Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

The single subunit nadh dehydrogenase reduces generation of reactive oxygen species from complex i

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Seo, B. B.
  • Marella, M.
  • Yagi, Takao
  • Matsuno-Yagi, A.

publication date

  • November 2006

journal

  • FEBS Letters  Journal

abstract

  • Using rat dopaminergic and human neuroblastoma cell lines transduced with the NDI1 gene encoding the internal NADH dehydrogenase (Ndi1) from Saccharomyces cerevisiae, we investigated reactive oxygen species (ROS) generation caused by complex I inhibition. Incubation of non-transduced cells with rotenone elicited oxidative damage to mitochondrial DNA as well as lipid peroxidation. In contrast, oxidative stress was significantly decreased when the cells were transduced with NDI1. Furthermore, mitochondria from the NDI1-transduced cells showed a suppressed rate of ROS formation by the complex I inhibitors. We conclude that the Ndi1 enzyme is able to suppress ROS overproduction from defective complex I.

subject areas

  • Animals
  • Cell Line
  • DNA Damage
  • DNA, Mitochondrial
  • Electron Transport Complex I
  • Humans
  • Lipid Peroxidation
  • NADH Dehydrogenase
  • Oxidative Stress
  • Protein Subunits
  • Rats
  • Reactive Oxygen Species
  • Rotenone
  • Saccharomyces cerevisiae Proteins
  • Transduction, Genetic
scroll to property group menus

Research

keywords

  • NDI1
  • complex I
  • dopaminergic cells
  • mitochondrial ROS
  • rotenone
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0014-5793

Digital Object Identifier (DOI)

  • 10.1016/j.febslet.2006.10.008

PubMed ID

  • 17055488
scroll to property group menus

Additional Document Info

start page

  • 6105

end page

  • 6108

volume

  • 580

issue

  • 26

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support