Dumansız Tütün "Maraş Otu"nun Homosistein ve Kardiyovasküler Risk Parametreleri Üzerine Etkileri

Abstract

Amaç: Bu çalışma, dumansız tütün (Maraş otu) ile sigara tüketiminin kardiyovasküler hastalıklar için bilinen risk faktörleri olan homosistein, Paraoksonaz-1 (PON-1), Arylesteraz (ARE) ve Lipoprotein-a (Lp (a)) ile ilişkisini araştırmayı amaçlamaktadır. . Gereç ve Yöntemler: Çalışmaya alınan bireyler Maraş otu kullananlar (n=38), sigara içenler (n=38) ve her iki tütün grubunu da kullanmayan sağlıklı gönüllüler (n=38) olarak üç gruba ayrıldı. Tüm katılımcıların serum homosistein, PON-1, ARE ve Lp(a) düzeylerine bakıldı. Bulgular: Gruplar karşılaştırıldığında en yüksek homosistein düzeyi Maraş otu grubundaydı. Kontrol grubu ile Maraş otu grubu arasındaki fark istatistiksel olarak anlamlıyken, kontrol grubu ile sigara içen grup arasındaki fark istatistiksel olarak anlamsızdı. Hem Maraş otu hem de sigara içen grupta PON değerleri kontrol grubuna göre daha düşük olmasına rağmen, fark sadece sigara içen grupta anlamlıydı. Kontrol grubuna göre her iki tütün içen grupta ARE anlamlı olarak daha düşüktü ve Lp (a) anlamlı olarak daha yüksekti. Sonuç: Serum homosistein, PON-1, ARE ve Lp(a) düzeyi Maraş otu kullanımı ile ilişkilidir. Homosistein, Maraş otu kullananlarda kardiyovasküler hastalık için yararlı bir erken belirteç olabilir.

Keywords

• Maraş otu,
• homosistein
• paraoksonaz-1
• arilesteraz
• lipoprotein-a

The Effects of Smokeless Tobacco "Maras Powder" on Homocysteine and Cardiovascular Risk Parameters

Abstract

Objective: This study aims to investigate the relationship between smokeless tobacco (Maras powder) and cigarette consumption with homocysteine, Paraoxonase-1 (PON-1), Arylesterase (ARE), and Lipoprotein-a (Lp (a)), which are known as risk factors for cardiovascular diseases. Material and Methods: The individuals included in the study were divided into three groups as Maras powder users (n = 38), cigarette smokers (n = 38), and healthy volunteers who did not use either tobacco group (n = 38). Serum homocysteine, PON-1, ARE, and Lp (a) levels of all participants were examined. Results: When the groups are compared, the highest homocysteine level was in the Maras powder group. While the difference between the control group and the Maras powder group was statistically significant, the difference between the control and smokers groups was statistically insignificant. Although PON values were lower in both the Maras powder and smokers groups than the control group, the difference was significant only in the smoking group. ARE was significantly lower, and Lp (a) was significantly higher in both tobacco smokers groups compared to the control group. Conclusion: Serum homocysteine, PON-1, ARE, and Lp (a) level are associated with Maras powder use. Homocysteine may be a useful early marker for cardiovascular disease in those who use Maras powder.

Keywords

• Maras powder
• homocysteine
• Paraoxonase-1
• Arylesterase
• Lipoprotein-a

References

1. 1. Cullen D, Keithly L, Kane K, Land T, Paskowsky M, Chen L, et al. Smokeless tobacco products sold in Massachusetts from 2003 to 2012: trends and variations in brand availability, nicotine contents and design features. Tob Control 2015;24:256–262.
2. 2. Leon ME, Lugo A, Boffetta P, Gilmore A, Ross H, Schüz J, et al. Smokeless tobacco use in Sweden and other 17 European countries. Eur J Public Health 2016;26:817–821.
3. 3. Shaik SS, Doshi D, Bandari SR, Madupu PR, Kulkarni S. Tobacco Use Cessation and Prevention - A Review. J Clin Diagn Res 2016;10:ZE13–17.
4. 4. Alsanosy RM. Smokeless tobacco (shammah) in Saudi Arabia: a review of its pattern of use, prevalence, and potential role in oral cancer. Asian Pac J Cancer Prev 2014;15:6477–6483.
5. 5. Erenmemisoglu A, Ustun H, Kartal M. Carcinoma of buccal mucosa in smokeless tobacco users: a preliminary study of the use of cytology for early detection. Cytopathology 1995;6:403–408.
6. 6. Saitoh F, Noma M, Kawashima N. The alkaloid contents of sixty Nicotiana species. Phytochemistry 1985;24:477–480.
7. 7. World Health Organization. WHO report on the global tobacco epidemic, 2015: Raising taxes on tobacco—Appendix VII: Country profiles. Available at: https://www.who.int/tobacco/global_report/2015/en/. Accessed May 28, 2017.
8. 8. Sucaklı HM, Ozkan F, Inci MF, Celik M, Keten HS, Bozdoğan O. Effects of smokeless tobacco (Maras powder) use on carotid intima media thickness. Med Sci Monit 2013;19:859-864.

9. 9. Aral M, Ekerbicer HC, Celik M, Ciragil P, Gul M. Comparison of Effects of Smoking and Smokeless Tobacco “Maras Powder” Use on Humoral Immune System Parameters. Hindawi Publishing Corporation Mediators of Inflammation 2006;1–4.
10. 10. Mushtaq N, Beebe LA, Thompson DM, Skaggs VJ. Smokeless tobacco and prevalence of cardiovascular disease. J Okla State Med Assoc 2010;103:539-544.
11. 11. Hergens MP, Alfredsson L, Bolinder G, Lambe M, Pershagen G, Ye W. Long-term use of Swedish moist snuff and the risk of myocardial infarction amongst men. J Intern Med 2007;262:351-359.
12. 12. Teo KK, Ounpuu S, Hawken S, Pandey MR, Valantin V, Hunt D, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet 2006;368:647-658.
13. 13. Gupta R, Gupta S, Sharma S, Sinha DN, Mehrotra R. A systematic review on association between smokeless tobacco & cardiovascular diseases. Indian J Med Res 2018;148(1):77-89.
14. 14. Choudhary AK, Qudeer A. Smokeless tobacco: Risk factor for cardiovascular and breathing in young Indian adolescent. Hipertens Riesgo Vasc 2019;36(4):176-183.
15. 15. Ganguly P, Alam SF. Role of homocysteine in the development of cardiovascular disease. Nutrition Journal 2015;14:6.
16. 16. Süner A, Cabioğlu DE, Kaya H, Köroğlu S, Sökmen A, Sökmen G. Genç erişkinlerde dumansız tütün “Maraş otu” ve sigaranın aort esnekliği üzerine etkileri. Arch Turk Soc Cardiol 2014;42(8):741-746.
17. 17. Güven A, Köksal N, Büyükbefle MA, Çetinkaya A, Sökmen G, Aksu E, et al. Effects of Using a Different Kind of Smokeless Tobacco on Cardiac Parameters: "Marafl Powder". Anadolu Kardiyol Derg 2003;3(3):230-235.
18. 18. Chistiakov DA, Melnichenko AA, Orekhov AN, Bobryshev YV. Paraoxonase and atherosclerosis-related cardiovascular diseases. Biochimie 2017;132:19-27.
19. 19. Kotur-Stevuljević J, Vekić J, Stefanović A, Zeljković A, Ninić A, Ivanišević J, et al. araoxonase 1 and atherosclerosis-related diseases. Biofactors 2020;46(2):193-205.
20. 20. Kondo T, Nakano Y, Adachi S, Murohara T. Effects of Tobacco Smoking on Cardiovascular Disease. Circ J 2019;83(10):1980-1985.
21. 21. Saracen A. Cigarette Smoking and Respiratory System Diseases in Adolescents. Adv Exp Med Biol 2017;944:81-85.
22. 22. Qiu F, Liang CL, Liu H, Zeng YQ, Hou S, Huang S, et al. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down? Oncotarget 20173;8(1):268-284.
23. 23. Eren E, Ellidag HY, Aydin O, Yılmaz N. Homocysteine, Paraoxonase-1 and Vascular Endothelial Dysfunction. Journal of Clinical and Diagnostic Research 2014; 8(9):CE01-4.
24. 24. Lai W.K.C. Kan M.Y. Homocysteine-Induced Endothelial Dysfunction. Ann Nutr Metab 2015;67:1–12.
25. 25. Iqbal MP, Yakub M. Smokeless Tobacco Use: A Risk Factor for Hyperhomocysteinemia in a Pakistani Population. PLoS One 2013;8(12):e83826.
26. 26. Eren E, Yılmaz N, Aydin O. Functionally Defective High-Density Lipoprotein and Paraoxonase: A Couple for Endothelial Dysfunction in Atherosclerosis. Hindawi Publishing Corporation Cholesterol 2013;2013:792090.
27. 27. Horke S, Witte I, Wilgenbus P, Krüger M, Strand D, Förstermann U. Paraoxonase-2 Reduces Oxidative Stress in Vascular Cells and Decreases Endoplasmic Reticulum Stress–Induced Caspase Activation. Circulation 2007;115:2055-2064.
28. 28. Jakubowski H. Homocysteine is a protein amino acid in humans. Implications for homocysteine-linked disease. J Biol Chem 2002;277:30425–30428.
29. 29. Perla-Kaján J, Jakubowski H. Paraoxonase 1 protects against protein N-homocysteinylation in humans. FASEB J 2010;24(3):931–936.
30. 30. Isik B, Ceylan A, Isik R. Oxidative stress in smokers and non-smokers. Inhal Toxicol 2007;9:767–769.
31. 31. Senti M, Tomas M, Anglada R, Elosua R, Marrugat J, Covas MI, et al. Interrelationship of smoking, paraoxonase activity, and leisure time physical activity: a population based study. Eur J Intern Med 2003;14(3):178-184.
32. 32. Kurtul N, Söylemez S, Çelik M. Plasma paraoxonase and arylesterase activities in smokers and smokeless tobacco users as Maras powder. Inhal Toxicol 2014;26(4):235–239.
33. 33. Boerwinkle E, Leffert CC, Lin J, lackner C, Chiesa G, Hobbs HH. Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J Clin Invest 1992;90:52–60.
34. 34. Maranhão RC, Carvalho PO, Strunz CC, Pileggi F. Lipoprotein (a): Structure, Pathophysiology and Clinical Implications. Arq Bras Cardiol 2014;103(1):76-84.
35. 35. Saleheen D, Haycock PC, Zhao W, Rasheed A, Taleb A, Imran A, et al. Apolipoprotein(a) isoform size, lipoprotein(a) concentration, and coronary artery disease: a mendelian randomisation analysis. Lancet Diabetes Endocrinol 2017;5(7):524-533.
36. 36. Wang Z, Zhai X, Xue M, Cheng W, Hu H. Prognostic value of lipoprotein (a) level in patients with coronary artery disease: a meta-analysis. Lipids Health Dis 2019;18(1):150.
37. 37. Adunmo GO, Adesokan AA, Desalu OO, Biliaminu SA, Adunmo EO. Novel Cardiovascular Risk Markers in Nigerian Cigarette Smokers. Int J Appl Basic Med Res 2017;7(3):160-164.