Oxidative modifications of blood serum proteins in myasthenia gravis

Myasthenia gravis (MG) is an autoimmune disease caused by production of antibodies against acetylcholine receptors of the neuromuscular junction (Ab). The aim of this study was to ascertain if oxidative stress accompanies MG by estimation of the several independent parameters of oxidative damage, mainly the levels of oxidative modifications of blood serum proteins. The group studied consisted of 50 MG patients (28 females and 22 males), 24 with ocular MG (OMG) and 26 with generalized MG (GMG), of mean age of 66.7 (30–81) years (y), mean disease duration of 9.5 (0.5–34) y, mean level of Ab of 8.9 (0.1–85) nmol/ml, and 25 age-matched healthy controls. MG patients were stratified into groups according to disease duration (<5 y or >5 y), Ab level (low, <3 or high, >3 nmol/l) as well as symptoms (GMG or OMG). Glycophore fluorescence was increased in OMGa. Dityrosine was increased in both types of MGc, in patients ill <5b and >5c y, with lowc and highc levels of Ab. N-formylkynurenine was increased in OMGa and GMGb, in both disease duration groupsa, in the group of low Aba. Kynurenine was increased in the group with high Aba. Tryptophan fluorescence was decreased in OMGb and GMGc, in patients ill for <5b and >5a y, with lowa and highc Ab. Serum thiol group concentration were decreased in GMGc, in patients ill for >5 yb. AOPP level was elevated in OMGa, in patients ill for >5 ya with high Aba. Protein carbonyls were increased in both OMGc and GMGc, in patients ill for >5a y, with lowb and highb Ab. FRAP and ABTS• scavenging by fast antioxidants were unchanged, but ABTS• scavenging by slow antioxidants was lower in OMGb and GMGc, in patients ill for >5c y, in patients with lowc and highb Ab (ap < 0.05, bp < 0.01, cp < 0.001). These results demonstrate systemic oxidative stress in MG, suggesting therapeutic use of antioxidants.