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RESEARCH PAPER
Mitogenic and functional responses by nicotine and hydrogen peroxide in AR42J cells: a comparative study
Azida Walker 1
,
 
Kodetthoor B Udupa 1,2,3
,
 
Parimal Chowdhury 1
 
 
 
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1
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, USA
 
2
Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, USA
 
3
Medical Research, Central Arkansas Veterans Healthcare System, Little Rock, USA
 
 
Submission date: 2008-06-13
 
 
Acceptance date: 2008-07-31
 
 
Publication date: 2008-07-31
 
 
Tobacco Induced Diseases 2008;4(July):5
DOI: https://doi.org/10.1186/1617-9625-4-5
 
 
Article (PDF)
Supplementary files
References (35) Citations (4)
 
KEYWORDS
nicotine
pancreatic acinar cell
amylase secretion
AR42J cell
H2O2 treated cell
 
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 μM H2O2 for 15 min or to 100 μM 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.
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CITATIONS (4):
1.
Menthol-enhanced cytotoxicity of cigarette smoke demonstrated in two bioassay models
Atsuko Noriyasu, Tadashi Konishi, Shinichi Mochizuki, Kazuo Sakurai, Yutaka Tanaike, Ken Matsuyama, Kazuya Uezu, Tomonori Kawano
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2.
Mechanisms for redox actions of nicotine and glutathione in cell culture, relevant to periodontitis
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3.
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
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Journal of Functional Biomaterials
 
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4.
Lethal impacts of cigarette smoke in cultured tobacco cells
Masaru Yukihiro, Takuya Hiramatsu, Tomonori Kawano
Tobacco Induced Diseases
 
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