Skip to main content

Advertisement

Log in

Plasma glutathione peroxidase (GSH-Px) concentration is elevated in rheumatoid arthritis: a case–control study

  • Original Article
  • Published:
Clinical Rheumatology Aims and scope Submit manuscript

Abstract

Plasma glutathione peroxidase (GSH-Px) by enzyme-linked immunosorbent assay (ELISA) offers a complimentary measurement approach to traditional GSH-Px activity methods. The aim was to investigate whether GSH-Px measured by ELISA in rheumatoid arthritis patients was elevated compared to controls. This was a case–control study with rheumatoid arthritis patients recruited from private practice and gender and age-matched controls randomly selected from the electoral role. GSH-Px concentration was measured by ELISA. Plasma malondialdehyde was used as a measure of oxidative stress, and antioxidant capacity was measured based on reduction of Cu++ to Cu+ by antioxidants in the sample. Disease severity was measured using the Health Assessment Questionnaire-Disability Index (HAQ-DI) and C-reactive protein was measured using an immunoturbidometric method. A total of 74 patients were recruited, consisting of 35 rheumatoid arthritis cases and 39 healthy controls. There were no differences between rheumatoid arthritis cases and controls for oxidative stress and antioxidant capacity; however, GSH-Px concentration was markedly elevated in the rheumatoid arthritis sufferers (85.9 ± 147.7 versus 17.3 ± 13.0 mg/L, respectively; mean ± SD; p < 0.01). GSH-Px levels were not associated with severity measured by the HAQ-DI or C-reactive protein. Patients with rheumatoid arthritis demonstrated increased GSH-Px consistent with an adaptive upregulation of GSH-Px to protect against oxidative stress.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Rahman I, Biswas SK, Kode A (2006) Oxidant and antioxidant balance in the airways and airway diseases. Eur J Pharmacol 533(1–3):222–239

    Article  PubMed  CAS  Google Scholar 

  2. Raes M, Michiels C, Remacle J (1987) Comparative study of the enzymatic defense systems against oxygen-derived free radicals: the key role of glutathione peroxidase. Free Radic Biol Med 3(1):3–7

    Article  PubMed  CAS  Google Scholar 

  3. Maddipati KR, Marnett LJ (1987) Characterization of the major hydroperoxide-reducing activity of human plasma. Purification and properties of a selenium-dependent glutathione peroxidase. J Biol Chem 262(36):17398–17403

    PubMed  CAS  Google Scholar 

  4. Takahashi K, Avissar N, Whitin J, Cohen H (1987) Purification and characterization of human plasma glutathione peroxidase: a selenoglycoprotein distinct from the known cellular enzyme. Arch Biochem Biophys 256(2):677–686

    Article  PubMed  CAS  Google Scholar 

  5. Reyes LH, Marchante-Gayon JM, Alonso JIG, Sanz-Medel A (2003) Quantitative speciation of selenium in human serum by affinity chromatography coupled to post-column isotope dilution analysis ICP-MS. J Anal At Spectrom 18(10):1210–1216

    Article  Google Scholar 

  6. Deagen JT, Butler JA, Zachara BA, Whanger PD (1993) Determination of the distribution of selenium between glutathione peroxidase, selenoprotein P, and albumin in plasma. Anal Biochem 208(1):176–181

    Article  PubMed  CAS  Google Scholar 

  7. Brown KM, Arthur JR (2001) Selenium, selenoproteins and human health: a review. Public Health Nutr 4(2B):593–599

    Article  PubMed  CAS  Google Scholar 

  8. Henrotin YE, Bruckner P, Pujol JP (2003) The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthr Cartil 11(10):747–755

    Article  PubMed  CAS  Google Scholar 

  9. Del Carlo M Jr, Loeser RF (2002) Nitric oxide-mediated chondrocyte cell death requires the generation of additional reactive oxygen species. Arthritis Rheum 46(2):394–403

    Article  PubMed  Google Scholar 

  10. Tiku ML, Gupta S, Deshmukh DR (1999) Aggrecan degradation in chondrocytes is mediated by reactive oxygen species and protected by antioxidants. Free Radic Res 30(5):395–405

    Article  PubMed  CAS  Google Scholar 

  11. Jovanovic DV, Mineau F, Notoya K, Reboul P, Martel-Pelletier J, Pelletier JP (2002) Nitric oxide induced cell death in human osteoarthritic synoviocytes is mediated by tyrosine kinase activation and hydrogen peroxide and/or superoxide formation. J Rheumatol 29(10):2165–2175

    PubMed  CAS  Google Scholar 

  12. Tiku ML, Shah R, Allison GT (2000) Evidence linking chondrocyte lipid peroxidation to cartilage matrix protein degradation. Possible role in cartilage aging and the pathogenesis of osteoarthritis. J Biol Chem 275(26):20069–20076

    Article  PubMed  CAS  Google Scholar 

  13. Suetens C, Moreno-Reyes R, Chasseur C et al (2001) Epidemiological support for a multifactorial aetiology of Kashin–Beck disease in Tibet. Int Orthop 25(3):180–187

    Article  PubMed  CAS  Google Scholar 

  14. Yang C, Wolf E, Roser K, Delling G, Muller PK (1993) Selenium deficiency and fulvic acid supplementation induces fibrosis of cartilage and disturbs subchondral ossification in knee joints of mice: an animal model study of Kashin–Beck disease. Virchows Arch A Pathol Anat Histopathol 423(6):483–491

    Article  PubMed  CAS  Google Scholar 

  15. Sasaki S, Iwata H, Ishiguro N, Habuchi O, Miura T (1994) Low-selenium diet, bone, and articular cartilage in rats. Nutrition 10(6):538–543

    PubMed  CAS  Google Scholar 

  16. Darlington LG, Stone TW (2001) Antioxidants and fatty acids in the amelioration of rheumatoid arthritis and related disorders. Br J Nutr 85(3):251–269

    Article  PubMed  CAS  Google Scholar 

  17. Aaseth J, Munthe E, Forre O, Steinnes E (1978) Trace elements in serum and urine of patients with rheumatoid arthritis. Scand J Rheumatol 7(4):237–240

    Article  PubMed  CAS  Google Scholar 

  18. Knekt P, Heliovaara M, Aho K, Alfthan G, Marniemi J, Aromaa A (2000) Serum selenium, serum alpha-tocopherol, and the risk of rheumatoid arthritis. Epidemiology 11(4):402–405

    Article  PubMed  CAS  Google Scholar 

  19. Peretz A, Siderova V, Neve J (2001) Selenium supplementation in rheumatoid arthritis investigated in a double blind, placebo-controlled trial. Scand J Rheumatol 30(4):208–212

    Article  PubMed  CAS  Google Scholar 

  20. Tarp U, Hansen JC, Overvad K, Thorling EB, Tarp BD, Graudal H (1987) Glutathione peroxidase activity in patients with rheumatoid arthritis and in normal subjects: effects of long-term selenium supplementation. Arthritis Rheum 30(10):1162–1166

    Article  PubMed  CAS  Google Scholar 

  21. Canter PH, Wider B, Ernst E (2007) The antioxidant vitamins A, C, E and selenium in the treatment of arthritis: a systematic review of randomized clinical trials. Rheumatology (Oxford) 46(8):1223–1233

    Article  CAS  Google Scholar 

  22. Jacobson GA, Narkowicz C, Tong YC, Peterson GM (2006) Plasma glutathione peroxidase by ELISA and relationship to selenium level. Clin Chim Acta 369(1):100–103

    Article  PubMed  CAS  Google Scholar 

  23. Jacobson GA, Yee KC, Ng CH (2007) Elevated plasma glutathione peroxidase concentration in acute severe asthma: comparison with plasma glutathione peroxidase activity, selenium and malondialdehyde. Scand J Clin Lab Invest 67(4):423–430

    Article  PubMed  CAS  Google Scholar 

  24. Fries JF, Spitz P, Kraines RG, Holman HR (1980) Measurement of patient outcome in arthritis. Arthritis Rheum 23(2):137–145

    Article  PubMed  CAS  Google Scholar 

  25. Cole JC, Motivala SJ, Khanna D, Lee JY, Paulus HE, Irwin MR (2005) Validation of single-factor structure and scoring protocol for the Health Assessment Questionnaire-Disability Index. Arthritis Rheum 53(4):536–542

    Article  PubMed  Google Scholar 

  26. Sokka T, Pincus T (2009) Erythrocyte sedimentation rate, C-reactive protein, or rheumatoid factor are normal at presentation in 35%–45% of patients with rheumatoid arthritis seen between 1980 and 2004: analyses from Finland and the United States. J Rheumatol 36(7):1387–1390

    Article  PubMed  CAS  Google Scholar 

  27. Anonymous. C-Reactive protein. Ref 8G65-21, Dec 2008. ARCHITECT c Systems. Abbott Diagnostics, Abbott Park, IL, USA

  28. Pincus T, Sokka T (2009) Laboratory tests to assess patients with rheumatoid arthritis: advantages and limitations. Rheum Dis Clin N Am 35(4):731–734, vi–vii

    Article  Google Scholar 

  29. Li K, Shang X, Chen Y (2004) High-performance liquid chromatographic detection of lipid peroxidation in human seminal plasma and its application to male infertility. Clin Chim Acta 346(2):199–203

    Article  PubMed  CAS  Google Scholar 

  30. Finaud J, Lac G, Filaire E (2006) Oxidative stress: relationship with exercise and training. Sports Med 36(4):327–358

    Article  PubMed  Google Scholar 

  31. Rokitzki L, Logemann E, Sagredos AN, Murphy M, Wetzel-Roth W, Keul J (1994) Lipid peroxidation and antioxidative vitamins under extreme endurance stress. Acta Physiol Scand 151(2):149–158

    Article  PubMed  CAS  Google Scholar 

  32. Tarp U, Overvad K, Hansen JC, Thorling EB (1985) Low selenium level in severe rheumatoid arthritis. Scand J Rheumatol 14(2):97–101

    Article  PubMed  CAS  Google Scholar 

  33. Tarp U, Graudal H, Overvad K, Thorling EB, Hansen JC (1989) Selenium in rheumatoid arthritis. A historical prospective approach. J Trace Elem Electrolyte Health Dis 3(2):93–95

    CAS  Google Scholar 

Download references

Acknowledgments

The authors wish to thank Catrina Boon for assistance with the provision of stored samples. This work was supported by the School of Pharmacy as part of a student project. TASOAC was funded by NHMRC and Arthritis Australia.

Disclosures

None.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Glenn A. Jacobson.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Jacobson, G.A., Ives, S.J., Narkowicz, C. et al. Plasma glutathione peroxidase (GSH-Px) concentration is elevated in rheumatoid arthritis: a case–control study. Clin Rheumatol 31, 1543–1547 (2012). https://doi.org/10.1007/s10067-012-2046-9

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10067-012-2046-9

Keywords

Navigation