ArticleLangenbeck's archives of surgery2008
A cell-based approach to study changes in the pancreas following nicotine exposure in an animal model of injury.
Article in Langenbeck's archives of surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Cholinergic Mechanisms in Gastrointestinal Neoplasia.International journal of molecular sciences · 2024Review
- The Risk Factors for Progression to Chronic Pancreatitis in Patients with Past-History of Acute Pancreatitis: A Retrospective Analysis Based on Mechanistic Definition.Journal of clinical medicine · 2022Article
- Risk Factors for Recurrent Pancreatitis After First Episode of Acute Pancreatitis.International journal of general medicine · 2022Article
- Prevalence of Panoramically Imaged Carotid Atheromas in Alcoholic Patients With Chronic Pancreatitis and Comorbid Diabetes.Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · 2018Observational
- Effects of a natural polyphenol on nicotine-induced pancreatic cancer cell proliferation.Tobacco induced diseases · 2018Article
- Impact of cigarette smoking on recurrence of hyperlipidemic acute pancreatitis.World journal of gastroenterology · 2017Article
- Nicotinic acetylcholine receptors and cancer.Biomedical reports · 2016Article
- β2-adrenogenic signaling regulates NNK-induced pancreatic cancer progression via upregulation of HIF-1α.Oncotarget · 2016Article
- Epidemiologic and Mechanistic Associations Between Smoking and Pancreatitis.Current treatment options in gastroenterology · 2015Article
- The Role of nAChR and Calcium Signaling in Pancreatic Cancer Initiation and Progression.Cancers · 2015Review
- Review
- Chronic Nicotine Exposure In Vivo and In Vitro Inhibits Vitamin B1 (Thiamin) Uptake by Pancreatic Acinar Cells.PloS one · 2015Article
- Smoking and Pancreatic Disease.Journal of cancer therapy · 2013Article
- Effect of nicotine on exocytotic pancreatic secretory response: role of calcium signaling.Tobacco induced diseases · 2013Article
- Effects of chronic nicotine on the autocrine regulation of pancreatic cancer cells and pancreatic duct epithelial cells by stimulatory and inhibitory neurotransmitters.Carcinogenesis · 2012Article
- Interplay between smoking-induced genotoxicity and altered signaling in pancreatic carcinogenesis.Carcinogenesis · 2012Review
- The pathobiological impact of cigarette smoke on pancreatic cancer development (review).International journal of oncology · 2012Review
- The emerging role of smoking in the development of pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2011Review
- Aldehyde dehydrogenase 3B1 (ALDH3B1): immunohistochemical tissue distribution and cellular-specific localization in normal and cancerous human tissues.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010Article
- Vitamin E reversed nicotine-induced toxic effects on bone biochemical markers in male rats.Archives of medical science : AMS · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCigarette smoking is a recognized risk factor for the induction of pancreatic diseases and is suspected to play a major role in the development of pancreatic cancer in smokers. MATERIALS AND
methodsThis study was designed to characterize the mechanisms of nicotine-induced injury to the pancreas. AR42Jcells, a stable mutant pancreatic tumor cell line, was chosen for the study because of its stability in culture media and also because of its known secretory capacity, which is like that of a normal pancreatic acinar cell. It is hypothesized that nicotine-induced effects on the pancreas are triggered by oxidative stress induced in pancreatic acinar cell via oxidative stress signaling pathways.
resultsThe results from our study showed that, in vitro, nicotine induced generation of oxygen free radicals measured as malondialdehyde, an end product of lipid peroxidation. Treatment of AR42J cells with nicotine induced p-ERK 1/2 activation as confirmed by Western blot and immunofluorescence imaging of cytoplasmic localization of mitogen-activated protein kinase (MAPK) signals. Nicotine enhanced AR42J cell proliferation and cholecystokinin-stimulated amylase release in AR42J cells. These effects of nicotine were confirmed by simultaneous studies conducted on the same cells by hydrogen peroxide, a known oxidative biomarker. Allopurinol, a XOD inhibitor, suppressed these effects induced by nicotine and H(2)O(2) with the exception that cholecystokinin-stimulated amylase release by H(2)O(2) remained unaltered when AR42J cells were preincubated with allopurinol. These results suggest that nicotine-induced effects on pancreatic acinar cells were associated with generation of oxyradical mediated via the XOD pathway. The results have a direct impact on cell proliferation, MAPK signaling, and acinar cell function.
conclusionWe conclude that nicotine induces oxidative stress in pancreatic acinar cells and that these events trigger pathophysiological changes in the pancreas, leading to increased cell proliferation and injury.
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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.