Mitochondrial injury caused by reactive oxygen species generation under high fluence low-power laser irradiation treatment

Shengnan Wu; Lei Huang; Xuegang Sun; Jiru Chu

doi:10.1117/12.808113

24 February 2009 Mitochondrial injury caused by reactive oxygen species generation under high fluence low-power laser irradiation treatment

Shengnan Wu, Lei Huang, Xuegang Sun, Jiru Chu

Author Affiliations +

Proceedings Volume 7178, Biophotonics and Immune Responses IV; 71780L (2009) https://doi.org/10.1117/12.808113
Event: SPIE BiOS, 2009, San Jose, California, United States

Abstract

Mitochondrial injury, characterized by its depolarization, is a key to cell apoptosis. High fluence low-power laser irradiation (HF-LPLI) through endogenous photosensitive reactions can cause mitochondrial injury. However, the exact mechanisms are not fully understood. Using fluorescent image techniques, we investigated cell apoptosis caused by mitochondrial photosensitization by HF-LPLI. Our results showed that the major step of the apoptosis, decrease of mitochondrial transmembrane potential (ΔΨm), occurred accompanying with high levels of mitochondrial reactive oxygen species (ROS) generation, indicating mitochondrial injury caused by ROS. Scavenging the photodynamical ROS completely prevented mitochondrial depolarization supported the view. Taken together, we demonstrated that HF-LPLI caused mitochondrial injury through a large amount of mitochondrial ROS generation. The specific mechanisms need to be further studied.

Citation Download Citation

Shengnan Wu, Lei Huang, Xuegang Sun, and Jiru Chu "Mitochondrial injury caused by reactive oxygen species generation under high fluence low-power laser irradiation treatment", Proc. SPIE 7178, Biophotonics and Immune Responses IV, 71780L (24 February 2009); https://doi.org/10.1117/12.808113

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