TY - GEN
T1 - The study on the mechanism of cell apoptosis induced by high fluence low-power laser irradiation
AU - Wu, Sheng Nan
AU - Xing, Da
PY - 2007
Y1 - 2007
N2 - 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 (Δ Ψm), 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 ΔΨm 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.
AB - 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 (Δ Ψm), 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 ΔΨm 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.
KW - Fluorescence resonance energy transfer (FRET)
KW - Low-power laser irradiation(LPLI)
KW - Mitochondria membrane potential (ΔΨm)
UR - http://www.scopus.com/inward/record.url?scp=48149088598&partnerID=8YFLogxK
U2 - 10.1109/ICCME.2007.4381890
DO - 10.1109/ICCME.2007.4381890
M3 - Conference contribution
AN - SCOPUS:48149088598
SN - 1424410789
SN - 9781424410781
T3 - 2007 IEEE/ICME International Conference on Complex Medical Engineering, CME 2007
SP - 998
EP - 1002
BT - 2007 IEEE/ICME International Conference on Complex Medical Engineering, CME 2007
T2 - 2007 IEEE/ICME International Conference on Complex Medical Engineering, CME 2007
Y2 - 23 May 2007 through 27 May 2007
ER -