Quick Search:

uzh logo
Browse by:
bullet
bullet
bullet
bullet

Zurich Open Repository and Archive 

Saini, N; Oelhafen, S; Hua, H; Georgiev, O; Schaffner, W; Büeler, H (2010). Extended lifespan of Drosophila parkin mutants through sequestration of redox-active metals and enhancement of anti-oxidative pathways. Neurobiology of Disease, 40(1):82-92.

Full text not available from this repository.

Abstract

The mechanisms underlying neuron death in Parkinson's disease are unknown, but both genetic defects and environmental factors are implicated in its pathogenesis. Mutations in the parkin gene lead to autosomal recessive juvenile Parkinsonism (AR-JP). Here we report that compared to control flies, Drosophila lacking parkin show significantly reduced lifespan but no difference in dopamine neuron numbers when raised on food supplemented with environmental pesticides or mitochondrial toxins. Moreover, chelation of redox-active metals, anti-oxidants and overexpression of superoxide dismutase 1 all significantly reversed the reduced longevity of parkin-deficient flies. Finally, parkin deficiency exacerbated the rough eye phenotype of Drosophila caused by overexpression of the copper importer B (Ctr1B). Taken together, our results demonstrate an important function of parkin in the protection against redox-active metals and pesticides implicated in the etiology of Parkinson's disease. They also corroborate that oxidative stress, perhaps as a consequence of mitochondrial dysfunction, is a major determinant of morbidity in parkin mutant flies.

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
DDC:570 Life sciences; biology
Language:English
Date:2010
Deposited On:09 Nov 2010 16:35
Last Modified:27 Nov 2013 20:39
Publisher:Elsevier
ISSN:0969-9961
Publisher DOI:10.1016/j.nbd.2010.05.011
PubMed ID:20483372
Citations:Web of Science®. Times Cited: 20
Google Scholar™
Scopus®. Citation Count: 21

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page