Mitogenic and functional responses by nicotine and hydrogen peroxide in AR42J cells: a comparative study
Azida Walker 1
Kodetthoor B Udupa 1, 2, 3
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Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, USA
Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, USA
Medical Research, Central Arkansas Veterans Healthcare System, Little Rock, USA
Publish date: 2008-07-31
Tobacco Induced Diseases 2008;4(July):5
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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