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Glutathione redox cycle enzymes and selenium in severe rheumatoid arthritis: lack of antioxidative response to selenium supplementation in polymorphonuclear leucocytes.
Ann Rheum Dis. 1992 Sep; 51(9):1044-9.AR

Abstract

The antioxidant capacity of the glutathione redox cycle and the concentrations of selenium in serum, red blood cells or whole blood, and polymorphonuclear leucocytes was evaluated in nine patients with severe rheumatoid arthritis (RA) and eight healthy controls receiving daily supplementation with 250 micrograms selenomethionine for six months. Serum and whole blood concentrations of selenium and the activity of the selenium dependent enzyme glutathione peroxidase (GSH-Px) were low in the serum, red blood cells, and polymorphonuclear leucocytes of patients with RA before selenium supplementation. During supplementation serum and whole blood concentrations of selenium and the activity of GSH-Px in serum and red blood cells of patients with RA and serum GSH-Px in controls increased. Selenium and GSH-Px in polymorphonuclear leucocytes were unaffected in patients with RA in contrast with the controls where both were augmented. Glutathione reductase activity in the red blood cells and polymorphonuclear leucocytes of patients with RA was low but increased during selenium supplementation. Whole blood concentrations of glutathione were slightly lower in patients with RA than controls and no difference in the content in polymorphonuclear leucocytes was found between the groups. The activity in red blood cells of glucose-6-phosphate dehydrogenase was high in patients with RA, indicating sufficient function of the hexose monophosphate pathway. The reduced antioxidant activity of the glutathione redox cycle in patients with severe RA was mainly due to the low availability of selenium. This was further supported by the response to selenium supplementation in serum and red blood cells. In the polymorphonuclear leucocytes, however, no biochemical effects of selenium supplementation were seen. This lack of antioxidative response could play a pathogenetic part in inflammation in patients with RA.

Authors+Show Affiliations

Institute of Environmental and Occupational Medicine, Aarhus University, Denmark.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1417134

Citation

Tarp, U, et al. "Glutathione Redox Cycle Enzymes and Selenium in Severe Rheumatoid Arthritis: Lack of Antioxidative Response to Selenium Supplementation in Polymorphonuclear Leucocytes." Annals of the Rheumatic Diseases, vol. 51, no. 9, 1992, pp. 1044-9.
Tarp U, Stengaard-Pedersen K, Hansen JC, et al. Glutathione redox cycle enzymes and selenium in severe rheumatoid arthritis: lack of antioxidative response to selenium supplementation in polymorphonuclear leucocytes. Ann Rheum Dis. 1992;51(9):1044-9.
Tarp, U., Stengaard-Pedersen, K., Hansen, J. C., & Thorling, E. B. (1992). Glutathione redox cycle enzymes and selenium in severe rheumatoid arthritis: lack of antioxidative response to selenium supplementation in polymorphonuclear leucocytes. Annals of the Rheumatic Diseases, 51(9), 1044-9.
Tarp U, et al. Glutathione Redox Cycle Enzymes and Selenium in Severe Rheumatoid Arthritis: Lack of Antioxidative Response to Selenium Supplementation in Polymorphonuclear Leucocytes. Ann Rheum Dis. 1992;51(9):1044-9. PubMed PMID: 1417134.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutathione redox cycle enzymes and selenium in severe rheumatoid arthritis: lack of antioxidative response to selenium supplementation in polymorphonuclear leucocytes. AU - Tarp,U, AU - Stengaard-Pedersen,K, AU - Hansen,J C, AU - Thorling,E B, PY - 1992/9/1/pubmed PY - 1992/9/1/medline PY - 1992/9/1/entrez SP - 1044 EP - 9 JF - Annals of the rheumatic diseases JO - Ann Rheum Dis VL - 51 IS - 9 N2 - The antioxidant capacity of the glutathione redox cycle and the concentrations of selenium in serum, red blood cells or whole blood, and polymorphonuclear leucocytes was evaluated in nine patients with severe rheumatoid arthritis (RA) and eight healthy controls receiving daily supplementation with 250 micrograms selenomethionine for six months. Serum and whole blood concentrations of selenium and the activity of the selenium dependent enzyme glutathione peroxidase (GSH-Px) were low in the serum, red blood cells, and polymorphonuclear leucocytes of patients with RA before selenium supplementation. During supplementation serum and whole blood concentrations of selenium and the activity of GSH-Px in serum and red blood cells of patients with RA and serum GSH-Px in controls increased. Selenium and GSH-Px in polymorphonuclear leucocytes were unaffected in patients with RA in contrast with the controls where both were augmented. Glutathione reductase activity in the red blood cells and polymorphonuclear leucocytes of patients with RA was low but increased during selenium supplementation. Whole blood concentrations of glutathione were slightly lower in patients with RA than controls and no difference in the content in polymorphonuclear leucocytes was found between the groups. The activity in red blood cells of glucose-6-phosphate dehydrogenase was high in patients with RA, indicating sufficient function of the hexose monophosphate pathway. The reduced antioxidant activity of the glutathione redox cycle in patients with severe RA was mainly due to the low availability of selenium. This was further supported by the response to selenium supplementation in serum and red blood cells. In the polymorphonuclear leucocytes, however, no biochemical effects of selenium supplementation were seen. This lack of antioxidative response could play a pathogenetic part in inflammation in patients with RA. SN - 0003-4967 UR - https://www.unboundmedicine.com/medline/citation/1417134/Glutathione_redox_cycle_enzymes_and_selenium_in_severe_rheumatoid_arthritis:_lack_of_antioxidative_response_to_selenium_supplementation_in_polymorphonuclear_leucocytes_ L2 - https://ard.bmj.com/lookup/pmidlookup?view=long&pmid=1417134 DB - PRIME DP - Unbound Medicine ER -