Parimal Chowdhury's work on smoking related pancreatic disorders

作     者：Parimal Chowdhury 

作者机构：Department of Physiology and BiophysicsFaculty of MedicineUniversity of Arkansas for Medical Sciences4301 W Markham StreetLittle RockAR 72205 United States 

出 版 物：《World Journal of Gastrointestinal Pathophysiology》 (世界胃肠病理生理学杂志（英文版）（电子版）)

年 卷 期：2011年第2卷第3期

页      面：57-60页

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Supported by the Earlier Grants from NIH and a Grant through University of Arkansas for Medical Sciences 

主　　题：Nicotine AR42J cell Effect on mechanisms Lipid peroxidation MAPK signaling Cell function 

摘      要：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 certain 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 bynicotine 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.