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World J Gastrointest Pathophysiol. Jun 15, 2011; 2(3): 57-60
Published online Jun 15, 2011. doi: 10.4291/wjgp.v2.i3.57
Parimal Chowdhury’s work on smoking related pancreatic disorders
Parimal Chowdhury
Parimal Chowdhury, Department of Physiology and Biophysics, Faculty of Medicine, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205 United States
Author contributions: Chowdhury P contributed solely to this manuscript.
Supported by the Earlier Grants from NIH and a Grant through University of Arkansas for Medical Sciences
Correspondence to: Parimal Chowdhury, PhD, Professor, Department of Physiology and Biophysics, Faculty of Medicine, University of Arkansas for Medical Sciences, 4301,W Markham Street, Nord, Little Rock, AR 72205, United States. pchowdhury@uams.edu
Telephone: +1-501-686-5443 Fax: +1-501-686-68167
Received: December 14, 2010
Revised: May 18, 2011
Accepted: May 25, 2011
Published online: June 15, 2011
Abstract

Cigarette smoking is a known risk factor for the development of numerous diseases. The role of nicotine in the induction of pancreatic inflammation and pancreatic cancer as a result of cigarette smoking has been recognized and reported in the literature. The mechanism by which nicotine induces such pathologies is as yet unknown. An understanding of the proliferative potential of nicotine in primary and tumor cells of the pancreas will allow us to develop measures that will ultimately lead to intervention, prevention and treatment of these diseases. Studies show that nicotine can increase the cell numbers of cer-tain cancer cell lines, suggesting that exposure to nicotine can lead to the disruption of the dynamic balance between cell death and proliferation, which is required for normal functioning of cells. We hypothesize that nicotine induces oxidative stress in pancreatic acinar cells and thus contributes to this disruption. We have used the AR42J cell line in our study because of its stability as an immortal tumor cell line and its known physiological similarity to primary acinar cells. Our studies show that mitogen activated protein kinase signaling is induced by nicotine in AR42J cells, causing an increase in lipid peroxidation and a subsequent decrease in cell function. Our data suggest that exposure to nicotine induces oxidative stress, leading to cell injury and compromised function, thus implicating cigarette smoking as a plausible mechanism.

Keywords: Nicotine; AR42J cell; Effect on mechanisms; Lipid peroxidation; MAPK signaling; Cell function