ARTICULAR CHONDROCYTES AND SYNOVIOCYTES IN CULTURE - INFLUENCE OF ANTIOXIDANTS ON LIPID-PEROXIDATION AND PROLIFERATION

Authors
Citation
B. Kurz et M. Schunke, ARTICULAR CHONDROCYTES AND SYNOVIOCYTES IN CULTURE - INFLUENCE OF ANTIOXIDANTS ON LIPID-PEROXIDATION AND PROLIFERATION, ANNALS OF ANATOMY-ANATOMISCHER ANZEIGER, 179(5), 1997, pp. 439-446
Citations number
35
Journal title
ANNALS OF ANATOMY-ANATOMISCHER ANZEIGER
ISSN journal
09409602 → ACNP
Volume
179
Issue
5
Year of publication
1997
Pages
439 - 446
Database
ISI
SICI code
0940-9602(1997)179:5<439:ACASIC>2.0.ZU;2-B
Abstract
Chondrocytes and synoviocytes are the main cell types in articular joi nts. Articular cartilage is fed by synoviocytes via synovial fluid and has a low partial oxygen pressure. Thus, chondrocytes show oxygen rad ical protective mechanisms in vivo and are unprotected against these f actors under common culture conditions. We investigated the influence of ascorbic acid, Fe2+, glutathione and alpha-tocopherol on lipid pero xidation and proliferation of rat articular chondrocytes and rabbit sy noviocytes (HIG-82) in vitro. A combination of ascorbic acid and Fe2induced the production of thiobarbituric acid-reactive material as a m arker of radical-mediated lipid peroxidation in homogenates and/or sup ernatants of cultured chondrocytes and synoviocytes. The amount of lip id peroxidation of chondrocytes was about 3-fold high er than that of synoviocytes. Ascorbic acid or Fe2+ alone had no significant influence on the production of thiobarbituric acid-reactive material. Lipid per oxidation could be abolished by addition of the radical scavenger alph a-tocopherol, whereas glutathione had no effect. 25-50 mu M alpha-toco pherol decreased the ascorbic acid - (100 mu g/ml) and Fe2+ - (3 mu M) induced lipid peroxidation to a basal level. Moreover, ascorbic acid inhibited the proliferation of rat chondrocytes and rabbit synoviocyte s measured by [H-3]-thymidine incorporation. Alpha-tocopherol and glut athione had no influence on the proliferation of chondrocytes but alph a-tocopherol decreased the growth of synoviocytes and increased the an ti-proliferative effect of ascorbic acid on these cells. The importanc e of these findings for the use of ascorbic acid, glutathione and alph a-tocopherol in chondrocyte and synoviocyte cultures, or the influence of these molecules on the etiology and treatment of articular disease s will be discussed.