Cited by 55Genetics, Aging, and Longevity in Model OrganismsRedox biology and oxidative stressAntioxidant Activity and Oxidative Stress

Involvement of Redox State in the Aging of Drosophila melanogaster

Open access
Orr, William C., Radyuk, Svetlana N., Sohal, Rajindar S.·2013·Antioxidants & Redox Signaling

Abstract

SIGNIFICANCE: The main objective of this review was to provide an exposition of investigations, conducted in Drosophila melanogaster, on the role of reactive oxygen species and redox state in the aging process. While early transgenic studies did not clearly support the validity of the oxidative stress hypothesis of aging, predicated on the accumulation of structural damage, they spawned a broader search for redox-related effects that might impact the aging process. RECENT ADVANCES: Initial evidence implicating the thiol redox state as a possible causative factor in aging has been obtained in Drosophila. Overexpression of genes, such as GCL, G6PD, Prx2, and Prx5, which are involved in the maintenance of thiol redox homeostasis, has strong positive effects on longevity. Further, the depletion of peroxiredoxin activity in the mitochondria through the double knockdown of Prx5 and Prx3 not only results in a redox crisis but also elicits a rapid aging phenotype. CRITICAL ISSUES: Herein, we summarize the present status of knowledge about the main components of the machinery controlling thiol redox homeostasis and describe how age-related redox fluctuations might impact aging more acutely through disruption of the redox-sensitive signaling mechanisms rather than via the simple accumulation of structural damage. FUTURE DIRECTIONS: Based on these initial insights into the plausible impact of redox fluctuations on redox signaling, future studies should focus on the pathways that have been explicitly implicated in aging, such as insulin signaling, TOR, and JNK/FOXO, with particular attention to elements that are redox sensitive.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1089/ars.2012.5002

Cites

131 of 131 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Over-expression of genes involved in the maintenance of thiol redox homeostasis or co-overexpression of Cu-Zn superoxide dismutase (Cu-ZnSOD) and catalase increase the lifespan of Drosophila melanogaster by 33-48%.

    “Over-expression of genes involved in the maintenance of thiol redox homeostasis or co-overexpression of Cu-Zn superoxide dismutase (Cu-ZnSOD) and catalase increase the lifespan of Drosophila melanogaster by 33–48% (Orr et al., 2013; Orr and Sohal, 1994).”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. [98]Rubner M. Das Problem der Lebensdauer und seine Beziehunger zum Wachstum und Ernaibrung. Oldenburg; Munchen: 1908. [Google Scholar]

Cited by

Sorted by citations

Authors
Orr, W. C., Radyuk, S. N., & Sohal, R. S.
Affiliations
  • Southern Methodist University (US)
  • University of Southern California (US)
Corresponding author
Orr, William C.
Venue
Antioxidants & Redox Signaling
Published
2013-09-10
Volume
19
Issue
8
Pages
788-803
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
OpenAlex
W2085223516
Cited by
55
References
131
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2022: 5 · 2021: 4 · 2020: 4 · 2019: 7 · 2018: 3 · 2017: 3 · 2016: 7 · 2015: 6 · 2014: 7 · 2013: 1
FWCI
0.42
Type
journal article
Language
en
Open access
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (RO1 AG7657)
  • National Institute on Aging (RO1 AG7657, RO1 AG15122, R01AG020715, R01AG032342, R01AG045830, R01AG007657, R01AG013563, R01AG017526, RO1 AG20715, R01AG015122, R01AG017077)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
aging, Drosophila melanogaster, redox state, thiol redox homeostasis, reactive oxygen species, longevity, glutathione peroxidase, peroxiredoxin, glutathione synthetase, glucose-6-phosphate dehydrogenase, redox signaling, insulin signaling, TOR signaling
MeSH terms
Aging, Animals, Drosophila melanogaster, Energy Metabolism, Humans, Longevity, Oxidation-Reduction, Oxidoreductases, Reactive Oxygen Species, Oxidative Stress, Drosophila Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review