Lipopolysaccharide (LPS) can cause damage to the epithelia of the respiratory tract. However, taurine can protect the lung tissue from such oxidant-induced inflammation. This study examined the effects of a LPS treatment on the intracellular calcium levels ([Ca(2+)]i) as well as the specific mechanisms of LPS-induced cell death in pneumocytes. In addition, the effects of taurine on the LPS-induced increase in the accumulation of reactive oxygen species (ROS) in pneumocytes were investigated. The [Ca(2+)]i in cultured pneumocytes was determined using microfluorescence techniques. The level of activation of the mitogen-activated protein kinases (MAPKs) and Bax protein were measured by Western blotting. LPS at 10 and 100 ng/ml induced cell death and decreased the viability of MRC-5 cells. Moreover, the intracellular Ca(2+) and ROS levels were increased by LPS. The LPS treatment led to the phosphorylation of ERK1/2, JNK and the activation of Bax. A pretreatment with 20 mM taurine reduced the LPS-induced production of ROS and MARK activity. These results show that a LPS treatment induces cell death in MRC-5 cells by increasing the intracellular ROS and Ca(2+) levels. The increase in the intracellular level of ROS promotes MAPKs activation and Bax translocation. Overall, LPS induces lung cell death by activating MAPKs. Furthermore, taurine decreased the LPS-induced generation of ROS and activation of MAPK and Bax.