Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1
5-Year Impact Factor – 2.2
Scopus CiteScore – 3.4 (CiteScore Tracker 3.4)
Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2014, vol. 23, nr 1, January-February, p. 49–55

Publication type: original article

Language: English

Arylestarase and Oxidative Stress in Operating Room Personnel

Neset Cerit1,A, Asuman Arslan Onuk1,B, Hamit Yasar Ellidag2,C,D, Esin Eren3,E, Nurullah Bulbuller4,E, Necat Yilmaz2,F

1 Anesthesia Clinic of the Antalya Education and Research Hospital of the Ministry of Health, Antalya, Turkey

2 Central Laboratories of the Antalya Education and Research Hospital of the Ministry of Health, Antalya, Turkey

3 Antalya Public Health Center of the Ministry of Health, Antalya, Turkey

4 General Surgery Clinic of the Antalya Education and Research Hospital of the Ministry of Health, Antalya, Turkey

Abstract

Background. Long-term occupational exposure to trace concentrations of volatile anesthetics is known to have adverse effects on the health of exposed personnel.
Objectives. We investigated paraoxonase-1 (PON1) and arylesterase (ARE), as well as antioxidant status (TAS) and total oxidant status (TOS) levels in anesthesia personnel (AP) who were chronically exposed to inhalation anesthetics, and compared them with levels in a control group.
Material and Methods. We designed a comparative prospective study with 50 female subjects. The first cohort included 25 full-time female workers in operating rooms in two locations in the Antalya Education and Research Hospital in Antalya, Turkey. The control group was comprised of 25 female individuals working in the same hospitals without any work-related exposure to hazardous agents.
Results. Serum ARE activity and TAS levels were significantly reduced (p = 0.04 and p < 0.0001, respectively), whereas TOS and OSI levels were found to be significantly higher (p = 0.01 and p < 0.0001, respectively) in AP. However, there were no significant differences in PON1 activity, PON1/HDL-C, ARE/HDL-C, and PON1/ /ARE (p = 0.30, p = 0.5, p = 0.1 and p = 0.7, respectively) when the two groups were contrasted.
Conclusion. According to the results of this study, depending on the putative role of PON/ARE in oxidant stress-related diseases, particularly atherosclerosis and cancer, AP might be considered a risk group for the development of atherosclerosis and many other diseases.

Key words

anesthesia personnel, paraoxonase, arylesterase, oxidative stress, operating room.

References (35)

  1. Vessey MP: Epidemiological studies of the occupational hazards of anaesthesia—a review. Anaesthesia 1978, 33, 430–438.
  2. Türkan H, Aydin A, Sayal A: Effect of volatile anesthetics on oxidative stress due to occupational exposure. World J Surg 2005, 29, 540–542.
  3. Cohen EN, Gift HC, Brown BW, Greenfield W, Wu ML, Jones TW, Whitcher CE, Driscoll EJ, Brodsky JB: Occupational disease in dentistry and chronic exposure to trace anesthetic gases. J Am Dent Assoc 1980, 101, 21–31.
  4. Venables H, Cherry N, Waldron HA, Buck L, Edling C,Wilson HK: Effects of trace levels of nitrous oxide on psychomotor performance. Scand J Work Environ Health 1983, 9, 391–396.
  5. Plummer JL, Beckwith AL, Bastin FN, Adams JF, Cousins MJ, Hall P: Free radical formation in vivo and hepatotoxicity due to anesthesia with halothane. Anesthesiology 1982, 57, 160–166.
  6. Malekirad AA, Ranjbar A, Rahzani K, Kadkhodaee M, Rezaie A, Taghavi B, Abdollahi M: Oxidative stress in operating room personnel: occupational exposure to anesthetic gases. Hum Exp Toxicol 2005, 24, 597–601.
  7. Yılmaz N: Relationship between paraoxonase and homocystein: crossroads of oxidative disease. Arch Med Sci 2012, 8, 138–153.
  8. Mackness MI, Arrol S, Durrington PN: Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Letters 1991, 286, 152–154.
  9. Mackness MI, Durrington PN, Mackness B: How high-density lipoprotein protects against the effects of lipid peroxidation. Cur Opin Lipidol 2000, 11, 383–388.
  10. Ahmed Z, Ravandi A, Maguire GF, Emili A, Draganov D, La Du BN, Kuksis A, Connelly PW: Apolipoprotein A-I promotes the formation of phosphatidylcholine core aldehydes that are hydrolyzed by paraoxonase (PON-1) during high density lipoprotein oxidation with a peroxynitrite donor. J Biol Chem 2001, 276, 24473–24481.
  11. Valko M, Rhodes CJ, Moncola J, Izakovic M, Mazura M: Free radicals, metals and antioxidants in oxidative stress-induced cancer. Mini-review. Chemico-Biological Interactions 2006, 160, 1–40.
  12. Eckerson HW, Wyte MC, La Du BN: The human serum paraoxonase/arylesterase polymorphism. Am J Hum Genet 1983, 35, 1126–1138.
  13. Haagen L, Brock A: A new automated method for phenotyping arylesterase (E.C.3.1.1.2.) based upon inhibition of enzymatic hydrolisis of 4-nitrophenyl acetate. Eur J Clin Chem Clin Biochem 1992, 30, 391–395.
  14. Erel O: A novel automated direct measurement method for total antioxidant capacity using a new generationmore stable ABTS radical cation. Clin Biochem 2004, 37, 277–285.
  15. Erel O: A new automated colorimetric method for measuring total oxidant status. Clin Biochem 2005, 38, 1103–1111.
  16. Harma M, Harma M, Erel O: Increased oxidative stress in patients with hydatidiform mole. Swiss MedWkly 2003, 133, 563–566.
  17. Chandrasekhar M, Rekhadevi PV, Sailaja N, Rahman MF, Reddy JP, Mahboob M, Grover P: Evaluation of genetic damage in operating room personnel exposed to anaesthetic gases. Mutagenesis 2006, 21, 249–254.
  18. Peric M, Vranes Z, Marusic M: Immunological disturbances in anaesthetic personnel chronically exposed to high occupational concentrations of nitrous oxide and halothane. Anaesthesia 1991, 46, 531–537.
  19. Wrońska-Nofer T, Nofer JR, Jajte J, Dziubałtowska E, Szymczak W, Krajewski W, Wąsowicz W, Rydzyński K: Oxidative DNA damage and oxidative stress in subjects occupationally exposed to nitrous oxide (N(2)O). Mutat Res 2012, 731, 58–63.
  20. Baysal Z, Cengiz M, Ozgonul A, Cakir M, Celik H, Kocyigit A: Oxidative status and DNA damage in operating room personel. Clin Biochem 2009, 42, 189–193.
  21. Sinclair AJ, Barnett AH, Lunec J: Free radicals and antioxidant systems in health and disease. Br J Hosp Med 1990, 43, 334–344.
  22. Andreoli TE: Free radicals and oxidative stress. Am J Med 2000, 108, 650–651.
  23. Kudou M, Kudou T, Matsuki A: Changes of plasma superoxide dismutase like activity during general anesthesia and surgery in man. Masui 1990, 39, 1172–1177.
  24. Durackova Z: Some current insights into oxidative stress. Physiol Res 2010, 59, 459–469.
  25. Schraufstatter I, Hyslop PA, Jackson JH, Cochrane CG: Oxidant-induced DNA damage of target cells. J Clin Invest 1988, 82, 1040–1050.
  26. Crawford A, Fassett RG, Geraghty DP, Kunde DA, Ball MJ, Robertson IK, Coombes JS: Relationships between single nucleotide polymorphisms of antioxidant enzymes and disease. Gene 2012, 501, 89–103.
  27. Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La Du BN: Paraoxonase inhibits highdensity lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest 1998, 101, 1581–1590.
  28. Li HL, Liu DP, Liang CC: Paraoxonase gene polymorphisms, oxidative stress, and diseases. J Mol Med 2003, 81, 766–779.
  29. Gan KN, Smolen A, Eckerson HW, La Du BN: Purification of human serum paraoxonase/arylesterase. Evidence for one esterase catalyzing both activities. Drug Metab Dispos 1991, 19, 100–106.
  30. Rosenblat M, Gaidukov L, Khersonsky O, Vaya J, Oren R, Tawfik DS, Aviram M: The catalytic histidine dyad of high density lipoprotein-associated serum paraoxonase-1 (PON1) is essential for PON1-mediated inhibition of low density lipoprotein oxidation and stimulation of macrophage cholesterol efflux. J Biol Chem 2006, 281, 7657–7665.
  31. Otocka-Kmiecik A, Orłowska-Majdak M: The role of genetic (PON1 polymorphism) and environmental factors, especially physical activity, in antioxidant function of paraoxonase. Post Hig Med Dosw 2009, 63, 668–677.
  32. Tang WH, Hartiala J, Fan Y, Wu Y, Stewart AF, Erdmann J, Kathiresan S; CARDIoGRAM Consortium, Roberts R, McPherson R, Allayee H, Hazen SL: Clinical and genetic association of serum paraoxonase and arylesterase activities with cardiovascular risk. Arterioscler Thromb Vasc Biol 2012, 32, 2803–2812.
  33. Kruth HS: Lipoprotein cholesterol and atherosclerosis. Curr Mol Med 2001, 1, 633–653.
  34. Berlier JA, Navab M, Fogelman AM, Frank JS, Demer LL, Edwards PA, Watson AD, Lusis AJ: Atherosclerosis: basic mechanism, oxidation, inflammation, genetics. Circulation 1995, 91, 2488–2496.
  35. Eren E, Aydın O, Yilmaz N: High Density Lipoprotein and it’s Dysfunction The Open Biochemistry Journal 2012, 6, 1–10.