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Proceedings Paper

Mechanism study on mitochondrial fragmentation under oxidative stress caused by high-fluence low-power laser irradiation
Author(s): Shengnan Wu; Feifan Zhou; Da Xing
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Paper Abstract

Mitochondria are dynamic organelles that undergo continual fusion and fission to maintain their morphology and functions, but the mechanism involved is still not clear. Here, we investigated the effect of mitochondrial oxidative stress triggered by high-fluence low-power laser irradiation (HF-LPLI) on mitochondrial dynamics in human lung adenocarcinoma cells (ASTC-a-1). Upon HF-LPLI-triggered oxidative stress, mitochondria displayed a fragmented structure, which was abolished by exposure to dehydroascorbic acid (DHA), a reactive oxygen species scavenger, indicating that oxidative stress can induce mitochondrial fragmentation. Mitochondrial translocation of the profission protein dynamin-related protein 1 (Drp1) was observed following HF-LPLI, demonstrating apoptosis-related activation of Drp1. Notably, DHA pre-treatment prevented HF-LPLI-induced Drp1 activation. We conclude that mitochondrial oxidative stress through activation of Drp1 causes mitochondrial fragmentation.

Paper Details

Date Published: 10 March 2012
PDF: 6 pages
Proc. SPIE 8211, Mechanisms for Low-Light Therapy VII, 82110K (10 March 2012); doi: 10.1117/12.905332
Show Author Affiliations
Shengnan Wu, South China Normal Univ. (China)
Feifan Zhou, South China Normal Univ. (China)
Da Xing, South China Normal Univ. (China)


Published in SPIE Proceedings Vol. 8211:
Mechanisms for Low-Light Therapy VII
Michael R. Hamblin; Juanita Anders; James D. Carroll, Editor(s)

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