AIM To study the growth inhibition of adenosine triphosphate (ATP) and adenosine (ADO) on cultured tumor cells in vitro. METHODS MTT assays were used to determine the inhibition of proliferation of ATP and ADO on several tumor cell lines, including human squamous esophageal carcinoma cells TE-13, human stomach carcinoma cells HGC-27 and human erythroleukemia cells K562. The morphological changes of ATP and ADO on the cell lines were observed under light microscope. RESULTS ATP and ADO produced a certain inhibition effect on TE-13, HGC-27, K562 cells at different concentration between 0.01～1.0 mmol?L -1. The maxium inhibition fraction of TE-13, HGC-27, K562 cells exposed to ATP for 72 h was 80.52%, 58.67% and 45.07%, respectively; and to ADO for 72 h, was 74.03%, 52% and 30.99%, respectively. Under light microscope, the tumor cells exposed to higher concentration(1 mmol?L -1) of ATP and ADO displayed morphological changes of apoptosis. CONCLUSION These results suggested that ATP has a certain cytotoxic effect on several tumor cell lines, it might partly be related to ADO. Its mechanism might involve apoptosis.

AIM: To study the mechanism responsible for ONOO --induced the airway epithelial injury. METHODS: Effects of 3-aminobenzamide(3-AB), a poly-(ADP-ribose) polymerase(PARP) inhibitor, and Ac-DEVD-CHO, a caspase-3 inhibitor, on LDH release and apoptosis of cultured rat tracheal epithelial (RTE) cells induced by ONOO - were examined. The cleavage of PARP was analysed by Western blot. RESULTS: 3-AB inhibited the release of LDH induced by ONOO - partially, and had no effect on the apoptosis of RTE cells. Caspase-3 inhibitor Ac-DEVD-CHO obviously prevented the apoptosis of RTE cells induced by ONOO - in a dose-dependent manner. The cleavage of PARP was observed in the process of apoptosis of RTE cells induced by ONOO -. CONCLUSIONS: PARP activation represents one of the pathways of ONOO --mediated epithelial injury, and the excessive activation of PARP contributes to the necrosis in RTE cells induced by ONOO -. Cleavage of PARP by activated caspase-3 plays a crucial role in the apoptosis of RTE cells induced by ONOO -.

AIM:To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on proliferation,apoptosis and caspase 3 expression in FN-stimulated HSCs in vitro. METHODS:[ 3H]-thymidine incorporation,Annexin-V/Propidium Iodide double-labeled flow cytometry(FCM),TUNEL,scanning electron microscope and transmission electron microscopy were employed to estimate the influence of RGDS on proliferation and apoptosis of HSCs. The adhesion rates were observed by toluidine blue colorimetric assay. The expression of caspase-3 protein was detected by FCM. RESULTS:①Compared with control and FN groups,RGDS tetrapeptide at concentrations of 25 mg?L -1 ,50 mg?L -1 and 100 mg?L2 1 inhibited the proliferation of HSCs ( P