Assessing risks of functional disorders of hepatobiliary system in workers employed at butyl rubber production allowing for analysis of the ogg1 gene polymorphic variant rs1052133

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PDF icon health-risk-analysis-2022-4-17.pdf
UDC: 
616.36-008.6:612.6.05
DOI: 
10.21668/health.risk/2022.4.17.eng
Authors: 

E.R. Kudoyarov1, D.O. Karimov1, A.B. Bakirov1,2, G.F. Mukhammadieva1, L.K. Karimova1, R.R. Galimova1,2

Organization: 

1Ufa Research Institute of Occupational Health and Human Ecology, 94 Stepana Kuvykina Str., Ufa, 450106, Russian Federation
2Bashkir State Medical University, 3 Lenina Str., Ufa, 450008, Russian Federation

Abstract: 

Contemporary petrochemical productions maintain strict control over contents of adverse chemicals in workplace air. Despite that, the chemical factor remains one of the major harmful occupational factors and can produce adverse effects on workers’ health by increasing, among other things, risks of general somatic diseases. Given that, prevention of chronic non-communicable diseases in workers employed at chemical productions remains a vital challenge for occupational medicine. A way to tackle it is to timely detect risk groups relying on, among other things, analysis of workers’ genetic peculiarities.
This article presents a study with 140 volunteers participating in it; they had basic occupations required at contemporary butyl rubber production. It was conducted within a periodical medical examination that involved using up-to-date hygienic, clinical-laboratory and genetic methods. The study included hygienic assessment of the chemical factor at the analyzed production, examination of hematologic and biochemical blood indicators, identification of workers’ genetic status as per the rs1052133 polymorphic variant of the OGG1 gene and the severity of DNA breaks.
The study revealed adverse effects produced by the chemical factors on health of workers with basic occupations based on deviations in biochemical blood indicators obtained by tests that included indicator enzyme identification, and DNA damage. Following the study results, a risk group was created as per the state of the hepatobiliary system. To preserve workers’ health, it is necessary to implement certain preventive measures that include providing safe working conditions as regards the chemical factor, timely detection of risk groups and rehabilitation activities.

Keywords: 
health, workers, blood, liver, polymorphic variant, OGG1 gene, DNA breaks, preventive medicine
Kudoyarov E.R., Karimov D.O., Bakirov A.B., Mukhammadieva G.F., Karimova L.K., Galimova R.R. Assessing risks of functional disorders of hepatobiliary system in workers employed at butyl rubber production allowing for analysis of the OGG1 gene polymorphic variant rs1052133. Health Risk Analysis, 2022, no. 4, pp. 177–185. DOI: 10.21668/health.risk/2022.4.17.eng
References: 
  1. Weber L.W.D., Boll M., Stampfl A. Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model. Crit. Rev. Toxicol., 2003, vol. 33, no. 2, pp. 105–136. DOI: 10.1080/713611034
  2. Döring B., Petzinger E. Phase 0 and phase III transport in various organs: combined concept of phases in xenobiotic transport and metabolism. Drug Metab. Rev., 2014, vol. 46, no. 3, pp. 261–282. DOI: 10.3109/03602532.2014.882353
  3. Reif R. Ghallab A., Beattie L., Günther G., Kuepfer L., Kaye P.M., Hengstler J.G. In vivo imaging of systemic transport and elimination of xenobiotics and endogenous molecules in mice. Arch. Toxicol., 2017, vol. 91, no. 3, pp. 1335–1352. DOI: 10.1007/s00204-016-1906-5
  4. Xu C., Li C.Y.-T., Kong A.-N.T. Induction of phase I, II and III drug metabolism/transport by xenobiotics. Arch. Pharm. Res., 2005, vol. 28, no. 3, pp. 249–268. DOI: 10.1007/BF02977789
  5. Myshkin V.A., Bakirov A.B. Okislitel'nyi stress i povrezhdenie pecheni pri khimicheskikh vozdeistviyakh [Oxidative stress and liver damage from chemical exposures]. Ufa, Mir pechati, 2010, 176 p. (in Russian).
  6. Khavinson V.Kh., Barinov V.A., Arutyunyan A.V., Malinin V.V. Svobodnoradikal'noe okislenie i starenie [Free radical oxidation and aging]. St. Petersburg, Nauka, 2003, 327 p. (in Russian).
  7. Galimova R.R., Valeeva E.T., Timasheva G.V., Bakirov A.B., Selezneva L.I., Karimova L.K., Karamova L.M. Kliniko-biokhimicheskie i geneticheskie markery toksicheskogo porazheniya pecheni na proizvodstvakh neftekhimii [Clinical, biochemical and genetic markers of toxic liver damage in petrochemical industries]. Ufa, FBUN Ufimskii NII meditsiny truda i ekologii cheloveka Publ., 2012, 35 p. (in Russian).
  8. Joshi-Barve S., Kirpich I., Cave M.C., Marsano L.S., McClain C.J. Alcoholic, nonalcoholic, and toxicant-associated steatohepatitis: mechanistic similarities and differences. Cell. Mol. Gastroenterol. Hepatol., 2015, vol. 1, no. 4, pp. 356–367. DOI: 10.1016/j.jcmgh.2015.05.006
  9. Browning J.D., Horton J.D. Molecular mediators of hepatic steatosis and liver injury. J. Clin. Invest., 2004, vol. 114, no. 2, pp. 147–152. DOI: 10.1172/JCI22422
  10. Alison M.R. Liver stem cells: implications for hepatocarcinogenesis. Stem Cell Rev., 2005, vol. 1, no. 3, pp. 253–260. DOI: 10.1385/SCR:1:3:253
  11. Idilman I.S., Ozdeniz I., Karcaaltincaba M. Hepatic steatosis: etiology, patterns, and quantification. Semin. Ultrasound CT MR, 2016, vol. 37, no. 6, pp. 501–510. DOI: 10.1053/j.sult.2016.08.003
  12. Mezale D., Strumfa I., Vanags A., Mezals M., Fridrihsone I., Strumfs B., Balodis D. Non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma: The molecular pathways. Liver Cirrhosis – Update and Current Challenges. In: G. Tsoulfas ed. London, InTech, 2017, pp. 1–35. DOI: 10.5772/intechopen.68771
  13. Rolo A.P., Oliveira P.J., Moreno A.J., Palmeira C.M. Bile acids affect liver mitochondrial bioenergetics: possible relevance for cholestasis therapy. Toxicol. Sci., 2000, vol. 57, no. 1, pp. 177–185. DOI: 10.1093/toxsci/57.1.177
  14. Caro A.A., Cederbaum A.I. Oxidative stress, toxicology and pharmacology of CYP2E1. Annu. Rev. Pharmacol. Toxicol., 2004, vol. 44, no. 1, pp. 27–42. DOI: 10.1146/annurev.pharmtox.44.101802.121704
  15. McGillicuddy F.C., de la Llera Moya M., Hinkle C.C., Joshi M.R., Chiquoine E.H., Billheimer J.T., Rothblat G.H., Reilly M.P. Inflammation impairs reverse cholesterol transport in vivo. Circulation, 2009, vol. 119, no. 8, pp. 1135–1145. DOI: 10.1161/CIRCULATIONAHA.108.810721
  16. Colombo C., Battezzati P.M., Strazzabosco M., Podda M. Liver and biliary problems in cystic fibrosis. Semin. Liver Dis., 1998, vol. 18, no. 3, pp. 227–235. DOI: 10.1055/s-2007-1007159
  17. Pérez Fernández T., López Serrano P., Tomás E., Gutiérrez M.L., Lledó J.L., Cacho G., Santander C., Fernández Rodríguez C.M. Diagnostic and therapeutic approach to cholestatic liver disease. Rev. Esp. Enferm. Dig., 2004, vol. 96, no. 1, pp. 60–73. DOI: 10.4321/s1130-01082004000100008
  18. Reshetnyak V.I. Primary biliary cirrhosis: Clinical and laboratory criteria for its diagnosis. World J. Gastroenterol., 2015, vol. 21, no. 25, pp. 7683–7708. DOI: 10.3748/wjg.v21.i25.7683
  19. Jansen P.L.M., Ghallab A., Vartak N., Reif R., Schaap F.G., Hampe J., Hengstler J.G. The ascending pathophysiology of cholestatic liver disease. Hepatology, 2017, vol. 65, no. 2, pp. 722–738. DOI: 10.1002/hep.28965
  20. Henkel R.R., Solomon M.C. Chapter 1.5 – Leucocytes as a cause of oxidative stress. Oхydants, antioxydants and impact of the oxidative status in male reproduction. In: R. Henkel, L. Samanta, A. Agarwal eds. London, Elsevier, Academic Press, 2019, pp. 37–44. DOI: 10.1016/B978-0-12-812501-4.00005-5
  21. Valverde M., Rojas E. Chapter 11. Comet assay in human biomonitoring. The Comet Assay in Toxicology, 2017, vol. 30, pp. 264–313. DOI: 10.1039/9781782622895-00264
  22. Somorovská M., Szabová E., Vodička P., Tulinská J., Barančoková M., Fábry R., Lísková A., Riegerová Z. [et al.]. Biomonitoring of genotoxic risk in workers in a rubber factory: Comparison of the Comet assay with cytogenetic methods and immunology. Mutat. Res., 1999, vol. 445, no. 2, pp. 181–192. DOI: 10.1016/s1383-5718(99)00125-4
  23. Kumar A.K., Balachandar V., Arun M., Ahamed S.A.K.M., Kumar S.S., Balamuralikrishnan B., Sankar K., Sasikala K. A comprehensive analysis of plausible genotoxic covariates among workers of a polyvinyl chloride plant exposed to vinyl chloride monomer. Arch. Environ. Contam. Toxicol., 2013, vol. 64, no. 4, pp. 652–658. DOI: 10.1007/s00244-012-9857-1
  24. Boiteux S., Radicella J.P. The human OGG1 gene: structure, functions, and its implication in the process of car-cinogenesis. Arch. Biochem. Biophys., 2000, vol. 377, no. 1, pp. 1–8. DOI: 10.1006/abbi.2000.1773
  25. Mahmoud A.A., Hassan M.H., Ghweil A.A., Abdelrahman A., Mohammad A.N., Ameen H.H. Urinary 8-hydroxy-deoxyguanosine in relation to XRCC1 rs25487 G/A (Arg399Gln) and OGG1 rs1052133 C/G (Ser326Cys) DNA repair genes polymorphisms in patients with chronic hepatitis C and related hepatocellular carcinoma. Cancer Manag. Res., 2019, vol. 11, pp. 5343–5351. DOI: 10.2147/CMAR.S209112
  26. Sampath H., Lloyd R.S. Roles of OGG1 in transcriptional regulation and maintenance of metabolic homeostasis. DNA Repair, 2019, vol. 81, pp. 102667. DOI: 10.1016/j.dnarep.2019.102667
  27. Guo J., Yang J., Li Y. Association of hOGG1 Ser326Cys polymorphism with susceptibility to hepatocellular car-cinoma. Int. J. Clin. Exp. Med., 2015, vol. 8, no. 6, pp. 8977–8985.
  28. Zou H., Li Q., Xia W., Liu Y., Wei X., Wang D. Association between the OGG1 Ser326Cys polymorphism and cancer risk: Evidence from 152 case-control studies. J. Cancer, 2016, vol. 7, no. 10, pp. 1273–1280. DOI: 10.7150/jca.15035
  29. Hill J.W., Evans M.K. Dimerization and opposite base-dependent catalytic impairment of polymorphic S326C OGG1 glycosylase. Nucleic Acids Res., 2006, vol. 34, no. 5, pp. 1620–1632. DOI: 10.1093/nar/gkl060
  30. Kotnis A., Namkung J., Kannan S., Jayakrupakar N., Park T., Sarin R., Mulherkar R. Multiple pathway-based genetic variations associated with tobacco related multiple primary neoplasms. PLoS One, 2012, vol. 7, no. 1, pp. e30013. DOI: 10.1371/journal.pone.0030013
  31. Milić M., Ceppi M., Bruzzone M., Azqueta A., Brunborg G., Godschalk R., Koppen G., Langie S. [et al.]. The hCOMET project: International database comparison of results with the comet assay in human biomonitoring. Baseline frequency of DNA damage and effect of main confounders. Mutat. Res. Rev. Mutat. Res., 2021, vol. 787, pp. 108371. DOI: 10.1016/j.mrrev.2021.108371
Received: 
26.09.2022
Approved: 
08.12.2022
Accepted for publication: 
18.12.2022

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