Mechanism study on mitochondrial fragmentation under oxidative stress caused by high fluence low-power laser irradiation

Shengnan Wu, Feifan Zhou, Da Xing*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

1 Citation (Scopus)

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.

Original languageEnglish
Title of host publicationMechanisms for Low-Light Therapy VII
DOIs
Publication statusPublished - 2012
Externally publishedYes
EventMechanisms for Low-Light Therapy VII - San Francisco, CA, United States
Duration: 21 Jan 201221 Jan 2012

Publication series

NameProgress in Biomedical Optics and Imaging - Proceedings of SPIE
Volume8211
ISSN (Print)1605-7422

Conference

ConferenceMechanisms for Low-Light Therapy VII
Country/TerritoryUnited States
CitySan Francisco, CA
Period21/01/1221/01/12

Keywords

  • Dynamin-related protein 1 (Drp1)
  • Fission
  • High fluence low-power laser irradiation (HF-LPLI)
  • Oxidative stress
  • Reactive oxygen species (ROS)

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