Skip to main content
Cellular and Molecular Life Sciences: CMLS logoLink to Cellular and Molecular Life Sciences: CMLS
. 2008 Feb 25;65(7-8):1272–1284. doi: 10.1007/s00018-008-7589-1

Mitochondrial association of alpha-synuclein causes oxidative stress

M S Parihar 1, A Parihar 1, M Fujita 2, M Hashimoto 2, P Ghafourifar 1,
PMCID: PMC11131648  PMID: 18322646

Abstract.

α-Synuclein is a neuron-specific protein that contributes to the pathology of Parkinson’s disease via mitochondria-related mechanisms. The present study investigated possible interaction of α-synuclein with mitochondria and consequences of such interaction. Using SHSY cells overexpressing α-synuclein A53T mutant or wild-type, as well as isolated rat brain mitochondria, the present study shows that α-synuclein localizes at the mitochondrial membrane. In both SHSY cells and isolated mitochondria, interaction of α-synuclein with mitochondria causes release of cytochrome c, increase of mitochondrial calcium and nitric oxide, and oxidative modification of mitochondrial components. These findings suggest a pivotal role for mitochondria in oxidative stress and apoptosis induced by α-synuclein.

Keywords. Alpha synuclein, mitochondria, nitric oxide, Parkinson’s disease, mitochondrial calcium, cytochrome c, mitochondrial nitric oxide synthase, oxidative stress

Footnotes

Received 27 December 2007; received after revision 7 February 2008; accepted 8 February 2008


Articles from Cellular and Molecular Life Sciences: CMLS are provided here courtesy of Springer

RESOURCES