skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Depletion of (/sup 3/H)methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy (42001)

Abstract

The present study was undertaken to determine cytosol binding properties of (/sup 3/H)methyltrienolone, a synthetic androgen, in comparison with (/sup 3/)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/sup -1/ body wt) or the vehicle, 1% carboxymethyl cellulose. Following treatment, both (/sup 3/H)dexamethansone and (/sup 3/H)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 (/sup 3/H)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, 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 (/sup 3/H)methyltrienolone binding in muscles of vehicle-treated animals were markedly reduced by CA treatment. In addition, the binding specificity data alsomore » showed strong competition by progesterone and methyltrienolone for (/sup 3/H)dexamethasone binding and estradiol-17..beta.. for (/sup 3/H)methyltrienolone binding.« less

Authors:
; ; ;
Publication Date:
Research Org.:
Univ. of Illinois, Chicago
OSTI Identifier:
5729728
Resource Type:
Journal Article
Journal Name:
Proc. Soc. Exp. Biol. Med.; (United States)
Additional Journal Information:
Journal Volume: 178:2
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; ANDROGENS; BIOCHEMICAL REACTION KINETICS; DEXAMETHASONE; MUSCLES; PHYSIOLOGY; AFFINITY; ATROPHY; CHEMICAL BONDS; CORTISONE; CYTOPLASM; EXPERIMENTAL DATA; LIGANDS; MATHEMATICAL MODELS; PROGESTERONE; RATS; RECEPTORS; SPECIFICITY; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ADRENAL HORMONES; ANDROSTANES; ANIMALS; CELL CONSTITUENTS; CORTICOSTEROIDS; DATA; GLUCOCORTICOIDS; HORMONES; HYDROXY COMPOUNDS; INFORMATION; ISOTOPE APPLICATIONS; KETONES; KINETICS; LABELLED COMPOUNDS; MAMMALS; NUMERICAL DATA; ORGANIC COMPOUNDS; PATHOLOGICAL CHANGES; PREGNANES; REACTION KINETICS; RODENTS; STEROID HORMONES; STEROIDS; VERTEBRATES; 550201* - Biochemistry- Tracer Techniques

Citation Formats

Kurowski, T T, Capaccio, J A, Chatterton, Jr, R T, and Hickson, R C. Depletion of (/sup 3/H)methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy (42001). United States: N. p., 1985. Web. doi:10.3181/00379727-178-42001.
Kurowski, T T, Capaccio, J A, Chatterton, Jr, R T, & Hickson, R C. Depletion of (/sup 3/H)methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy (42001). United States. https://doi.org/10.3181/00379727-178-42001
Kurowski, T T, Capaccio, J A, Chatterton, Jr, R T, and Hickson, R C. 1985. "Depletion of (/sup 3/H)methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy (42001)". United States. https://doi.org/10.3181/00379727-178-42001.
@article{osti_5729728,
title = {Depletion of (/sup 3/H)methyltrienolone cytosol binding in glucocorticoid-induced muscle atrophy (42001)},
author = {Kurowski, T T and Capaccio, J A and Chatterton, Jr, R T and Hickson, R C},
abstractNote = {The present study was undertaken to determine cytosol binding properties of (/sup 3/H)methyltrienolone, a synthetic androgen, in comparison with (/sup 3/)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/sup -1/ body wt) or the vehicle, 1% carboxymethyl cellulose. Following treatment, both (/sup 3/H)dexamethansone and (/sup 3/H)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 (/sup 3/H)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, 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 (/sup 3/H)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 (/sup 3/H)dexamethasone binding and estradiol-17..beta.. for (/sup 3/H)methyltrienolone binding.},
doi = {10.3181/00379727-178-42001},
url = {https://www.osti.gov/biblio/5729728}, journal = {Proc. Soc. Exp. Biol. Med.; (United States)},
number = ,
volume = 178:2,
place = {United States},
year = {Tue Jan 01 00:00:00 EST 1985},
month = {Tue Jan 01 00:00:00 EST 1985}
}