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Apoptosis induced by high fluence low-power laser irradiation (LPLI) is observed in several cell models. However, the underlying mechanisms have not been elucidated as yet. To study the mechanism of high fluence LPLI-induced apoptosis, we used special fluorescence probes to measure and analyze the alteration of mitochondria membrane potential (Deltapsim), bax/bid activity of human lung adenocarcinoma cells (ASTC-a-1) irradiated by He-Ne laser at a high fluence of 200 J/cm2. We also further tested the activity of caspase-3 using fluorescence resonance energy transfer (FRET) imaging and the release of cytochrome c using the plasmid GFP-cyto c and DsRed-mit. Results showed that Deltapsim decrease, caspase-3 activation, and cytochrome c release occurred in sequence in cells exposed to high fluence LPLI. While bax and bid were not activated. Taken together, these results suggest that apoptosis induced by high fluence LPLI is initiated from mitochondrial and major involves photoacceptors, which are responsible for the subsequent generation of mitochondrial reactive oxygen species (mROS), the damage of mitochondria and finally cell death.