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 (<5y or >5y), Ab level (low, <3 or high, >3nmol/l) as well as symptoms (GMG or OMG). Glycophore fluorescence was increased in OMG^a. Dityrosine was increased in both types of MG^c, in patients ill <5^b and >5^cy, with low^c and high^c levels of Ab. N-formylkynurenine was increased in OMG^a and GMG^b, in both disease duration groups^a, in the group of low Ab^a. Kynurenine was increased in the group with high Ab^a. Tryptophan fluorescence was decreased in OMG^b and GMG^c, in patients ill for <5^b and >5^ay, with low^a and high^c Ab. Serum thiol group concentration were decreased in GMG^c, in patients ill for >5y^b. AOPP level was elevated in OMG^a, in patients ill for >5y^a with high Ab^a. Protein carbonyls were increased in both OMG^c and GMG^c, in patients ill for >5^ay, with low^b and high^b Ab. FRAP and ABTS^• scavenging by fast antioxidants were unchanged, but ABTS^• scavenging by slow antioxidants was lower in OMG^b and GMG^c, in patients ill for >5^cy, in patients with low^c and high^b Ab (^ap<0.05, ^bp<0.01, ^cp<0.001). These results demonstrate systemic oxidative stress in MG, suggesting therapeutic use of antioxidants.