Our previous studies showed intragastric administration of Aflatoxin G 1 (AFG 1 ) could induce lung adenocarcinoma, which derived from alveolar type II cells (AT-II cells). AT-II cells contribute to Aflatoxin B 1 (AFB 1 ) metabolism and also serve as the potential progenitor cells for AFB 1 -induced tumorigenesis. Thus, AT-II cells may constitute a target for AFG 1 exposure and serve as progenitor cells for tumorigenesis induced by AFG 1 . The current experiment was designed to identify the acute toxicity of AFG 1 in AT-II cells following a single intratracheal administration of AFG 1 . We observed inflammatory changes in the alveolar septum at days 3 and 7 after AFG 1 treatment, which resolved by 14days. We also found AFG 1 caused lamellar bodies damage in AT-II cells at days 3 and 7 post-treatment. Surfactant protein C (SP-C) expression, an AT-II cell-specific marker, was reduced at day 7 post-treatment. The structural and functional impairment in AT-II cells returned to normal by day 14. Moreover, we found that AFG 1 induced a elevation of intracellular calcium concentration [Ca 2+ ]i in AT-II cells in vitro, which may contribute to the decreased SP-C expression. In conclusion, our results show AFG 1 induces structural and functional impairment in AT-II cells involved in the acute toxicity of AFG 1 in lung.