In the present study, we show that the thymus atrophy inducing compound DBTC stimulates the intracellular release, but not the influx, of Ca2+ elicited by cross-linking of the TcR alpha beta-CD3-complex on rat thymocytes and inhibits capping of TcR alpha beta. Similarities with the effects of cytochalasin B together with the finding that DBTC also inhibited capping of CD8, whereas cross-linking of CD8 did not cause a Ca(2+)-response, suggest that DBTC interferes with TcR alpha beta-CD3-signalling by selective interference with cytoskeletal functioning. The responding thymocytes were CD53- and FSClow, thus possibly including the non proliferating counterpart of the presumed immature CD4-CD8+CD53-target cells of DBTC. The present effects may therefore relate to the mechanisms of organotin-induced thymus atrophy.