Abstract: OBJECTIVE: To study the protective effect and mechanism of ethyl pyruvate (EP) on acute lung injury (ALI) and oxidative stress induced by chlorine gas. METHODS：Adult male SD rats (200±20 g，about 8 weeks of age) were exposed to chlorine gas of 2536 mg/m3 or normal air for 20 min in a whole-body dynamic exposure chamber. EP (40 mg/kg) or vehicle (saline) was given by intraperitoneal injections immediately after chlorine gas exposure. Rats were killed at 6 hours after chlorine gas exposure，and the wet：dry weight ratio，PaO2/FiO2 ratio，the concentration of thiobarbituric acid reactive substances (TBARs)，glutathione disulfide (GSSG)，glutathione (GSH) and the activity of glutathione peroxidase (GSH-PX)，glutathione reductase (GR)，total superoxide dismutase (T-SOD)，catalase (CAT) in the lung were measured. RESULTS：After chlorine gas exposure，the wet：dry weight ratio，TBARs and GSSG in the lung increased significantly (P<0.05). However，PaO2/FiO2 ratio，GSH and the activities of GSH-PX，GR，T-SOD and CAT deceased (P<0.05). EP treatment attenuated these changes (P<0.05). CONCLUSION：EP treatment attenuated ALI and oxidative stress in the lung induced by chlorine gas.

Key words: chlorine gas, ethyl pyruvate, acute lung injury, oxidative stress