scholarly journals Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans

2008 ◽  
Vol 22 (23) ◽  
pp. 3236-3241 ◽  
Author(s):  
R. Doonan ◽  
J. J. McElwee ◽  
F. Matthijssens ◽  
G. A. Walker ◽  
K. Houthoofd ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span ◽  
Superoxide Dismutases ◽  
Theory Of Aging ◽  
Damage Theory

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

scholarly journals Multimarker Screening of Oxidative Stress in Aging

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Kamila Syslová ◽  
Adéla Böhmová ◽  
Miloš Mikoška ◽  
Marek Kuzma ◽  
Daniela Pelclová ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Nucleic Acids ◽  
Body Fluids ◽  
Physiological Concentration ◽  
Stress Theory ◽  
Complex Process ◽  
Prostaglandin F ◽  
Theory Of Aging ◽  
Biomarkers Of Oxidative Stress

Aging is a complex process of organism decline in physiological functions. There is no clear theory explaining this phenomenon, but the most accepted one is the oxidative stress theory of aging. Biomarkers of oxidative stress, substances, which are formed during oxidative damage of phospholipids, proteins, and nucleic acids, are present in body fluids of diseased people as well as the healthy ones (in a physiological concentration). 8-isoprostaglandin F2αis the most prominent biomarker of phospholipid oxidative damage,o-tyrosine, 3-chlorotyrosine, and 3-nitrotyrosine are biomarkers of protein oxidative damage, and 8-hydroxy-2′-deoxyguanosine and 8-hydroxyguanosine are biomarkers of oxidative damage of nucleic acids. It is thought that the concentration of biomarkers increases as the age of people increases. However, the concentration of biomarkers in body fluids is very low and, therefore, it is necessary to use a sensitive analytical method. A combination of HPLC and MS was chosen to determine biomarker concentration in three groups of healthy people of a different age (twenty, forty, and sixty years) in order to find a difference among the groups.

scholarly journals Proteostasis collapse is a driver of cell aging and death

2019 ◽  
Vol 116 (44) ◽  
pp. 22173-22178 ◽  
Author(s):  
Mantu Santra ◽  
Ken A. Dill ◽  
Adam M. R. de Graff
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span ◽  
Protein Function ◽  
Tipping Point ◽  
Cell Aging ◽  
Molecular Processes ◽  
Increased Temperature ◽  
Oxidant Concentration

What molecular processes drive cell aging and death? Here, we model how proteostasis—i.e., the folding, chaperoning, and maintenance of protein function—collapses with age from slowed translation and cumulative oxidative damage. Irreparably damaged proteins accumulate with age, increasingly distracting the chaperones from folding the healthy proteins the cell needs. The tipping point to death occurs when replenishing good proteins no longer keeps up with depletion from misfolding, aggregation, and damage. The model agrees with experiments in the worm Caenorhabditis elegans that show the following: Life span shortens nonlinearly with increased temperature or added oxidant concentration, and life span increases in mutants having more chaperones or proteasomes. It predicts observed increases in cellular oxidative damage with age and provides a mechanism for the Gompertz-like rise in mortality observed in humans and other organisms. Overall, the model shows how the instability of proteins sets the rate at which damage accumulates with age and upends a cell’s normal proteostasis balance.

scholarly journals Production of YP170 Vitellogenins Promotes Intestinal Senescence in Caenorhabditis elegans

2019 ◽  
Vol 74 (8) ◽  
pp. 1180-1188 ◽  
Author(s):  
Thanet Sornda ◽  
Marina Ezcurra ◽  
Carina Kern ◽  
Evgeniy R Galimov ◽  
Catherine Au ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Stress Resistance ◽  
Later Life ◽  
Abundant Species ◽  
Yolk Proteins ◽  
Oxidative Stress Resistance ◽  
Vitellogenin Synthesis ◽  
Intestinal Atrophy

Abstract During aging, etiologies of senescence cause multiple pathologies, leading to morbidity and death. To understand aging requires identification of these etiologies. For example, Caenorhabditis elegans hermaphrodites consume their own intestinal biomass to support yolk production, which in later life drives intestinal atrophy and ectopic yolk deposition. Yolk proteins (YPs; vitellogenins) exist as three abundant species: YP170, derived from vit-1–vit-5; and YP115 and YP88, derived from vit-6. Here, we show that inhibiting YP170 synthesis leads to a reciprocal increase in YP115/YP88 levels and vice versa, an effect involving posttranscriptional mechanisms. Inhibiting YP170 production alone, despite increasing YP115/YP88 synthesis, reduces intestinal atrophy as much as inhibition of all YP synthesis, which increases life span. By contrast, inhibiting YP115/YP88 production alone accelerates intestinal atrophy and reduces life span, an effect that is dependent on increased YP170 production. Thus, despite copious abundance of both YP170 and YP115/YP88, only YP170 production is coupled to intestinal atrophy and shortened life span. In addition, increasing levels of YP115/YP88 but not of YP170 increases resistance to oxidative stress; thus, longevity resulting from reduced vitellogenin synthesis is not attributable to oxidative stress resistance.

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