CoChat
Sign Up
Cited by 25Exercise and Physiological ResponsesCell death mechanisms and regulationImmunotoxicology and immune responses

Mouse thymocyte apoptosis and cell loss in response to exercise and antioxidant administration

Quadrilatero, Joe, Hoffman-Goetz, Laurie·2005·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2004.12.004
Open this paper in CoChat — free account

Abstract

Various physical and psychological stressors can cause thymocyte apoptosis and cell loss in rodents. Although glucocorticoids (GC) are commonly implicated, oxidative stress may also play a role. The purpose of this study was to examine the effect of an acute bout of strenuous treadmill running, and the antioxidant N-acetyl-L-cysteine (NAC) on thymocyte loss and apoptosis. Eighty-eight female C57BL/6 mice were given NAC (1 g/kg, i.p.) or saline (SAL) 30 min before 90 min of treadmill exercise at a 2 degrees slope (EX; 30 min at 22 m/min; 30 min at 25 m/min; and 30 min at 28 m/min) and sacrificed immediately (Imm) or 24 h following EX. Control mice (NonEX) were exposed to treadmill noise and vibration without running. Thymocytes were isolated and analyzed for phosphatidylserine (PS) externalization (Annexin V), loss of membrane integrity, mitochondria membrane depolarization, intracellular hydrogen peroxide (H(2)O(2)) production, and intracellular glutathione (GSH) as well as protein levels of caspase 3, Bcl-2, and cytosolic cytochrome c. Blood was analyzed for corticosterone (CORT) concentrations by radioimmunoassay. Exercise stress caused a significant increase in plasma CORT concentrations in EX + SAL + Imm and EX + NAC + Imm groups compared to NonEX mice. Relative to NonEX mice, thymocytes isolated from EX + SAL + Imm mice showed signs of an early apoptotic profile as indicated by decreased GSH stores and increased mitochondrial membrane depolarization. These effects were followed by a 50% reduction in thymocyte numbers 24 h post-exercise (EX + SAL + 24 h). Alterations in GSH levels, mitochondrial membrane depolarization, and thymocyte loss were not observed in mice receiving NAC. These results suggest that exercise-induced thymocyte apoptosis and cell loss may be mediated via an oxidative stress pathway.

Integrity signals

Registry

Crossref · 10.1016/j.bbi.2004.12.004

Cites

57 of 57 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • A murine study has shown that N-acetyl-cysteine prevents thymocyte apoptosis and cell loss caused by exercise-induced oxidative stress.

    “Encouragingly however, a murine study has shown that N-acetyl-cysteine prevents thymocyte apoptosis and cell loss caused by exercise-induced oxidative stress (Quadrilatero and Hoffman-Goetz 2005).”

    From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as Quadrilatero and Hoffman-Goetz 2005

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Quadrilatero, J., & Hoffman-Goetz, L.
Affiliations
University of Waterloo (CA)
ORCID
Quadrilatero, Joe
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2005-09
Volume
19
Issue
5
Pages
436-444
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2004.12.004
OpenAlex
W2001159835
Cited by
25
References
57
Citations by year
2026: 1 · 2025: 1 · 2021: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 2 · 2013: 2 · 2012: 1
FWCI
1.05
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
Natural Sciences and Engineering Research Council of Canada
Topics
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords
thymocyte apoptosis, exercise stress, treadmill running, N-acetylcysteine, antioxidant supplementation, oxidative stress, corticosterone, glucocorticoids, mitochondrial depolarization, hydrogen peroxide, glutathione, caspase-3, Bcl-2, cytochrome c, phosphatidylserine exposure
MeSH terms
Acetylglucosamine, Animals, Antioxidants, Cell Survival, Corticosterone, Physical Exertion, Female, Flow Cytometry, Glutathione, Hydrogen Peroxide, Membrane Potentials, Mice, Inbred C57BL, Mitochondria, Oxidation-Reduction, Phosphatidylserines, T-Lymphocytes, Blotting, Western, Apoptosis, Annexin A5, Lymphocyte Count, Proto-Oncogene Proteins c-bcl-2, Caspases, Cytochromes c, Mice, Caspase 3

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