Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/9911
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dc.contributor.authorTopsakal, Şenay-
dc.contributor.authorÖzmen, Ö.-
dc.contributor.authorAslankoç, R.-
dc.contributor.authorAydemir, D.H.-
dc.date.accessioned2019-08-16T13:07:33Z
dc.date.available2019-08-16T13:07:33Z
dc.date.issued2016-
dc.identifier.issn2045-452X-
dc.identifier.urihttps://hdl.handle.net/11499/9911-
dc.identifier.urihttps://doi.org/10.1039/c5tx00496a-
dc.description.abstractIn recent years, pancreatic pathologies have become common problems and their etiology and pathogenesis are generally unknown. Studies have shown that smoking may increase the risk of pancreatic disorders but very scant knowledge is available about the pathogenesis of cigarette induced pancreatic pathology. This study aimed to evaluate the oxidative stress status, biochemical, pathological and immunohistochemical findings of rats exposed to cigarette smoke, pathogenesis of smoking related pancreatic damage and usability of Alpha Lipoic Acid (ALA) for amelioration of cigarette smoking induced harmful effects on rat pancreas. Twenty eight female, Sprague Dawley rats were randomly distributed into three groups. The sham group (S) (n = 8), rats were given 0.1 ml of physiological serum by oral gavage for 8 weeks. The cigarette smoke exposed group (CSE) (n = 10), rats were exposed to successive periods of cigarette smoke for 2 hours per day per 8 weeks and given 0.1 ml of physiological serum orally during the study. The cigarette smoke exposed and ALA treated group (CSE + ALA) (n = 10), animals were exposed to cigarette smoke (2 hours per day per 8 weeks) and simultaneously treated with 100 mg per kg per day ALA orally during the study. At the end of the study, the serum samples were collected for insulin, glucagon, glucose and amylase analyses. Tissue samples were collected for biochemical, histopathological and immunohistochemical examinations. Total oxidant status (TOS), total antioxidant status (TAS) levels and oxidative stress index (OSI) were evaluated in the pancreas samples. Immunohistochemical analyses of insulin, glucagon, calcitonin gene related protein (CGRP), active caspase-3, hypoxia inducible factor-1 (Hif-1), Hif-2 and tumor necrosis factor (TNF-?) expressions of pancreas were examined. Cigarette smoke caused statistically significant increase in serum amylase and glucose but decreased insulin levels indicating both endocrine and exocrine cell damage. There were no statistically significant differences in serum glucagon levels between the groups. Histopathological examination of the pancreas exhibited generally normal tissue architecture but slightly degenerative and apoptotic cells were noticed both in the endocrine and exocrine part of the pancreas in the CSE group. Immunohistochemical analyses revealed marked increase in active caspase-3, Hif-1 and Hif-2, CGRP and TNF-? expressions with a slight increase in glucagon immunoreactivity in cells while a marked decrease was observed in insulin expression in some Langerhans islets in the CSE group. ALA ameliorated biochemical and pathological findings in the CSE + ALA group. These findings clearly demonstrated that cigarette smoke can cause damage in both endocrine and exocrine cells in rat pancreas and ALA has an ameliorative effect of cigarette induced lesions. © 2016 The Royal Society of Chemistry.en_US
dc.language.isoenen_US
dc.publisherRoyal Society of Chemistryen_US
dc.relation.ispartofToxicology Researchen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectamylaseen_US
dc.subjectcalcitonin gene related peptideen_US
dc.subjectcaspase 3en_US
dc.subjectcigarette smokeen_US
dc.subjectglucagonen_US
dc.subjectglucoseen_US
dc.subjecthypoxia inducible factoren_US
dc.subjecthypoxia inducible factor 1en_US
dc.subjecthypoxia inducible factor 2en_US
dc.subjectinsulinen_US
dc.subjectthioctic aciden_US
dc.subjecttumor necrosis factor alphaen_US
dc.subjectunclassified drugen_US
dc.subjectamylase blood levelen_US
dc.subjectanimal cellen_US
dc.subjectanimal experimenten_US
dc.subjectanimal modelen_US
dc.subjectanimal tissueen_US
dc.subjectArticleen_US
dc.subjectblood biochemistryen_US
dc.subjectcell damageen_US
dc.subjectcontrolled studyen_US
dc.subjectendocrine cellen_US
dc.subjectexocrine cellen_US
dc.subjectfemaleen_US
dc.subjectglucagon blood levelen_US
dc.subjectglucose blood levelen_US
dc.subjecthistopathologyen_US
dc.subjectimmunohistochemistryen_US
dc.subjectimmunoreactivityen_US
dc.subjectinsulin blood levelen_US
dc.subjectnonhumanen_US
dc.subjectoxidative stressen_US
dc.subjectpancreas injuryen_US
dc.subjectpancreatic tissueen_US
dc.subjectpriority journalen_US
dc.subjectprotein expressionen_US
dc.subjectraten_US
dc.subjectsmokingen_US
dc.subjectSprague Dawley raten_US
dc.titlePancreatic damage induced by cigarette smoke: The specific pathological effects of cigarette smoke in the rat modelen_US
dc.typeArticleen_US
dc.identifier.volume5en_US
dc.identifier.issue3en_US
dc.identifier.startpage938
dc.identifier.startpage938en_US
dc.identifier.endpage945en_US
dc.identifier.doi10.1039/c5tx00496a-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.pmid30090402en_US
dc.identifier.scopus2-s2.0-84968735771en_US
dc.identifier.wosWOS:000375488900019en_US
dc.identifier.scopusqualityQ2-
dc.ownerPamukkale University-
item.languageiso639-1en-
item.fulltextWith Fulltext-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept14.02. Internal Medicine-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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