Exp Clin Endocrinol Diabetes 2007; 115(8): 522-526
DOI: 10.1055/s-2007-981457
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG · Stuttgart · New York

Oxidative Stress and Enzymatic Antioxidant Status in Patients with Hypothyroidism before and after Treatment

G. Baskol 1 , H. Atmaca 2 , F. Tanrıverdi 2 , M. Baskol 3 , D. Kocer 1 , F. Bayram 2
  • 1Department of Biochemistry and Clinical Biochemistry, Erciyes University Faculty of Medicine, Kayseri, Turkey
  • 2Department of Endocrinology, Erciyes University Faculty of Medicine, Kayseri, Turkey
  • 3Department of Internal Medicine, Erciyes University Faculty of Medicine, Kayseri, Turkey
Further Information

Publication History

received 18. 01. 2007 first decision 23. 03. 2007

accepted 02. 05. 2007

Publication Date:
12 September 2007 (online)

Abstract

The present study was designed to investigate the relationship between the serum levels of oxidant-antioxidant system (malondialdehyde (MDA) level, Paraoxonase (PON1) activity, nitric oxide (NO) level and superoxide dismutase (SOD) activity) and thyroid hormone status in hypothyroidism pre and posttreatment. The study group comprised 33 patients with primary hypothyoidism. 18 of these patients were reevaluated after euthyroid state i.e. at least 6 months of thyroxine replacement. The patients were compared with 26 normal healthy controls. Serum MDA level, PON1 activity, NO level and SOD activity were measured according to an enzymatic spectrophotometric method. MDA levels were found higher in patients with hypothyroidism before the treatment than the controls. MDA levels were also found to be decreased after the treatment in patients with hyothyroidism. However MDA were found still higher than the controls after the treatment. PON1 activity was found to be lower in patients pretreatment when compared to posttreatment hypothyroidism and controls. Posttreatment of hypothyroidism mean PON1 activity significantly increased compared to pretreatment level but it was still significantly lower than control level. NO level was higher in pretreatment hypothyroidism when compared to controls. SOD activity was not found different in patients before treatment when compared to controls. SOD activity was significantly higher in after treatment when compared to both pretreatment and control levels. In conclusion, increased ROS levels in hypothyroidism may result in a pro-oxidation environment, which in turn could result in decreased antioxidant PON1 activity, increased MDA and NO levels. As a result, lipid peroxidation may have a role in the pathogenesis of the atherosclerosis in hypothyroidism.

References

  • 1 Halliwell B. Free radicals, antioxidants and human disease: curiosity, cause or consequence?.  Lancet. 1994;  344 721-724
  • 2 Paller MS. Hypothyroidism protects against free radical damage in ischemic acute renal failure.  Kidney Int. 1986;  29 1162-1166
  • 3 Dumitriu L, Bartoc R, Ursu H. et al . Significance of high levels of serum malonyl dialdehyde (MDA) and ceruloplasmin (CP) in hyper- and hypothyroidism.  Endocrinologie. 1988;  26 35-38
  • 4 Costantini F, Pierdomenico SD, Cesare D De, Remigis P De, Bucciarelli T, Bittolo Bon G, Cazzolato G, Nubile G, Guanano MT, Sensi S, Cuccurullo F, Mezzetti A. Effect of thyroid function on LDL oxidation.  Arterioscler Thromb Vasc Biol. 1998;  18 732-737
  • 5 Pereira B, Rosa LF, Safi DA. et al . Control of superoxide dismutase, catalase and glutathione peroxidase activities in rat lymphoid organs by thyroid hormones.  J Endocrinol. 1994;  140 73-77
  • 6 Swaroop A, Ramasarma T. Heat exposure and hypothyroid conditions decrease hydrogen peroxide generation in liver mitocondria.  Biochem J. 1985;  226 403-408
  • 7 Sundaram V, Hanna AN, Koneru L. et al . Both hypothyroidism and hyperthyroidism enhance low density lipoprotein oxidation.  J Clin Endocrinol Metab. 1997;  82 3421-3424
  • 8 Gutteridge JM. Free radicals in disease processes: a compilation of cause and consequence.  Free Radic Res Commun. 1993;  19 141-158
  • 9 Fridovich I. Superoxide anion radical (O2 -), superoxide dismutases, and related matters.  J Biol Chem. 1997;  272 18515-18518
  • 10 Berlett BS, Stadtman ER. Protein oxidation in aging, disease and oxidative stress.  J Biol Chem. 1997;  272 20313-20316
  • 11 Gambhir JK, Lali P, Jain AK. Correlation between blood antioxidant levels and lipid peroxidation in rheumatoid arthritis.  Clin Biochem. 1997;  30 351-355
  • 12 Draper HH, Hadley M. A review of recent studies on the metabolism of exogenous and endogenous malondialdehyde.  Xenobiotica. 1990;  20 901-907
  • 13 Romero FJ, Morell B, Romero MJ, Jareno EJ, Romero B, Marin N, Roma J. Lipid peroxidation products and antioxidants in human disease.  Environmental Health Perspectives. 1998;  106 1229-1234
  • 14 Aviram M, Rosenblat M, Bisgaier CL. et al . Paraoxonase inhibits high-density lipoprotein oxidation and preserves its function: A possible peroxidative role for paraoxonase.  J Clin Invest. 1998;  101 1581-1590
  • 15 Gan KN, Smolen A, Eckerson HW. et al . Purification of human serum paraoxonase/arylesterase: evidence for one esterase catalyzing both activities.  Drug Metab Dispos. 1991;  19 100-106
  • 16 Rozenberg O, Rosenblat M, Coleman R. et al . Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knockout mice.  Free Rad Biol Med. 2003;  34 774-784
  • 17 Ayub A, Mackness MI, Arrol S. et al . Serum paraoxonase after myocardial infarction.  Arterioscler Thromb Vasc Biol. 1999;  19 330-335
  • 18 Mackness MI, Harty D, Bhatnagar D. et al . Serum paraoxonase activity in familial hypercholesterolaemia and insulin dependent diabetes mellitus.  Atherosclerosis. 1991;  86 193-199
  • 19 Stichtenoth DO, Frölich JC. Nitric oxide and inflammatory joint disease.  Br J Rhumatol. 1998;  37 246-257
  • 20 Beckman JS, Beckman TW, Chen J, Marshall PA, Freeman BA. Apparent hydroxyl radical production by peroxynitrite: implications for endothelial cell injury from nitric oxide and superoxide.  Proc Natl Acad Sci USA. 1990;  87 1620-1624
  • 21 Beckman JS, Koppenol WH. Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and the ugly.  Am J Physiol. 1996;  271 3424-3437
  • 22 Jain SK. Evidence for membrane lipid peroxidation during the invivo aging of human erythrocytes.  Biochem Biophys Acta. 1988;  937 205-210
  • 23 Eckerson EW, Romson J, Wyte C. et al . The human serum paraoxonase polymorphism: Identification of phenotypes by their response to salts.  Am J Hum Genet. 1983;  35 214-227
  • 24 Sun Y, Oberley LW, Li YA. A simple method for clinical assay of superoxide dismutase.  Clin Chem. 1988;  34 497-500
  • 25 Bories PN, Bories C. Nitrate determination in biological fluids by an enzymatic one-step assay with nitrate reductase.  Clin Chem. 1995;  41 904-907
  • 26 Halliwell B, Chirico S. Lipid peroxidation: its mechanism, measurement and significance.  Am J Clin Nutr. 1993;  57 715-724
  • 27 Halliwell B. Reactive oxygen species in living system: source, biochemistry, and role in human disease.  Am J Med. 1991;  91 14S-22S
  • 28 Azizi F, Raiszadeh F, Solati M. et al . Serum paraoxonase 1 activity is decreased in thyroid dysfunction.  J Endocrinol Invest. 2003;  26 703-709
  • 29 Sarandol E, Tas S, Dirican M. et al . Oxidative stress and serum paraoxonase activity in experimental hypothyroidism: effect of vitamin E supplementation.  Cell Biochem Funct. 2005;  23 1-8
  • 30 Aviram M, Rosenblat M, Billecke S, Erogul J, Sorenson R, Bisgaier CL, Newton RS, La Du B. Human serum paraoxonase (PON1) is inactivated by oxidized low density lipoprotein and preserved by antioxidants.  Free Radic Biol Med. 1999;  26 892-904
  • 31 Baskol G, Demir H, Baskol M, Kilic E, Ates F, Kocer D, Muhtaroglu S. Assessment of paraoxonase 1 activity and malondialdehyde levels in patients with rheumatoid arthritis.  Clinical Biochemistry. 2005;  38 951-955
  • 32 Baskol G, Karakucuk S, Oner AO, Baskol M, Kocer D, Mirza E, Saraymen R, Ustdal M. Serum paraoxonase 1 activity and lipid peroxidation levels in patients with age related macular degeneration.  Ophthalmologica. 2006;  220 12-16
  • 33 Baskol G, Baskol M, Yurci A, Ozbakır O. et al . Serum paraoxonase 1 activity and malondialdehyde levels in patients with ulcerative colitis.  Cell Biochem Funct. 2006;  24 283-286
  • 34 Baskol M, Baskol G, Deniz K. et al . A new marker for lipid peroxidation: serum paraoxonase activity in non-alcoholic steatohepatitis.  Turk J Gastroenterol. 2005;  16 119-123
  • 35 Karakucuk S, Baskol G, Oner A. et al . Serum paraoxonase activity is decreased in the active stage of Behcet's disease.  Br J Ophthalmol. 2004;  88 1256-1258
  • 36 Kumon Y, Nakauchi Y, Suehiro T, Shiinoki T, Tanimoto N, Inoue M, Nakamura T, Hashimoto K, Sipe JD. Proinflammatory cytokines but not acute phase serum amyloid A or C-reactive protein, down regulate paraoxonase 1 (PON1) expression by Hep G2.  Amyloid. 2002;  9 160-164
  • 37 Weetman AP. Cellular immune responses in autoimmune thyroid disease.  Clin Endocrinol (Oxf). 2004;  61 405-413
  • 38 Van Lenten BJ, Wagner AC, Nayak DP. et al . High-density lipoprotein loses its anti-inflammatory properties during acute influenza a infection.  Circulation. 2001;  103 2283-2288
  • 39 Feingold KR, Memon RA, Moser AH. et al . Paraoxonase activity in the serum and hepatic mRNA levels decrease during the acute phase response.  Atherosclerosis. 1998;  139 307-315
  • 40 Evereklioglu C, Türköz Y, Er H. et al . Increased nitric oxide production in patients with Behçet's disease: Is it a new activity marker?.  J Am Acad Dermatol. 2002;  46 50-54

Correspondence

Asst. Prof. G. BaskolMD 

Erciyes University Faculty of Medicine

Department of Biochemistry and Clinical Biochemistry

Kayseri

Turkey

Phone: +90/352/437 49 37 ext. 23289

Fax: +90/352/437 55 65

Email: gbaskol@yahoo.com