RABBIT ARTICULAR CHONDROCYTES: AN IN VITRO MODEL FOR STUDYING THE EFFECT OF SODIUM AURO‐THIOPROPANOL SULFONATE ON PROLIFERATION KINETICS, TYPE II COLLAGEN PHENOTYPE AND MITOCHONDRIAL ACTIVITY

Summary— Despite the benefits of chrysotherapy the responsible mechanism of action of gold compounds remains unclear. At a concentration of 5 times 10−4 M, sodium aurothiopropanol sulfonate (SAS) modified the in vitro proliferation kinetics of articular chondrocytes by reducing growth, viability and plating efficiency. Flow cytometry analysis, using propidium iodide DNA staining, revealed slight but significant cell arrest in G2 + M which, in fact, represents an increase in the proportion of binucleate cells. SAS did not induce any variations in chondrocyte phenotype stability as far as the biosynthesis of type II collagen was concerned, and no appreciable changes in overall mitochondrial activity reflected by rhodamine 123 incorporation.

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