The Mitochondrial Apoptotic Pathway Effects Of Fine Particulate From Cooking Oil Fumes On Fetal Alveolar Type â…¡ Epithelial Cells

ObjectiveTo investigate the effects of cell proliferation and mitochondrial pathwayapoptosis-related protein’s expression in alveolar type II epithelial cells(AECII) induced by fine particulate matter (PM2.5) from cooking oil fumes. In order toprovide the theoretical and experimental basis for further study the lungtoxicological mechanisms of PM2.5from cooking oil fumes.MethodPM2.5sample from cooking oil fumes was collected as poisonous substances andextracted AEC Ⅱcell from18days fetal rats’ lung tissue as experimental target cell. Todetected the influence of different PM2.5concentration to survival by measuring MTT.Flow cytometry to detect the influence of PM2.5to the cell cycle and evaluated the cellproliferation. Western Blot detect the protein expression of mitochondria apoptoticwhich inclouding Bax/Bcl-2, Cyt-c, Caspase-9and Caspase-3.Result1. AECⅡ survival rates was no statistical difference in12h phase and24h phasebetween12.5ug/ml exposure group and control group. There was statistical differencebetween low-dose group (12.5ug/ml) and control group in36h phase. There all havesignificant difference in other concentration of exposure group to control group indifferent time. And present time-response relationship and dose-response relationship. 2. Along the higher concentrations of PM2.5act on AECⅡ, the higher scale of celldistribution in G0-G1phase, and present dose-response relationship. Along the higherconcentrations of PM2.5act on AECⅡ, the lower scale of cell distribution in S phase,and present dose-response relationship. The scale of AECⅡ distribution in G2-Mphase affected by different concentrations of PM2.5but there was not presentdose-response relationship. Along the higher concentrations of PM2.5act on AECⅡ, theProliferation Index was become lower, and present dose-response relationship.3. The Bax protein expression of AECⅡwas higher than control group in36h phase inall different concentrations of PM2.5, and present dose-response relationship. The Bcl-2protein expression of AEC Ⅱ was higher than control group in low-dose group(12.5ug/ml), but the other groups was no difference. Along the higher concentrations ofPM2.5, the ratio of Bax/Bcl-2was become higher. The Cyt-c protein expression of AECⅡwas lower than control group in low-dose group (12.5ug/ml). The protein expressionof Cyt-c, Caspase-9and Caspase-3were all higher than control group in50ug/ml and75ug/ml concentrations.ConclusionCooking oil fumes PM2.5can lead down AECⅡsurvival rate which through affect cellproliferation and mitochondrial injury to occurred apoptosis.