Evidence map›Paper›PMID 23748015›Full record

ArticleMutation research2013

Effects of side-stream tobacco smoke and smoke extract on glutathione- and oxidative DNA damage repair-deficient mice and blood cells.

Mitsuko L Yamamoto, Aaron M Chapman, Robert H Schiestl

Abstract read
In one paragraph

Article in Mutation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Mitsuko L YamamotoDavid Geffen School of Medicine at UCLA, Department of Pathology, Los Angeles, CA, United States; David Geffen School of Medicine at UCLA, Department of Environmental Health, Los Angeles, CA, United States; Pfizer Inc., Experimental Medicine, South San Francisco, California 94080, United States.
Aaron M Chapman
Robert H Schiestl
University of California, Los Angeles · USPfizer (United States) · US

Funding

Mechanisms of Intestinal Inflammation - Associated Systemic GenotoxicityR56AI094756 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRAUN, JONATHAN, SCHIESTL, ROBERT H · 2012 to 2012
$378k
NIAID NIH HHS R56 AI094756NIAID NIH HHS R56AI094756-0
6 · The paper itself

Abstract

Cigarette smoke causes direct oxidative DNA damage as well as indirect damage through inflammation. Epidemiological studies show a strong relationship between secondhand smoke and cancer; however, the mechanisms of secondhand smoke-induced cancer are not well understood. Animal models with either (i) deficient oxidative DNA damage repair, or (ii) a decreased capacity to combat oxidative stress may help determine the pathways important in mitigating damage caused by smoke. In this study, we used mice lacking Ogg1 and Myh, both of which are involved in base excision repair by removing oxidatively damaged DNA bases. Gclm-deficient mice, which have decreased levels of glutathione (GSH), were used to look at the role of smoke-induced oxidative damage. Ex vivo experiments show significantly elevated levels of DNA single-strand breaks and chromosomal aberrations in peripheral blood lymphocytes from Ogg1(-/-)Myh(-/-) double knockout mice compared to wild type (WT) mice after 24h of exposure to cigarette smoke extract (CSE). The average γH2AX foci per cell was significantly elevated 3h after exposure to CSE in cells from Ogg1(-/-)Myh(-/-) double knockout mice compared to wildtype mice. In vivo we found that all mice had increased markers of DNA damage after exposure to side-stream tobacco smoke (SSTS). Ogg1(-/-)Myh(-/-) and Gclm(-/-) mice had altered levels of peripheral blood glutathione after SSTS exposure whereas wild type mice did not. This may be due to differential regulation of glutathione synthesis in the lung. We also found that Ogg1(-/-)Myh(-/-) mice had a decreased lifespan after oral gavage with benzo[a]pyrene compared to wildtype mice and sham-exposed Ogg1(-/-)Myh(-/-) mice. Our results are important in investigating the roles of oxidative stress and oxidative DNA damage repair in cigarette smoke-induced cancers and characterizing the role of genetic polymorphisms in smoke-related disease susceptibility.

Indexed as

AnimalsBlood CellsDNA DamageDNA GlycosylasesDNA Repair-Deficiency DisordersFemaleGlutamate-Cysteine LigaseGlutathioneMaleMiceMice, Inbred C57BLMice, KnockoutOxidative StressTobacco Smoke PollutionDNA GlycosylasesGCLM protein, mouseGlutamate-Cysteine LigaseGlutathionemutY adenine glycosylaseOgg1 protein, mouseTobacco Smoke Pollutioncigarette smoke extractCSEDNA damageDNA repairdouble stranded breaksDSBsenvironmental tobacco smokeETSGlutathionemicro-nucleusMNMyhOgg1Ogg1(−/−)Myh(−/−)OMMside stream tobacco smokeSSTSwild typeWT

Identifiers

PMID23748015
PMCPMC3810249
OpenAlexW1986198509

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.