Testing the rate-of-living/oxidative damage theory of aging in the nematode model Caenorhabditis elegans

2007 ◽  
Vol 42 (9) ◽  
pp. 845-851 ◽  
Author(s):  
Kristel Brys ◽  
Jacques R. Vanfleteren ◽  
Bart P. Braeckman
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Theory Of Aging ◽  
Damage Theory

The oxidative damage theory of aging

2003 ◽  
Vol 2 (5-6) ◽  
pp. 305-315 ◽  
Author(s):  
Michael T. Lin ◽  
M. Flint Beal
Keyword(s):  
Oxidative Damage ◽  
Theory Of Aging ◽  
Damage Theory

Knock-down of transcription factor skinhead-1 exacerbates arsenite-induced oxidative damage in Caenorhabditis elegans

BioMetals ◽  
2021 ◽  
Author(s):  
Yijie Mao ◽  
Ling Yao ◽  
Xuejun Jiang ◽  
Golamaully Sumayyah ◽  
Zhen Zou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Knock Down

scholarly journals The Exacerbation of Aging and Oxidative Stress in the Epididymis of Sod1 Null Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 151 ◽  
Author(s):  
Anaīs Noblanc ◽  
Alicia Klaassen ◽  
Bernard Robaire
Keyword(s):  
Oxidative Damage ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Theory Of Aging ◽  
Accumulation Of Damage ◽  
Effects Of Aging ◽  
And Oxidative Stress

There is growing evidence that the quality of spermatozoa decreases with age and that children of older fathers have a higher incidence of birth defects and genetic mutations. The free radical theory of aging proposes that changes with aging are due to the accumulation of damage induced by exposure to excess reactive oxygen species. We showed previously that absence of the superoxide dismutase 1 (Sod1) antioxidant gene results in impaired mechanisms of repairing DNA damage in the testis in young Sod1−/− mice. In this study, we examined the effects of aging and the Sod−/− mutation on mice epididymal histology and the expression of markers of oxidative damage. We found that both oxidative nucleic acid damage (via 8-hydroxyguanosine) and lipid peroxidation (via 4-hydroxynonenal) increased with age and in Sod1−/− mice. These findings indicate that lack of SOD1 results in an exacerbation of the oxidative damage accumulation-related aging phenotype.

scholarly journals Increased life span from overexpression of superoxide dismutase in Caenorhabditis elegans is not caused by decreased oxidative damage

2011 ◽  
Vol 51 (8) ◽  
pp. 1575-1582 ◽  
Author(s):  
Filipe Cabreiro ◽  
Daniel Ackerman ◽  
Ryan Doonan ◽  
Caroline Araiz ◽  
Patricia Back ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span

Mitochondrial Complex I Function Affects Halothane Sensitivity in Caenorhabditis elegans 

2004 ◽  
Vol 101 (2) ◽  
pp. 365-372 ◽  
Author(s):  
Ernst-Bernhard Kayser ◽  
Phil G. Morgan ◽  
Margaret M. Sedensky
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Phosphorylation ◽  
Oxidative Damage ◽  
Adenosine Triphosphate ◽  
Complex I ◽  
Volatile Anesthetics ◽  
Mitochondrial Proteins ◽  
Wild Type ◽  
Complex Ii ◽  
C Elegans

Background : The gene gas-1 encodes a subunit of complex I of the mitochondrial electron transport chain in Caenorhabditis elegans. A mutation in gas-1 profoundly increases sensitivity of C. elegans to volatile anesthetics. It is unclear which aspects of mitochondrial function account for the hypersensitivity of the mutant. Methods : Oxidative phosphorylation was determined by measuring mitochondrial oxygen consumption using electron donors specific for either complex I or complex II. Adenosine triphosphate concentrations were determined by measuring luciferase activity. Oxidative damage to mitochondrial proteins was identified using specific antibodies. Results : Halothane inhibited oxidative phosphorylation in isolated wild-type mitochondria within a concentration range that immobilizes intact worms. At equal halothane concentrations, complex I activity but not complex II activity was lower in mitochondria from mutant (gas-1) animals than from wild-type (N2) animals. The halothane concentrations needed to immobilize 50% of N2 or gas-1 animals, respectively, did not reduce oxidative phosphorylation to identical rates in the two strains. In air, adenosine triphosphate concentrations were similar for N2 and gas-1 but were decreased in the presence of halothane only in gas-1 animals. Oxygen tension changed the sensitivity of both strains to halothane. When nematodes were raised in room air, oxidative damage to mitochondrial proteins was increased in the mutant animal compared with the wild type. Conclusions : Rates of oxidative phosphorylation and changes in adenosine triphosphate concentrations by themselves do not control anesthetic-induced immobility of wild-type C. elegans. However, they may contribute to the increased sensitivity to volatile anesthetics of the gas-1 mutant. Oxidative damage to proteins may be an important contributor to sensitivity to volatile anesthetics in C. elegans.

Sign in / Sign up

Export Citation Format

Share Document