Journal of Neurology

, Volume 246, Issue 7, pp 533–539

Nonenzymatic antioxidants of blood in multiple sclerosis

Authors

  • Eszter Karg
    • Department of Pediatrics, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 471, Hungary
  • Péter Klivényi
    • Department of Neurology, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 397, Hungary Tel.: +36-62-455597, Fax: +36-62-455597
  • Ilona Németh
    • Department of Pediatrics, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 471, Hungary
  • Krisztina Bencsik
    • Department of Neurology, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 397, Hungary Tel.: +36-62-455597, Fax: +36-62-455597
  • Sándor Pintér
    • Department of Pediatrics, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 471, Hungary
  • László Vécsei
    • Department of Neurology, Albert Szent-Györgyi University Medical School, H-6701 Szeged, P.O. Box 397, Hungary Tel.: +36-62-455597, Fax: +36-62-455597
Original communication

DOI: 10.1007/s004150050399

Cite this article as:
Karg, E., Klivényi, P., Németh, I. et al. J Neurol (1999) 246: 533. doi:10.1007/s004150050399

Abstract

Free radical action has been suggested as a causal factor in multiple sclerosis. We investigated the plasma level of lipid peroxides expressed in terms of malone dialdehyde and changes in blood nonenzymatic antioxidants (glutathione, α-tocopherol, retinol, plasma sulfhydryl groups, and uric acid) in multiple sclerosis patients with exacerbation or in remission, including a group treated with β-interferon. The malone dialdehyde level was increased by 38% (n.s.) during exacerbations. The blood concentration of oxidized glutathione was likewise elevated (P < 0.05), while the ratio of plasma α-tocopherol to cholesterol plus triglyceride was decreased (P < 0.001). These changes suggest increased free radical production and consumption of the scavenger molecules during the active phase of the disease. Blood reduced glutathione level was increased (P < 0.01) during exacerbation and remission as well. The rise in this thiol is likely to be a compensatory mechanism defending the cells from further oxidant injuries. β-Interferon increased plasma α-tocopherol levels (P < 0.001) but not the lipid corrected α-tocopherol value. Other parameters were not influenced by the drug.

Key words Glutathioneβ-InterferonMalone dialdehydeRetinolA-Tocopherol

Copyright information

© Steinkopff Verlag 1999