The apoptotic pathways effect of fine particulate from cooking oil fumes in primary fetal alveolar type II epithelial cells

• COFs exposure led to the cytotoxicity of AEC II cells.
• The alterations of apoptosis proteins showed apoptosis of cells exposed to COFs.
• The cell cycle distribution of AEC II cells exposed to COFs showed G1 arrest.

Apoptosis occurs along three major pathways: (i) an extrinsic pathway, mediated by death receptors; (ii) an intrinsic pathway centered on mitochondria; and (iii) an ER-stress pathway. We investigated the apoptotic pathway effects of cooking oil fumes (COF) in fetal lung type II-like epithelium cells (AEC II). Exposure to COF caused up-regulation of the pro-apoptotic protein Bax and down-regulation of the anti-apoptotic protein Bcl-2. COF induced the mitochondrial permeability transition, an early event in apoptosis; cytochrome c was translocated from the mitochondria to the cytoplasm and nucleus. Caspase-9 and caspase-3 were activated, as a consequence of the mitochondrial permeability transition. The death receptor apoptotic pathway was triggered by COF, as indicated by a change in Fas expression, resulting in increased caspase-8 content. COF exposure arrested the cell cycle the at G0-G1 phase. In summary, COF can lead to apoptosis via mitochondrial and death receptor pathways in AEC II cells.