 2, 1985, pp. 215-21.
Kurowski TT, Capaccio JA, Chatterton RT, et al. Depletion of [3H]methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy. Proc Soc Exp Biol Med. 1985;178(2):215-21.
Kurowski, T. T., Capaccio, J. A., Chatterton, R. T., & Hickson, R. C. (1985). Depletion of [3H]methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 178(2), 215-21.
Kurowski TT, et al. Depletion of [3H]methyltrienolone Cytosol Binding in Glucocorticoid-induced Muscle Atrophy. Proc Soc Exp Biol Med. 1985;178(2):215-21. PubMed PMID: 3871528.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Depletion of [3H]methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy. AU - Kurowski,T T, AU - Capaccio,J A, AU - Chatterton,R T,Jr AU - Hickson,R C, PY - 1985/2/1/pubmed PY - 2001/3/28/medline PY - 1985/2/1/entrez SP - 215 EP - 21 JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) JO - Proc. Soc. Exp. Biol. Med. VL - 178 IS - 2 N2 - The present study was undertaken to determine cytosol binding properties of [3H]methyltrienolone, a synthetic androgen, in comparison with [3H]dexamethasone, a synthetic glucocorticoid, under conditions of glucocorticoid excess in skeletal muscle. Male hypophysectomized rats received either seven daily subcutaneous injections of cortisone acetate (CA) (100 mg X kg-1 body wt) or the vehicle, 1% carboxymethyl cellulose. Following treatment, both [3H]dexamethasone and [3H]methyltrienolone-receptor concentrations were decreased from those in vehicle-treated rats by more than 90 and 80%, respectively, in CA-treated animals. Scatchard analysis of [3H]methyltrienolone binding in muscles of vehicle-treated animals became nonlinear at high concentrations of labeled ligand and were reanalyzed by a two-component binding model. The lower affinity, higher capacity component, which was attributed to binding of methyltrienolone to a "dexamethasone" component, disappeared in muscles of CA-treated rats and Scatchard plots were linear. Receptor concentrations of the higher affinity lower capacity "methyltrienolone" component were similar in muscles of vehicle-treated and CA-treated groups. From competition studies, the high relative specificities of glucocorticoids for [3H]methyltrienolone binding in muscles of vehicle-treated animals were markedly reduced by CA treatment. In addition, the binding specificity data also showed strong competition by progesterone and methyltrienolone for [3H]dexamethasone binding and estradiol-17 beta for [3H]methyltrienolone binding. These results demonstrate that most of the [3H]methyltrienolone binding is eliminated under in vivo conditions of glucocorticoid excess. Furthermore, the competitiveness of various steroids for receptor binding suggests that rat muscle may not contain classic (ligand-specific) glucocorticoid and androgen receptors. SN - 0037-9727 UR - https://www.unboundmedicine.com/medline/citation/3871528/Depletion_of_[3H]methyltrienolone_cytosol_binding_in_glucocorticoid_induced_muscle_atrophy_ L2 - https://medlineplus.gov/steroids.html DB - PRIME DP - Unbound Medicine ER -