Mouse models of mitochondrial disease, oxidative stress, and senescence
Language: 
English
Abstract: 

During the course of normal respiration, reactive oxygen species are produced which are particularly detrimental to mitochondrial function. This is shown by recent studies with a mouse that lacks the mitochondrial form of superoxide dismutase (Sod2). Tissues that are heavily dependent on mitochondrial function such as the brain and heart are most severely affected in the Sod2 mutant mouse. Recent work with a mouse mutant for the heart/muscle specific isoform of the mitochondrial adenine nuclear translocator (Ant1) demonstrates a potential link between mitochondrial oxidative stress and mitochondrial DNA mutations. These mutations can be detected by Long-extension PCR, a method for detecting a wide variety of mutations of the mitochondrial genome. Such mutations have also been observed in the mitochondrial genome with senescence regardless of the mean or maximal lifespan of the organism being studied. Mutations have been detected with age in Caenorhabditis elegans, mice, chimpanzees, and humans. This implies that a causal relationship may exist between mitochondrial reactive oxygen species production, and the senescence specific occurrence of mitochondrial DNA mutations.

Author(s): 
Melov, S.
Coskun, P. E.
Wallace, D. C.
Item Type: 
Journal Article
Publication Title: 
Mutation Research
Journal Abbreviation: 
Mutat. Res.
Publication Date: 
7/30/1999
Publication Year: 
1999
Pages: 
233-242
Volume: 
434
Issue: 
3
ISSN: 
0027-5107
Library Catalog: 
NCBI Published Medical (?)
Extra: 
PMID: 10486594

Turabian/Chicago Citation

S. Melov, P. E. Coskun and D. C. Wallace. 7/30/1999. "Mouse models of mitochondrial disease, oxidative stress, and senescence." Mutation Research 434: 3: 233-242.

Wikipedia Citation

<ref> {{Cite journal | doi = | issn = 0027-5107 | volume = 434 | pages = 233-242 | last = Melov | first = S. | coauthors = Coskun, P. E., Wallace, D. C. | title = Mouse models of mitochondrial disease, oxidative stress, and senescence | journal = Mutation Research | date = 7/30/1999 | pmid = | pmc = }} </ref>