Lithium inhibits the cytolytic glucocorticoid effect on S49 mouse lymphoma cells |
| |
Authors: | K Junker M Svenson S Junker |
| |
Affiliation: | 1. Department of Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark;2. The Laboratory of Immunology, University Clinic for Infectious Diseases, Copenhagen, Denmark;3. Institute of Human Genetics, University of Aarhus, Aarhus, Denmark |
| |
Abstract: | Cytolysis is the end point of receptor-mediated effects of glucocorticoids on S49 mouse lymphoma cells of wild-type. In the presence of 5 mM LiCl this effect of triamcinolone or dexamethasone was markedly delayed. The cytoprotective effect of Li+ against 10(-7) M triamcinolone acetonide was already manifest after 24 h of steroid incubation, and on the fifth day 50-fold more Li+-treated than control cells were viable. This effect of Li+ was not exerted through changes of the doubling time of the cells, and thus could not be ascribed to an overall reduction of protein- or RNA synthesis. Data on accumulation and effect of cyclic AMP indicated that the cytoprotective effect was independent on cyclic AMP. Furthermore Li+ did not affect the amount or affinity of glucocorticoid receptors in intact cells. By use of aqueous 2-phase partitioning and DNA-Sepharose binding of [3H]triamcinolone acetonide labelled cytosols we demonstrate that Li+ inhibits the in vitro salt-activation of the glucocorticoid-receptor complexes by 60-100%. The nuclear bound fraction of hormone-receptor complexes in intact cells at 37 degrees C was not affected by Li+. The data suggest that Li+ inhibits the cytolytic glucocorticoid effect by interacting with the hormone-receptor complexes. |
| |
Keywords: | |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|