Rheumatoid arthritis is an autoimmune disease where diagnosis is based on clinical and radiological features and presence of rheumatoid factor in serum. It is characterized by chronic inflammation leading to joints’ destruction. The pathogenesis of RA is not fully understood yet. RA is not generally recognized as a disease of oxidative stress but it has been suggested that the level of reactive oxygen species (ROS) in patients with RA is higher than in healthy subjects. Oxidative stress in RA is due to the fact that the antioxidant systems are impaired [¹, ²].

The aim of this paper is to study the antioxidant system in erythrocyte from patients with RA. The increase in ROS leads to significant changes in the structure of membrane lipids and proteins that may impair membrane functions and influence the antioxidant enzymes activity.

Level of the lipid peroxidation is shown in Table 1. Concentration of TBARs [μmol MDA/g_Hb] in the erythrocyte membranes from the RA was determined and compared to the control group. It was significantly higher in RA patients than in healthy individuals.

The plasma membrane protein damage was determined by total ATPase and Na⁺K⁺ ATPase activities and concentration of –SH groups (Table 2). The level of the total ATPase was about 10% higher, and the level of the Na⁺K⁺ ATPase was about 20% higher in the control group than in RA patients. These differences were statistically significant. The –SH groups’ concentration in the erythrocyte plasma membranes from RA patients was significantly lower than in healthy individuals.

Antioxidant enzymes activities and concentration of GHS are given in Table 3. SOD activity is significantly lower in RA patients than in control group (P < 0.005). There are no significant differences in CAT and GSH-Px activities. Concentration of the GSH is about 20% lower in RA patients than in healthy subjects.

Imbalance in the human oxidative/antioxidative status leads to oxidative stress, which is involved in ageing and number of disorders: vascular diseases (e.g. atherosclerosis, stroke, reperfusion damage), neurodegenerative diseases (e.g. Parkinson’s, Alzheimer’s, multiple sclerosis), lung diseases (e.g. pneumonia), eye diseases (e.g. cataract, retinopathy), autoimmune diseases (e.g. rheumatoid arthritis) [¹⁴–¹⁷]. The result of the present study showed that oxidative stress in RA patients is higher than in control group. Similar conclusion is presented in another studies, e.g. Altindag et al. [¹⁸] stated higher oxidative stress on the basis of increasing oxidative DNA damage.

In RA, damage to the plasma membranes of red blood cells is observed. This may result from the peroxidation of polyunsaturated fatty acids and changes in proteins. It is known that MDA, which is one of the final products of lipid peroxidation, could cause erythrocytes plasma membrane stiffness. It impairs the cells ability to change shape. Phosphatidyloserine movement from the inner to the outer layer under the influence of free radicals affects the losing of membrane fluidity.

Level of the lipid peroxidation is significantly higher in the patients with RA than in the control group and it is in agreement with most studies [¹⁹, ²⁰]. On the basis of the obtained results and the literature data, it can be concluded that in RA, red blood cells are more susceptible to the influence of free radicals.

Thiol groups play an important role in a variety of activities of cell membranes. As described by Deuticke [²¹], membrane thiol groups are liable to be modified by oxidants or alkylating agents. Oxidation of thiol groups of erythrocyte membrane can increase their permeability to ions such as K⁺, Na⁺ and Ca⁺, indicating that membrane permeability to these ions is correlated with membrane thiol groups.

Free radicals’ processes lead to lipid peroxidation and decreased concentration of –SH groups in membrane proteins. Our data illustrate the decrease in the concentration of thiol groups about 30%. A decrease in the accessible –SH groups should be correlated with increased aggregation of membrane proteins since a significant fraction of the oxidized groups can be involved in the formation of the disulphide bridges [²²].

Na⁺K⁺-ATPase is the membrane lipid–protein complex. It contains 30% lipids, most of them are phosphate lipids and cholesterol. It produces energy by hydrolysing ATP and transports ions for keeping the stable ion content which is needed for normal physiological activity [²³, ²⁴]. Total ATPase and Na⁺K⁺ ATPase activities were lower in RA patients than in the control groups. It is in agreement with another data that indicate inhibitory influence of free radicals on ATPase activity [²⁵, ²⁶].

Antioxidant enzymes are responsible for defence against free radicals. There are some reports on erythrocyte SOD, CAT and GSH-Px activities in patients with RA, but the results are controversial. In the present study, inhibition of the SOD activity was observed. Sarban [¹⁹] observed no changes, and Akyol [²⁰] noticed no change in erythrocytes SOD and inhibition of plasma SOD. Cimen [²⁷] observed increase in erythrocyte SOD activity. In the present study, significant differences in CAT and GSH-Px activities were not noticed and it is in agreement with most of studies but there are some differences between researchers too—Sarban observed inhibition of CAT and GSH-Px activities. His results confirm increase in oxidative stress in RA patients.

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