Abstract

Drug effects on the size of the exchangeable sulphate pool and the incorporation rate into costal cartilage in vivo were studied by a new double isotope method in growing mice of the N. M. R. I. strain. Adrenalectomy caused a significant decrease both in the size of the sulphate pool and the rate of sul‐phation in cartilage. Hydrocortisone (a water soluble form), acetylsalicylic acid, oxyphenylbutazone and dimethyl‐sulphoxide given in rather high doses had no effect on the sulphate pools or the sulphate incorporation rates. Hydrocortisone‐acetate (in oil or suspension), prednisolone‐acetate and dexamethasone all elicited a dose‐dependent retardation of body growth and a considerable increase in the size both of the total sulphate pool and the pool per g body weight. The sulphation rate of the cartilage samples even at high doses was only moderately depressed by the steroids studied. Only prednisolone elicited a marked inhibition with a dose above 40 μg. Salazopyrin® (4 mg/day × 6) considerably decreased sulphate incorporation without affecting the size of the sulphate pool. Vitamin A caused a marked and dose‐dependent increase in the sulphate pool and a moderate and dose‐independent decrease in the sulphation of cartilage. l‐Thyroxine up to a dose of 1 μg/day depressed sulphate incorporation, but a 10 times higher dose stimulated it. The sulphate pools displayed a graded elevation after increasing doses of l‐thyroxine.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.