Mechanisms of aging: an appraisal of the oxidative stress hypothesis.

By R. S. Sohal, R. J. Mockett, W. Orr. Free Radical Biology & Medicine, 2002

647 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Physiology

View Paper: https://www.semanticscholar.org/paper/0ea87f549993c10722edd466a26b8334c36a5c11

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. Barry Halliwell
2. R. Ricklefs
3. Hannah J. Zhang
4. K. Kregel
5. D. Bohmann
6. Gerasimos P. Sykiotis
7. A. Valavanidis

In Endocrine and Autonomic Systems

1. R. Ricklefs
2. Hannah J. Zhang
3. K. Kregel
4. D. Bohmann
5. Gerasimos P. Sykiotis

In Physiology

1. Barry Halliwell
2. K. Rahman
3. M. Whiteman
4. R. Ricklefs
5. Hannah J. Zhang
6. K. Kregel
7. D. Del Rio
8. D. Bohmann

Citations in the corpus

• A review of recent studies on malondialdehyde as toxic molecule and biological marker of oxidative stress. (2005, background): “Oxidative stress has been related to the etiopathogenesis of several chronic diseases and plays a paramount role in the aging process [1,2].”
• Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean? (2004, background): “…of these terms see Table 1) are widely believed to contribute to the development of several age-related diseases, and perhaps, even to the aging process itself (Halliwell & Gutteridge, 1999; Sohal et al., 2002) by causing ‘oxidative stress’ and ‘oxidative damage’ (terms explained in Table 2).”
• Studies on free radicals, antioxidants, and co-factors (2007, background): “These are the main byproducts formed in the cells of aerobic organisms, and can initiate autocatalytic reactions so that molecules to which they react are themselves converted into free radicals to propagate the chain of damage.”
• The evolution of senescence from a comparative perspective (2008, background): “For example, the production of ROS, which play a role in cellular ageing, can be balanced to some extent by the maintenance of mechanisms to counteract ROS, such as antioxidants (Finkel & Holbrook 2000; Sohal et al. 2002).”
• Molecular biomarkers of oxidative stress in aquatic organisms in relation to toxic environmental pollutants. (2006, background): “This situation initiates oxidative stress in biological systems, damage to tissues, inflammation, degenerative diseases, and aging (Sohal et al., 2002; Finkel and Holbrook, 2000).”
• Keap1/Nrf2 signaling regulates oxidative stress tolerance and lifespan in Drosophila. (2008, background): “On the other hand, some of the model organism studies showing lifespan extension by “longevity genes” have been performed using short-lived control strains; this suggests that the observed lifespan extensions may represent a rescue of pathology rather than a genuine effect on lifespan (Sohal et al.,”
• Mechanisms of nanotoxicity: Generation of reactive oxygen species (2014, background): “associated with many age-related degenerative diseases [41,45,58,59], including amyotrophic lateral sclerosis, arthritis, cardiovascular disease, inflammation, Alzheimer’s disease, Parkinson’s disease, diabetes, and cancer [8,40,43,52,60e64].”
• An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “There are certainly studies supporting the notion that a decline in antioxidant defenses occurs with aging (91), but substantial data also exist indicating that there is no generalized decrease in antioxidant enzyme function (159, 221, 243).”