نمایش مختصر رکورد

dc.contributor.authorJalili, Cyrusen_US
dc.contributor.authorSalahshoor, Mohammad Rezaen_US
dc.contributor.authorMoradi, Mohammad Taheren_US
dc.contributor.authorAhookhash, Maryamen_US
dc.contributor.authorTaghadosi, Mehdien_US
dc.contributor.authorSohrabi, Maryamen_US
dc.date.accessioned1399-07-08T17:50:25Zfa_IR
dc.date.accessioned2020-09-29T17:50:26Z
dc.date.available1399-07-08T17:50:25Zfa_IR
dc.date.available2020-09-29T17:50:26Z
dc.date.issued2017-01-01en_US
dc.date.issued1395-10-12fa_IR
dc.date.submitted2016-12-21en_US
dc.date.submitted1395-10-01fa_IR
dc.identifier.citationJalili, Cyrus, Salahshoor, Mohammad Reza, Moradi, Mohammad Taher, Ahookhash, Maryam, Taghadosi, Mehdi, Sohrabi, Maryam. (2017). Expression Changes of Apoptotic Genes in Tissues from Mice Exposed to Nicotine. Asian Pacific Journal of Cancer Prevention, 18(1), 239-244. doi: 10.22034/APJCP.2017.18.1.239en_US
dc.identifier.issn1513-7368
dc.identifier.issn2476-762X
dc.identifier.urihttps://dx.doi.org/10.22034/APJCP.2017.18.1.239
dc.identifier.urihttp://journal.waocp.org/article_43070.html
dc.identifier.urihttps://iranjournals.nlai.ir/handle/123456789/30360
dc.description.abstract<br /> <strong><span style="font-size: small;">Objective: S</span></strong><span style="font-family: Times New Roman,Times New Roman; font-size: small;"><span style="font-family: Times New Roman,Times New Roman; font-size: small;">moking is the leading preventable cause of various diseases such as lung cancer, chronic obstructive pulmonary disease and cardiovascular disease. Nicotine, one of the major toxic components of tobacco, contributes to the pathogenesis of different diseases. </span></span><strong><span style="font-size: small;">Methods: </span></strong><span style="font-family: Times New Roman,Times New Roman; font-size: small;"><span style="font-family: Times New Roman,Times New Roman; font-size: small;">Given the controversy about nicotine toxicity, the present study was conducted to determine apoptotic effects of nicotine on the heart, kidney, lung and liver of male mice. Real-time PCR was performed to identify mRNA expression changes in apoptotic-related genes between nicotine treated and control mice. </span></span><strong><span style="font-size: small;">Result: </span></strong><span style="font-family: Times New Roman,Times New Roman; font-size: small;"><span style="font-family: Times New Roman,Times New Roman; font-size: small;">In the heart and lung, nicotine caused significant decrease in P53, Bax and Caspase-3 mRNA expression levels compared to the control group. However, in the kidney and liver, the result was significant increase in Bax, Caspase-2, Caspase-3 and a significant decrease in P53 mRNA expression (p<0.01). DNA fragmentation assays indicated no fragmentation in the heart and lung, but in the kidney and liver of nicotine treated mice, isolated DNA was </span></span><span style="font-family: Times New Roman,Times New Roman; font-size: small;"><span style="font-family: Times New Roman,Times New Roman; font-size: small;">fragmented. </span></span><strong><span style="font-size: small;">Conclusion: </span></strong><span style="font-family: Times New Roman,Times New Roman; font-size: small;"><span style="font-family: Times New Roman,Times New Roman; font-size: small;">Our study provided insight into the molecular mechanisms of nicotine anti-apoptotic effects on the heart and lung as well as pro-apoptotic effects on kidney and liver via a P53-independent pathway. </span></span>en_US
dc.format.extent295
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoen_US
dc.publisherWest Asia Organization for Cancer Prevention (WAOCP)en_US
dc.relation.ispartofAsian Pacific Journal of Cancer Preventionen_US
dc.relation.isversionofhttps://dx.doi.org/10.22034/APJCP.2017.18.1.239
dc.subjectNicotineen_US
dc.subjectApoptosisen_US
dc.subjectLiveren_US
dc.subjectCaspase-2en_US
dc.subjectp53en_US
dc.subjectMolecular and cellularen_US
dc.titleExpression Changes of Apoptotic Genes in Tissues from Mice Exposed to Nicotineen_US
dc.typeTexten_US
dc.typeResearch Articlesen_US
dc.contributor.departmentFertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.contributor.departmentMedical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.contributor.departmentFertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.contributor.departmentStudents Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.contributor.departmentDepartment of Immunology, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.contributor.departmentFertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.en_US
dc.citation.volume18
dc.citation.issue1
dc.citation.spage239
dc.citation.epage244


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