Evaluation of Dynamic Disulphide/Thiol Homeostasis in Silica Exposed Workers

Year 2017, Volume: 34 Issue: 2, 102 - 107, 01.03.2017

Meşide Gündüzöz Ceylan Bal Murat Büyükşekerci Salim Neşelioğlu Türkan Nadir Öziş Servet İritaş Halil Kara Özcan Erel

Abstract

Background: Oxidative stress is implicated as one of the main molecular mechanism underlying silicosis. Aims: In this study, our aim was to asses the redox status in occupationally silica-exposed workers, by evaluating the dynamic thiol-disulphide homeostasis. Study Design: Case-control study. Methods: Thirty-six male workers occupationally exposed to silica particles and 30 healthy volunteers, working as office workers were included to the study. Posteroanterior chest radiographs and pulmonary function tests of both groups were evaluated. Also serum thiol disulphide levels were measured using the spectrophotometric method described by Erel and Neşelioğlu. Results: Among the 36 workers that underwent pulmonary function tests 6 (17%) had obstructive, 7 (19%) had restrictive, 6 (17%) had obstructive and restrictive signs whereas 17 (47%) had no signs. The mean PFTs results of silica-exposed workers were significantly lower than control subjects. The serum disulphide levels of silica-exposed workers were significantly higher than control subjects (23.84±5.89 μmol/L and 21.18±3.44 μmol/L, respectively p=0.02). Conclusion: The serum disulphide levels, a biomarker of oxidative stress, are found to be higher in silica-exposed workers.

Keywords

Disulphide, thiol, oxidative stress, silica, exposure

References

• 1. Mazurek JM, Schleiff PL, Wood JM, Hendricks SA, Weston A; Centers for Disease Control and Prevention (CDC). Notes from the Field: Update: Silicosis Mortality-United States, 1999–2013. MMWR. MMWR Morb Mortal Wkly Rep 2015;64:653-4.
• 2. Fubini B, Hubbard A. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by silica in inflammation and fibrosis. Free Radic Biol Med 2003;34:1507-16.
• 3. Rimal B, Greenberg AK, Rom WN. Basic pathogenetic mechanisms in silicosis: current understanding. Curr Opin Pulm Med 200511:169-73.
• 4. Mossman BT, Churg A. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med 1998;157:1666-80.
• 5. Robeldo R, Mossman B. Cellular and molecular mechanisms of asbestosinduced fibrosis. J Cell Physiol 1999;180:158-66.
• 6. Cheresh P, Kim SJ, Tulasiram S, Kamp DW. Oxidative stress and pulmonary fibrosis. Biochim Biophys Acta 2013;1832:1028-40.
• 7. Sato T, Takeno M, Honma K, Yamauchi H, Saito Y, Sasaki T, et al. Heme oxygenase-1. apotential biomarker of chronic silicosis. attenuates silicainduced lung injury. Am J Respir Crit Care Med 2006;174:906-14.
• 8. Shi XL, Dalal NS, Vallyathan V. ESR evidence for the hydroxyl radical formation in aqueous suspension of quartz particles and its possible significanceto lipid peroxidation in silicosis. J Toxicol Environ Health 1988;25:237-45.
• 9. Turell L, Radi R, Alvarez B. The thiol pool in human plasma: the central contribution of albumin to redox processes. Free Radic Biol Med 2013;65:244-53.
• 10. Jones DP, Liang Y. Measuring the poise of thiol/disulfide couples in vivo. Free Radic Biol Med 2009;47:1329-38.
• 11. International Labour Office (ILO). Guidelines for the use ofthe ILO International Classification of Radiographs of Pneumoconioses. Revised Edition. ILO occupational safety and health series. No. 22. Geneva: ILO; 2011.
• 12. Standardization of Spirometry, 1994 Update. American Thoracic Society. Am J Respir Crit Care Med 1995;152:1107-36.
• 13. Erel O, Neselioglu S. A novel and automated assay for thiol/disulphide homeostasis. Clin Biochem 2014;47:326-32.
• 14. Vallyathan V, Leonard S, Kuppusamy P, Pack D, Chzhan M, Sanders SP, et al. Oxidative stress in silicosis: evidence for the enhanced clearance of freeradicals from whole lungs. Mol Cell Biochem 1997;168:125-32.
• 15. Perez-Alonso A, Cordoba-Dona JA, Millares-Lorenzo JL, FigueroaMurillo E, Garcia-Vadillo C, Romero-Morillos J. Outbreak of silicosis in Spanish quartzconglomerate workers. Int J Occup Environ Health 2014;20:26-32.
• 16. Ergün D, Ergün R, Ozdemir C, Oziş TN, Yilmaz H, Akkurt I. Pneumoconiosis and respiratory problems in dental laboratory technicians: analysis of 893 dental technicians. Int J Occup Med Environ Health 2014;27:785-96.
• 17. Yoldas O, Karaca T, Bilgin BC, Yilmaz OH, Simsek GG, Alici IO, et al. Tamoxifen citrate: a glimmer of hope for silicosis. J Surg Res 2015;193:429- 34.
• 18. Vallyathan V, Mega JF, Shi X, Dalal NS. Enhanced generation of free radicalsfrom phagocytes induced by mineral dusts. Am J Respir Cell Mol Biol 1992;6:404-13.
• 19. Zhang Z, Shen HM, Zhang QF, Ong CN. Involvement of oxidative stress in crystalline silica-induced cytotoxicity and genotoxicity in rat alveolar macrophages. Environ Res 2000;82:245-52.
• 20. Vallyathan V, Castranova V, Pack D, Leonard S, Shumaker J, Hubbs AF, et al. Freshly fractured quartz inhalationleads to enhanced lung injury and inflammation. Potential role of free radicals. Am J Respir Crit Care Med 1995;152:1003-9.
• 21. Kaushik R, Khaliq F, Subramaneyaan M, Ahmed RS. Pulmonary dysfunctions. oxidative stress and DNA damage in brick kiln workers. Hum Exp Toxicol 2012;31:1083-91.
• 22. Villarini M, Moretti M, Fatigoni C, Agea E, Dominici L, Mattioli A, et al. Evaluation of primary DNA damage. cytogenetic biomarkers and genetic polymorphisms for CYP1A1 and GSTM1 in road tunnel construction workers. J Toxicol Environ Health A 2008;71:1430-9.
• 23. Wallaert B, Lassalle P, Fortin F, Aerts C, Bart F, Fournier E, et al. Superoxide anion generation by alveolar inflammatory cells in simple pneumoconiosis and in progressive massive fibrosis of nonsmoking coal workers. Am Rev Respir Dis 1990;141:129-33.
• 24. Palabiyik SS, Girgin G, Tutkun E, Yilmaz OH, Baydar T. Immunomodulation andoxidative stress in denim sandblasting workers: changes caused by silican exposure. Arh Hig Rada Toksikol 2013;64:431-7.
• 25. Orman A, Kahraman A, Cakar H, Ellidokuz H, Serteser M. Plasma malondialdehyde and erythrocyte glutathione levels in workers with cement dust-exposure [corrected]. Toxicology 2005;207:15-20.
• 26. Schafer F, Garry R. Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple. Free Radic Biol Med 2001;30:1191-212.
• 27. Jones DP. Redox potential of GSH/GSSG couple: assay and biological significance. Methods Enzymol 2002;348:93-112.
• 28. Sen CK, Packer L. Thiol homeostasis and supplements in physical exercise. Am J Clin Nutr 2000;72(2 Suppl):653S-69S.
• 29. Comini M. Measurement and meaning of cellular thiol: disulphide redox status. Free radical research just-accepted 2015;1-57.
• 30. Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010;48:749-62.
• 31. Kundi H, Ates I, Kiziltunc E, Cetin M, Cicekcioglu H, Neselioglu S, et al. A novel oxidative stress marker in acute myocardial infarction; thiol/ disulphide homeostasis. Am J Emerg Med 2015;33:1567-71.
• 32. Ates I, Kaplan M, Yuksel M, Mese D, Alisik M, Erel Ö, et al. Determination of thiol/disulphide homeostasis in type 1 diabetes mellitus and the factors associated with thiol oxidation. Endocrine 2016;51:47-51.
• 33. Bektas H, Vural G, Gumusyayla S, Deniz O, Alisik M, Erel O. Dynamic thiol-disulfide homeostasis in acute ischemic stroke patients. Acta Neurol Belg 2016;116:489-94.