ارزیابی مقایسه‌ای سطح ادراری آفلاتوکسین M1 در افراد مبتلا به Hepatitis C Virus (HCV) و افراد سالم

نوع مقاله : مقاله های پژوهشی

نویسندگان

1 دانشجوی کارشناسی ارشد، گروه قارچ‌شناسی و انگل‌شناسی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

2 استادیار، گروه قارچ‌شناسی و انگل‌شناسی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

3 استادیار، گروه داخلی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی شهرکرد، شهرکرد، ایران

4 دانشجوی دکتری، گروه مدیریت خدمات بهداشتی و درمانی، دانشگاه آزاد اسلامی، واحد علوم و تحقیقات تهران، تهران، ایران

5 دانشجوی کارشناسی پرستاری، دانشکده‌ی پرستاری، دانشگاه آزاد اسلامی، واحد شهرکرد، شهرکرد، ایران

چکیده

مقدمه: آفلاتوکسین‌ها، متابولیت ثانویه‌ی گونه‌های سکشن فلاوی (Aspergillus section flavi) می‌باشند. آفلاتوکسین B1، (AFB1 یا Aflatoxin B1) هپاتوکارسینوژن، تراتوژن و موتاژن است. آفلاتوکسین M1 (AFM1)، فرم هیدروکسیله شده‌ی AFB1 است. با توجه به اثرات تخریبی کبد در اثر هپاتیت و آفلاتوکسین، این مطالعه با هدف ارزیابی میزان میانگین سطح ادراری AFM1 در دو گروه افراد سالم (گروه شاهد) و مبتلایان به ویروس هپاتیت C (HCV یا Hepatitis C virus) (گروه مورد) انجام گرفت.روش‌ها: از 71 فرد مبتلا به HCV و 71 فرد سالم نمونه‌ی خون و ادرار گرفته شد. نمونه‌ی ادرار به روش Enzyme-linked immunosorbent assay (ELISA) از نظر میزان AFM1 مورد بررسی قرار گرفت. نمونه‌ی خون از نظر آنزیم‌های Serum glutamic-oxaloacetic transaminase (SGOT)، Serum glutamic-pyruvic transaminase (SGPT)، آلکالن فسفاتاز، بیلی‌روبین توتال و بیلی‌روبین دایرکت بررسی شد.یافته‌ها: 57/29 درصد از افراد گروه مورد و 57/19 درصد از افراد گروه شاهد در ادرار خود دارای AFM1 بودند. میانگین AFM1 افراد مبتلا به HCV، معادل 45/2 پیکوگرم بر میلی‌لیتر و میانگین AFM1 موجود در ادرار گروه شاهد 66/1 پیکوگرم بر میلی‌لیتر به دست آمد. نتایج به دست آمده از سطح AFM1 در دو گروه دارای تفاوت معنی‌داری بود (050/0 = P). غلظت سرمی SGPT و آلکالن فسفاتاز در افراد گروه مورد دارای AFM1 بیشتر از افراد فاقد AFM1 بود و این تفاوت غلظت معنی‌دار بود (012/0 = P). غلظت سرمی SGOT، بیلی‌روبین توتال و بیلی‌روبین مستقیم در دو گروه پیش‌گفته تفاوت معنی‌داری نداشت.نتیجه‌گیری: وجود AFB1 در مبتلایان به HCV ممکن است سبب تسریع پیشرفت بیماری مزمن کبدی گردد. از این رو، پیشنهاد می‌گردد با اصلاح الگوی مصرف مواد غذایی، از مصرف آفلاتوکسین‌ها جلوگیری گردد و در نتیجه، از سرعت پیشرفت فرم مزمن بیماری کاسته شود.

کلیدواژه‌ها

عنوان مقاله [English]

Comparative Study of the Urinary Level of Aflatoxin M1 in Patients with Hepatitis C Virus (HCV) and Healthy People

نویسندگان [English]

  • Amin Soltanpour 1
  • Parvin Dehghan 2
  • Mohammad Hadi Shafigh-Ardestani 3
  • Abbasali Asgari 4
  • Sahar Soltanpour 5
1 MSc Student, Department of Mycology and Parasitology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
2 Assistant Professor, Department of Mycology and Parasitology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
3 Assistant Professor, Department of Internal Medicine, School of Medicine, Shahrekord University of Medical Sciences, Shahrekord, Iran
4 PhD Student, Department of Health Service Management, Science and Research Branch, Islamic Azad University, Tehran, Iran
5 Student, Department of Nursing, School of Nursing, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
چکیده [English]

B1 (AFB1) is hepatocarcinogen, teratogen and mutagen. Aflatoxin M1 (AFM1) is the hydroxylated metabolite of AFB1. The liver protects the body by lowering the toxicity of AFB1 to form different hydroxylates like AFM1. According to the synergistic effect of hepatitis and also AFB1 as the parent molecule of AFM1, the main purpose of this study was to assess the relationship between the mean levels of AFM1, in the hepatitis-C-virus (HCV)-positive patients compared to healthy individuals.Methods: After the tests of liver function enzymes, the level of AFM1 was measured and compared in the urine sample of 71 patients with HCV and 71 healthy individuals. The AFM1 of urine samples were tested using enzyme-linked immunosorbent assay (ELISA) method. Besides, the levels of serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), alkaline phosphatase, total bilirubin and direct bilirubin were assessed in the blood samples.Findings: The urine of 29.7% of HCV-positive patients and 19.71% of healthy individuals consisted of some amount of AFM1. The mean level of AFM1 was 2.45 and 1.66 pg/ml in patients and controls, respectively; which was significantly different (P = 0.005). The mean levels of SGPT and alkaline phosphatase were significantly more among HCV-positive patients with AFM1 compared to those without AFM1 (P = 0.012). But, there was not any significant difference between the mean levels of SGOT and total and direct bilirubin between the HCV-positive patients with and without AFM1.Conclusion: The mean levels of SGPT and Alkaline phosphatase, which are more exclusive to survey of liver function, were significantly different between HCV-positive patients with and without AFM1. Consequently, progression of the chronic liver disease is caused by the existence of AFB1 in HCV-positive patients; therefore, the reduction of AFM1 via improving the food consumption pattern can prevent this progression.

کلیدواژه‌ها [English]

  • Aflatoxin M1
  • Hepatitis C virus (HCV)
  • Liver dysfunctions

مراجع

  1. Samson RA, Hoekstra ES, Frisvad JC, Filtenborg O. Introduction to food-borne fungi. Utrecht, Netherlands: Centraalbureau voor Schimmelcultures; 1995.
  2. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Some traditional herbal medicines, some mycotoxins, naphthalene and styrene. IARC Monogr Eval Carcinog Risks Hum 2002; 82: 1-556.
  3. Kew MC. Aflatoxins as a cause of hepatocellular carcinoma. J Gastrointestin Liver Dis 2013; 22(3): 305-10.
  4. Strosnider H, Azziz-Baumgartner E, Banziger M, Bhat RV, Breiman R, Brune MN, et al. Workgroup report: public health strategies for reducing aflatoxin exposure in developing countries. Environ Health Perspect 2006; 114(12): 1898-903.
  5. Ricordy R, Cacci E, ugusti-Tocco G. Aflatoxin B 1 and Cell cycle perturbation. In: Preedy VR, Watson RR, editors. Reviews in food and nutrition toxicity. Boca Raton, FL: CRC Press; 2005.
  6. Wild CP, Hasegawa R, Barraud L, Chutimataewin S, Chapot B, Ito N, et al. Aflatoxin-albumin adducts: a basis for comparative carcinogenesis between animals and humans. Cancer Epidemiol Biomarkers Prev 1996; 5(3): 179-89.
  7. Kensler TW, Qian GS, Chen JG, Groopman JD. Translational strategies for cancer prevention in liver. Nat Rev Cancer 2003; 3(5): 321-9.
  8. Wild CP, Gong YY. Mycotoxins and human disease: a largely ignored global health issue. Carcinogenesis 2010; 31(1): 71-82.
  9. Coulombe RA, Jr., Sharma RP. Clearance and excretion of intratracheally and orally administered aflatoxin B1 in the rat. Food Chem Toxicol 1985; 23(9): 827-30.
  10. Mykkanen H, Zhu H, Salminen E, Juvonen RO, Ling W, Ma J, et al. Fecal and urinary excretion of aflatoxin B1 metabolites (AFQ1, AFM1 and AFB-N7-guanine) in young Chinese males. Int J Cancer 2005; 115(6): 879-84.
  11. Wilson R, Ziprin R, Ragsdale S, Busbee D. Uptake and vascular transport of ingested aflatoxin. Toxicol Lett 1985; 29(2-3): 169-76.
  12. Wogan GN, Edwards GS, Shank RC. Excretion and tissue distribution of radioactivity from aflatoxin B1-14-C in rats. Cancer Res 1967; 27(10): 1729-36.
  13. Essigmann JM, Croy RG, Bennett RA, Wogan GN. Metabolic activation of aflatoxin B1: patterns of DNA adduct formation, removal, and excretion in relation to carcinogenesis. Drug Metab Rev 1982; 13(4): 581-602.
  14. Forrester LM, Neal GE, Judah DJ, Glancey MJ, Wolf CR. Evidence for involvement of multiple forms of cytochrome P-450 in aflatoxin B1 metabolism in human liver. Proc Natl Acad Sci USA 1990; 87(21): 8306-10.
  15. Foster PL, Eisenstadt E, Miller JH. Base substitution mutations induced by metabolically activated aflatoxin B1. Proc Natl Acad Sci USA 1983; 80(9): 2695-8.
  16. Jeannot E, Boorman GA, Kosyk O, Bradford BU, Shymoniak S, Tumurbaatar B, et al. Increased incidence of aflatoxin B1-induced liver tumors in hepatitis virus C transgenic mice. Int J Cancer 2012; 130(6): 1347-56.
  17. El-Shahat EA, Swelim MA, Mohamed AF, Abdel-Wahhab MA. correlation study between aflatoxin M1 and hepatitis C virus in Egyptian patients with chronic liver disease. World J Med Sci 2012; 7(4): 224-31.
  18. Hnatyszyn HJ. Chronic hepatitis C and genotyping: the clinical significance of determining HCV genotypes. Antivir Ther 2005; 10(1): 1-11.
  19. Sharma SD. Hepatitis C virus: molecular biology and current therapeutic options. Indian J Med Res 2010; 131: 17-34.
  20. Nguyen MH, Keeffe EB. Prevalence and treatment of hepatitis C virus genotypes 4, 5, and 6. Clin Gastroenterol Hepatol 2005; 3(10 Suppl 2): S97-S101.
  21. Shepard CW, Finelli L, Alter MJ. Global epidemiology of hepatitis C virus infection. Lancet Infect Dis 2005; 5(9): 558-67.
  22. Alavian Sm, Adibi P, Zali Mr. Hepatitis C virus in Iran: epidemiology of an emerging infection. Arch Iran Med 2005; 8(2): 84-90.
  23. Njei B, Rotman Y, Ditah I, Lim JK. Emerging trends in hepatocellular carcinoma incidence and mortality. Hepatology 2015; 61(1): 191-9.
  24. El-Serag HB. Epidemiology of viral hepatitis and hepatocellular carcinoma. Gastroenterology 2012; 142(6): 1264-73.
  25. Altekruse SF, McGlynn KA, Reichman ME. Hepatocellular carcinoma incidence, mortality, and survival trends in the United States from 1975 to 2005. J Clin Oncol 2009; 27(9): 1485-91.
  26. Jepsen P, Vilstrup H, Tarone RE, Friis S, Sorensen HT. Incidence rates of hepatocellular carcinoma in the U.S. and Denmark: recent trends. Int J Cancer 2007; 121(7): 1624-6.
  27. London WT, Evans AA, McGlynn K, Buetow K, An P, Gao L, et al. Viral, host and environmental risk factors for hepatocellular carcinoma: a prospective study in Haimen City, China. Intervirology 1995; 38(3-4): 155-61.
  28. Abdel-Wahab M, Mostafa M, Sabry M, el-Farrash M, Yousef T. Aflatoxins as a risk factor for hepatocellular carcinoma in Egypt, Mansoura Gastroenterology Center study. Hepatogastroenterology 2008; 55(86-87): 1754-9.
  29. Chen CH, Wang MH, Wang JH, Hung CH, Hu TH, Lee SC, et al. Aflatoxin exposure and hepatitis C virus in advanced liver disease in a hepatitis C virus endemic area in Taiwan. Am J Trop Med Hyg 2007; 77(4): 747-52.
  30. Williams JH, Phillips TD, Jolly PE, Stiles JK, Jolly CM, Aggarwal D. Human aflatoxicosis in developing countries: a review of toxicology, exposure, potential health consequences, and interventions. Am J Clin Nutr 2004; 80(5): 1106-22.
  31. Khoshpey B, Farhud D, Zaini F. Aflatoxins in Iran: nature, hazards and carcinogenicity. Iran J Public Health 2011; 40(4): 1-30.
  32. Institute of Standards and Industrial Research of Iran (ISIRI). Food and feed-mycotoxins: maximum tolerated level (ISIRI 5925). Tehran, Iran: ISIRI; 2001. p. 3-20. [In Persian].
  33. Vandercamme G. New EU aflatoxin levels and sampling plan. Gain report number: E50018 [Online]. [cited 2010 Sep 3]; Available from: URL: http://gain.fas.usda.gov/Recent%20GAIN%20Publications/New%20EU%20Aflatoxin%20Levels%20and%20Sampling%20Plan_Brussels%20USEU_EU-27_3-9-2010.pdf
  34. Mason S, Hajimohammadi B, Ehrampoush M, Khabiri F, Soltani M. A survey on relationship between diet and urinary excretion of aflatoxin M1: a screening pilot study on Iranian population. J Food Qual Hazards Control 2015; 2(2): 66-70.
  35. Lereau M, Gouas D, Villar S, Besaratinia A, Hautefeuille A, Berthillon P, et al. Interactions between hepatitis B virus and aflatoxin B(1): effects on p53 induction in HepaRG cells. J Gen Virol 2012; 93(Pt 3): 640-50.
  36. Wild CP, Montesano R. A model of interaction: aflatoxins and hepatitis viruses in liver cancer aetiology and prevention. Cancer Lett 2009; 286(1): 22-8.
  37. Sun Z, Lu P, Gail MH, Pee D, Zhang Q, Ming L, et al. Increased risk of hepatocellular carcinoma in male hepatitis B surface antigen carriers with chronic hepatitis who have detectable urinary aflatoxin metabolite M1. Hepatology 1999; 30(2): 379-83.
مجله دانشکده پزشکی اصفهان
دوره 34، شماره 404 - شماره پیاپی 404
آذر و دی 1395
صفحه 1275-1281

فایل ها

سابقه مقاله

  • تاریخ دریافت: 01 شهریور 1395
  • تاریخ بازنگری: 01 اردیبهشت 1403
  • تاریخ پذیرش: 17 فروردین 1401

هم رسانی

ارجاع به این مقاله

آمار