9 March 2012 Mechanism study on mitochondrial fragmentation under oxidative stress caused by high-fluence low-power laser irradiation
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Proceedings Volume 8211, Mechanisms for Low-Light Therapy VII; 82110K (2012) https://doi.org/10.1117/12.905332
Event: SPIE BiOS, 2012, San Francisco, California, United States
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.
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Shengnan Wu, Feifan Zhou, Da Xing, "Mechanism study on mitochondrial fragmentation under oxidative stress caused by high-fluence low-power laser irradiation", Proc. SPIE 8211, Mechanisms for Low-Light Therapy VII, 82110K (9 March 2012); doi: 10.1117/12.905332; https://doi.org/10.1117/12.905332
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