IMPACT OF GLUTATHIONE PEROXIDASE ACTIVITY (GPX) AS OXIDATIVE-STRESS MARKER AND ITS ROLE ON INFLAMMATION WITH OSTEOARTHRITIS PATIENTS

Osteoarthritis is an important issue for both the individual and society and its public health impact continues to grow due to the ageing population. It is the common form of arthritis and characterized by softening and disintegration of articular cartilage. The deterioration and loss of articular cartilage leading to an impairment of joint structure are the final pathogenic events common to osteoarthritis. Free radicals are produced in large amounts in tissues under physiologic conditions, these are controlled by several antioxidant protective mechanisms. Biologic tissues maintain a balance between antioxidant reserve and ROS or pro-oxidants, but under the pathophysiologic conditions this balance is upset because of an increase in ROS production and an alteration in the antioxidant defense system. This condition is oxidative stress. The objective was to determine the effect of blood glutathione peroxidise activity with OA patients, as well as to determine the p-value of controls, combined( all age groups) and two separate age groups(age<45; age>45). The study carried out 20 controls and 40 patients, has been suffering from OA and patient blood samples were carried out from OPTM health care and research institute. It was observed that mean ± SD value of GPx activity of OA patients in combined group (all age groups) and in two separate age groups (age<45; age>45) showed a significant decrease as compared to controls. Then it indicates that the glutathione redox enzymatic cycle is the most important intracellular defense against toxicity induced by oxygen free radicals. This incident could be explained by the reduction of GSH found in OA patients. The enzyme itself may be inactive under conditions of intense oxidative stress, which contributes to low GPx activity. Besides, It was reported that synovial cavity damage correlates with fluctuating oxygen pressure in the joint, overproduction of free radicals and free radical-scavenging molecules. This result confirm the role of oxidative stress in the pathogenesis of OA and suggesting that in this condition treatment is required.