ArticleTobacco induced diseases2008
Mitogenic and functional responses by nicotine and hydrogen peroxide in AR42J cells: a comparative study.
Article in Tobacco induced diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Menthol-enhanced cytotoxicity of cigarette smoke demonstrated in two bioassay models.Tobacco induced diseases · 2013Article
- Anabolic Actions of the Regenerative Agent Enamel Matrix Derivative (EMD) in Oral Periosteal Fibroblasts and MG 63 Osteoblasts, Modulation by Nicotine and Glutathione in a Redox Environment.Journal of functional biomaterials · 2012Article
- Mechanisms for redox actions of nicotine and glutathione in cell culture, relevant to periodontitis.Scientific reports · 2012Article
- Lethal impacts of cigarette smoke in cultured tobacco cells.Tobacco induced diseases · 2011Article
- Tobacco Induced Diseases moves to BioMed Central.Tobacco induced diseases · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the current study was to investigate the oxidative effects of nicotine by examining the mitogenic and functional responses in AR42J cells. As a control and for comparison, hydrogen peroxide (H2O2) was used as a source of known oxidative biomarker. Responses were examined by determining cell proliferation through the activation of ERK signaling, basal and CCK-stimulated cell function and measuring lipid peroxidation. AR42J cells have been exposed to either a non-cytotoxic dose of 20 muM H2O2 for 15 min or to 100 muM of nicotine for 3 min respectively. Nicotine and H2O2 at these dose and time intervals produced similar levels of malondialdyde (MDA) production and p-ERK1/2 activation. Immunofluorescence studies employing specific antibody to p-ERK1/2 confirmed the latter. Nicotine-induced increase in the proliferation of AR42J cells was significantly higher in comparison to H2O2 exposed cells. CCK-stimulated cell function induced by nicotine was significantly higher in AR42J cells as compared to the response by H2O2. These results suggest that nicotine- induced mitogenic and functional response in AR42J cells are associated with ERK signaling and increase in reactive oxygen species production. The data suggests that nicotine-induced mitogenic response in AR42J cells closely identifies the response induced by an oxidative biomarker.
Identifiers
What OpenQuestion holds
Registered trials
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.