Chelidonine, a tertiary hexahydro-benzophenanthridine alkaloid is an inhibitor of tubulin polymerisation and has been revealed to arrest cells in G2/M. Since enhanced tyrosine kinase (TK) activity is linked to the transition from normal to the immortal malignant phenotype, the effect of 10 mM chelidonine was evaluated on TK activity in normal, transformed and malignant cell lines after 2 hours of exposure. Chelidonine caused a stimulation of TK activity in two normal cell lines (human foreskin fibroblast (Hs27) and normal monkey kidney (NMK)). In contrast, an inhibition of TK activity was observed in transformed human embryonic kidney (Graham 293) and transformed African green monkey kidney (Vero), as well as in human cervical carcinoma (HeLa) and squamous oesophageal carcinoma (WHCO5) cells. Hs27 cells exposed to chelidonine, revealed an increase in TK activity of 1.27-fold (P < 0.05). NMK cells showed a 1.15-fold increase in TK activity. A decrease in TK activity was observed in Graham 293 (0.91-fold) and Vero (0.45-fold) (P < 0.005) cells. In both HeLa and WHCO5 cells, the TK activity was reduced to 0.68-fold (P < 0.05) and 0.56-fold (P < 0.005) respectively. These data, including results from our previous studies, suggest a potential cross talk between the SAPK/JNK and TK signal transduction pathways and a possible differential effect of chelidonine on the phosphorylation status of role players involved in determining the length of G2 arrest in normal versus transformed and malignant cells.