The effect of zinc rich diet to the cytokine profile in the Rat Bladder on cigarette smoke exposure

Abstract

OBJECTIVE: Cigarette smoking causes lung, larynx, esophagus, stomach, bladder and kidney cancers and chronic diseases. Cytokines are important in initiating and maintaining inflammation. Smoking is the cause of zinc deficiency. Zinc is an antioxidant and protects cells from free radical damage. In our study, it was aimed to investigate the effect of cigarette smoke exposure on expression of Toll-like receptor 2, Toll-like receptor 4, nuclear factor kappa B, interleukin 1β and interleukin 10 in the bladder tissue of rats fed with zinc rich diet.METHODS: In this study 24 adult male Wistar-Albino rats were used. The rats were divided into 4 groups. First group was fed with normal diet, the 2nd group was fed with zinc rich diet. Third and 4th groups were exposed to cigarette inhalation and fed with normal and zinc rich diet respectively. The bladder tissues were taken at the end of the experiment and evaluated histologically. The remaining tissue samples were evaluated by the method of Real time polymerase chain reaction to show cytokine expression.RESULTS: No changes in urinary bladder epithelium was observed in all study groups. Edema and inflammatory cells in the smooth muscle layers with intense hemorrhage and congestion were observed in cigarette smoke given group. Less inflammatory cells, congestion and edema have been found in the rats fed with zinc rich diet. Cytokine expression in bladder tissue of all groups of rats compared in pairs and significant difference was found for the NF-κb2 gene in zinc rich supplemented and normally supplemented rats exposed to cigarette smoke.CONCLUSION: As a result, a significant increase in expression of NF-κb2 caused by the use of zinc in rats exposed to cigarette smoke suggests that zinc can contribute the treatment of bladder cancer due to smoking by increasing cancer cell.

Keywords

• Cigarette smoke exposure,RT-PCR,Zinc,NFκB2

Çinkodan Zengin Diyetin, Sigara Dumanı Maruziyetindeki Sıçan Mesane Dokusu Sitokin Profiline Etkisi

Abstract

AMAÇ: Sigara içimi akciğer, larinks, özefagus, mide, mesane ve böbrek kanserleri ile kronik hastalıkların sebebidir. Sitokinler, inflamasyonun başlatılması ve sürdürülmesinde önemlidirler. Sigara, çinko eksikliği sebebidir. Çinko, antioksidan olup serbest radikallerin zararlarından hücreleri korur. Çalışmamızda sigara dumanına maruz bırakılarak çinkodan zengin diyet ile beslenen sıçanların mesane dokusundaki TLR 2, TLR 4, Nükleer faktör kapa B, İnterlökin 1β ve İnterlökin 10 ekspresyonuna etkisi incelenmesi amaçlanmıştır. YÖNTEMLER: Çalışmada 24 adet erişkin erkek Wistar-Albino sıçanlar kullanıldı. Sıçanlar 4 gruba ayrıldı. Birinci grup normal, 2. grup ise çinkodan zengin diyetle beslendi. Üçüncü ve 4. gruplar sigara inhalasyonu yapılan gruplar olup sırasıyla normal ve çinkodan zengin diyetle beslenen gruplardı. Deney sonunda alınan mesane dokuları histolojik olarak değerlendirildi. Kalan doku örnekleri ise Real time polymerase chain reaction yöntemi ile sitokin ekspresyonları gösterilerek değerlendirildi. BULGULAR: Çalışmadaki hiçbir grup mesane epitelinde değişiklik izlenmemiştir. Sigara verilen grupta sadece düz kas yapılarında tabakalar arasında ödem ve bazı alanlarda yoğun inflamatuar hücreler ile bu alanlarda hemoraji ve konjesyona rastlanılmıştır. Çinkodan zengin diyetle beslenen denekler de ise inflamatuar hücrelere, konjesyona ve ödeme daha az rastlandı. Tüm sıçan gruplarının mesane dokularında sitokin ekspresyonları ikili olarak karşılaştırmalarda sigaraya maruz kalmış sıçanlarda çinko almayan ve çinko alan sıçanlar için NF-κB2 geni için anlamlı farklılık bulundu. SONUÇ: Sonuç olarak sigara maruz kalan sıçanlarda çinko kullanımının anlamı bir şekilde NF-κB2 ekpresyonunu artışına neden olması, çinkonun sigaraya bağlı gelişen mesane kanserlerinde kanserli hücre apopitozunu arttırarak tedaviye katkı yapabileceğini düşündürmektedir.

Keywords

• Sigara Dumanı Maruziyeti,RT-PCR,Çinko,NF-κB2

References

1. 1. World Health Organization. Tobacco: Deadly in Any Form or Disguise. Geneva: World Health Organization; 2006. [accessed: July 13, 2007]. < http://wwwwho.int/tobacco/communications/even ts/wntd/2006/Tfi_Rapport.pdf>.
2. 2. Centers for Disease Control and Prevention. Smoking attributable mortality, years of potential life lost, and productivity losses—United States, 2000– 2004. Morbidity and Mortality Weekly Report. 2008;57(45):1226–8
3. 3. Uluslararası Katılımlı Üçüncü Sigara veya Sağlık Ulusal Kongresi Sonuç bildirgesi 1 Aralık 2006 ANKARA http://www.tutunsuzyasam.org/dosya/SonucBildirg esi.doc
4. 4. International Agency for Research on Cancer [IARC] 2004
5. 5. Rodgman A, Perfetti TA. The Chemical Components of Tobacco and Tobacco Smoke. Boca Raton (FL): CRC Press Taylor & Francis Group; 2009
6. 6. US Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Atlanta (GA). 2010.
7. 7. US Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2004.
8. 8. Kato M, Wei M, Yamano S, Fujioka M, Kakehashi A, Wanibuchi H. Evaluation of the modifying effect of inhalation of mainstream cigarette smoke on mouse bladder carcinogenesis. J Toxicol Pathol. 2013 Dec;26(4):447-51. doi: 10.1293/tox.2013- 0039.

9. 9. Freedman ND, Silverman DT, Hollenbeck AR, Schatzkin A, and Abnet CC. Association between smoking and risk of bladder cancer among men and women. JAMA. 306: 737–745. 2011.
10. 10. Ward EM, Sabbioni G, DeBord DG, Teass AW, Brown KK, Talaska GG, Roberts DR, Ruder AM, and Streicher RP. Monitoring of aromatic amine exposures in workers at a chemical plant with a known bladder cancer excess. J Natl Cancer Inst. 88: 1046– 1052. 1996
11. 11. Lesmes GR, Donofrio KH. Passive smoking: the medical and economic issues. Am J Med. 1992 Jul 15;93(1A):38S-42S.
12. 12. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. International journal of cancer Journal international du cancer. 2010 Dec 15;127(12):2893-917. PubMed PMID: 21351269. Epub 2011/02/26.
13. 13. Hebda PA, Piltcher OB, Swarts JD, Alper CM, Zeevi A, Doyle WJ. Cytokine profiles in a rat model of otitis media with effusion caused by eustachian tube obstruction with and without Streptococcus pneumoniae infection. Laryngoscope. 2002 Sep;112(9):1657-62.
14. 14. Mortaz E, Lazar Z, Koenderman L. Cigarette smoke attenuates the production of cytokines by human plasmacytoid dendritic cells and enhances the release of IL-8 inresponse to TLR-9 stimulation Respiratory Research 2009 Respir Res. 2009 Jun 10;10:47.
15. 15. Lang C, Hansen M, Roscioli E. Dietary zinc mediates inflammation and protects against wasting and metabolic derangement caused by sustained cigarette smoke exposure in mice. Biometals. 2011 Feb;24(1):23-39
16. 16. Livak KJ,Schmittgen TD., Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001;25(4):402-8.
17. 17. Fielding JE. Smoking: health effects and control (1).N Engl J Med. 1985 Aug 22;313(8):491-8
18. 18. Lesmes GR, Donofrio KH. Passive smoking: the medical and economic issues. Am J Med. 1992 Jul 15;93(1A):38S-42S.
19. 19. Salganik RI, Solovyova NA, Dikalov SI, Grishaeva ON, Semenova LA, Popovsky AV. Inherited enhancement of hydroxyl radical generation and lipid peroxidation in the S strain rats results in DNA rearrangements, degenerative diseases, and premature aging. Biochemical and biophysical research communications. 1994 Mar 15;199(2):726-33.
20. 20. Akcay T, Saygili I, Andican G, Yalcin V. Increased formation of 8-hydroxy-2'-deoxyguanosine in peripheral blood leukocytes in bladder cancer. Urologia internationalis. 2003;71(3):271-4.
21. 21. Mao S, Huang S. Zinc and copper levels in bladder cancer: a systematic review and meta-analysis. Biological trace element research. 2013 Jun;153(1- 3):5-10.
22. 22. Mazdak H, Yazdekhasti F, Movahedian A, Mirkheshti N, Shafieian M. The comparative study of serum iron, copper, and zinc levels between bladder cancer patients and a control group. International urology and nephrology. 2010 Mar;42(1):89-93.
23. 23. Preciado D, Lin J, Wuertz B. Cigarette Smoke Activates NFκB and Induces Muc5b Expression in Mouse Middle Ear Cells Laryngoscope. 2008 March; 118(3): 464–471.
24. 24. Zhang GJ, Zhang Z. Effect of Bcl-2 on apoptosis and transcription factor NF-κB activation induced by adriamycin in bladder carcinoma BIU87 cells. Asian Pac J Cancer Prev. 2013; 14(4):2387-91
25. 25. Hamajima N, Katsuda N, Matsuo K, Saito T, Ito LS, Ando M, Inoue M, Takezaki T, Tajima K. Smoking habit and interleukin lB C-31T polymorphism. J Epidemiol. 2001 May;11(3):120-5.
26. 26. Ouyang Y, Virasch N, Hao P, et al. Suppression of human IL-1β , IL-2, IFN- γ , and TNF- α production by cigarette smoke extractions. J Allergy Clin Immunol 2000; 106: 280-287.
27. 28. Unless else specified in boxes then ref is: Lippincott's Illustrated Reviews: Immunology. Paperback: 384 pages. Publisher: Lippincott Williams & Wilkins; (July 1, 2007). Language: English. ISBN 0781795435. ISBN 978-0781795432. Page 17.