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Proceedings Paper

Mitochondrial injury caused by reactive oxygen species generation under high fluence low-power laser irradiation treatment
Author(s): Shengnan Wu; Lei Huang; Xuegang Sun; Jiru Chu
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Paper 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.

Paper Details

Date Published: 24 February 2009
PDF: 8 pages
Proc. SPIE 7178, Biophotonics and Immune Responses IV, 71780L (24 February 2009); doi: 10.1117/12.808113
Show Author Affiliations
Shengnan Wu, South China Normal Univ. (China)
Lei Huang, South China Normal Univ. (China)
Xuegang Sun, South China Normal Univ. (China)
Jiru Chu, South China Normal Univ. (China)

Published in SPIE Proceedings Vol. 7178:
Biophotonics and Immune Responses IV
Wei R. Chen, Editor(s)

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