Mitochondrial Respiratory Dysfunction in Familiar Parkinsonism Associated with PINK1 Mutation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-05-13

AUTHORS

Claudia Piccoli, Annamaria Sardanelli, Rosella Scrima, Maria Ripoli, Giovanni Quarato, Annamaria D’Aprile, Francesco Bellomo, Salvatore Scacco, Giuseppe De Michele, Alessandro Filla, Arcangela Iuso, Domenico Boffoli, Nazzareno Capitanio, Sergio Papa

ABSTRACT

In the present study mitochondrial respiratory function of fibroblasts from a patient affected by early-onset Parkinsonism carrying the homozygous W437X nonsense mutation in the PINK1 gene has been thoroughly characterized. When compared with normal fibroblasts, the patient’s fibroblast mitochondria exhibited a lower respiratory activity and a decreased respiratory control ratio with cellular ATP supply relying mainly on enhanced glycolytic production. The quantity, specific activity and subunit pattern of the oxidative phosphorylation complexes were normal. However, a significant decrease of the cellular cytochrome c content was observed and this correlated with a reduced cytochrome c oxidase in situ-activity. Measurement of ROS revealed in mitochondria of the patient’s fibroblasts enhanced O2•− and H2O2 production abrogated by inhibition of complex I. No change in the glutathione-based redox buffering was, however, observed. More... »

PAGES

2565

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11064-008-9729-2

DOI

http://dx.doi.org/10.1007/s11064-008-9729-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044999310

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18473170


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