Pathologic Cellular Events in Smoking-Related Pancreatitis

Thrower, Edwin C.

doi:10.3390/cancers7020723

Cited by 13 publications

(11 citation statements)

References 65 publications

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“…The nicotine content of cigarettes has important biological effects and plays a key role in the pathogenesis of many diseases. Thrower [18] have shown that nicotine is a major contributor to pancreatic anomalies. The present study evaluates the effects of genistein against toxic properties of nicotine to the pancreas weight, total antioxidant capacity, nitrite oxide, diameter, and the number of pancreatic islets and serum level of insulin.…”

Section: Discussionmentioning

confidence: 99%

Genistein improve nicotine toxicity on male mice pancreas

et al. 2019

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Nicotine is the most toxic factor of tobacco. Genistein is a phytoestrogen and antioxidant that has numerous health benefits. The aim of this study is to evaluate the effects of genistein against toxic properties of nicotine to the pancreas of mice. For this purpose, 48 male mice were randomly assigned into six groups (n=8): normal control, nicotine control (2.5 mg/kg), genistein (25 and 50 mg/kg), and nicotine+genistein (25 and 50 mg/kg) treated groups. Various doses of genistein and genistein+nicotine were administered intraperitoneally to animals for 4 weeks. The weight of pancreas, total antioxidant capacity and nitrite oxide of serum, insulin levels, and the number and diameter of islets of Langerhans were investigated. Nicotine administration reduced significantly total antioxidant capacity, insulin, pancreas weight, and the number and diameter of islets of Langerhans and increased nitrite oxide in serum compared to the control normal group ( P <0.05). Conversely, genistein and genistein+nicotine increased significantly insulin, total antioxidant capacity, and the number and diameter islets of Langerhans and decreased serum nitrite oxide compared to the nicotine control group. It seems that the genistein can improve pancreas damage following the nicotine administration.

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Section: Discussionmentioning

confidence: 99%

Genistein improve nicotine toxicity on male mice pancreas

et al. 2019

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“…Les cellules pancréatiques stellaires, d'origine mésenchymateuse, sont responsables de la production de tissu fibreux dans la pancréatite chronique, ce qui serait favorisé par la consommation d'alcool (20) (21). L'intoxication alcooliquechronique entraîne des anomalies de la sécrétion des protéinespancréatiques ainsi qu'une diminution de la synthèse de la lithostatine expliquant la formation des calculs intra parenchymateux et intracanalaires (15).…”

Section: Introductionunclassified

Pancreatic cancer in patients with chronic calcifying pancreatitis: Computed tomography findings – a retrospective analysis of 48 patients

Mohamed

Ayav

Belle

et al. 2017

European Journal of Radiology

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“…Nicotine is known to accumulate in the pancreas [ 27 ], and has been implicated in the production of free radicals that lead to oxidative stress and consequently pancreatic injury [ 28 ]. Furthermore, animal studies have shown that nicotine exposure induces changes in the pancreas that are similar to those seen in experimental models of pancreatitis [ 29 ]. The effect(s) of nicotine on pancreatic physiology appears to be mediated mainly by the nicotinic acetylcholine receptor and elevated levels of intracellular calcium [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic Nicotine Exposure In Vivo and In Vitro Inhibits Vitamin B1 (Thiamin) Uptake by Pancreatic Acinar Cells

et al. 2015

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Thiamin (vitamin B1), a member of the water-soluble family of vitamins, is essential for normal cellular functions; its deficiency results in oxidative stress and mitochondrial dysfunction. Pancreatic acinar cells (PAC) obtain thiamin from the circulation using a specific carrier-mediated process mediated by both thiamin transporters -1 and -2 (THTR-1 and THTR-2; encoded by the SLC19A2 and SLC19A3 genes, respectively). The aim of the current study was to examine the effect of chronic exposure of mouse PAC in vivo and human PAC in vitro to nicotine (a major component of cigarette smoke that has been implicated in pancreatic diseases) on thiamin uptake and to delineate the mechanism involved. The results showed that chronic exposure of mice to nicotine significantly inhibits thiamin uptake in murine PAC, and that this inhibition is associated with a marked decrease in expression of THTR-1 and THTR-2 at the protein, mRNA and hnRNAs level. Furthermore, expression of the important thiamin-metabolizing enzyme, thiamin pyrophosphokinase (TPKase), was significantly reduced in PAC of mice exposed to nicotine. Similarly, chronic exposure of cultured human PAC to nicotine (0.5 μM, 48 h) significantly inhibited thiamin uptake, which was also associated with a decrease in expression of THTR-1 and THTR-2 proteins and mRNAs. This study demonstrates that chronic exposure of PAC to nicotine impairs the physiology and the molecular biology of the thiamin uptake process. Furthermore, the study suggests that the effect is, in part, mediated through transcriptional mechanism(s) affecting the SLC19A2 and SLC19A3 genes.

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Pathologic Cellular Events in Smoking-Related Pancreatitis

Cited by 13 publications

References 65 publications

Genistein improve nicotine toxicity on male mice pancreas

Genistein improve nicotine toxicity on male mice pancreas

Pancreatic cancer in patients with chronic calcifying pancreatitis: Computed tomography findings – a retrospective analysis of 48 patients

Chronic Nicotine Exposure In Vivo and In Vitro Inhibits Vitamin B1 (Thiamin) Uptake by Pancreatic Acinar Cells

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