© 2013. Al Ameen Charitable Fund Trust, Bangalore 134 Al Ameen J Med Sci 2013; 6(2):134-137 ● US National Library of Medicine enlisted journal ● ISSN 0974-1143 ORIGINAL ARTICLE CODEN: AAJMBG A study of oxidative stress, thiol proteins and role of vitamin E supplementation in chronic obstructive pulmonary disease (COPD) Anita M. Raut 1* , Adinath N. Suryakar 2 and Dilip Mhaisekar 3 1 Department of Biochemistry, Dr. Vikhe Patil Institute of Medical Sciences, Post: MIDC, Vadgaon Gupta, Ahmednagar-414111, Maharashtra, India, 2 Registrar, Maharashtra University of Health Sciences, Mhasrul, Dindori Road, Nashik-422004 Maharashtra, India and 3 Department of Resp. Medicine, Government Medical College, Vazirabad, Nanded-431601 Maharashtra, India Abstract: Background: Lipid peroxide plays an important role in inflammatory lung disease. Increased epithelial permeability produced by cigarette smoke is likely to be mediated through depletion of thiol proteins. Imbalance between oxidants and thiol proteins is also an established fact in these patients. Materials & methods: In the present study 30 healthy non-smokers were served as controls and 20 patients with stable COPD were included. Their base line clinical examination, Malondialdehyde (MDA) as an oxidant, alpha tocopherol and erythrocyte superoxide dismutase (SOD) as an antioxidants and thiol proteins levels were measured. All above parameters were repeated after 12 weeks of supplementation with 400 IU of vitamin E daily. Results: We observed that the mean malondialdehyde levels in these patients at base line were high (p<0.001) than Control Plasma alpha-tocopherol, SOD and thiol proteins levels were low (p<0.001) in the patients compared to controls. Exogenous vitamin E (400 IU twice daily) Supplementation did not bring about any significant change in plasma Erythrocyte Superoxide Dismutase and vitamin E. But slight increase in the plasma thiol proteins levels was seen. The present study shows that initially the plasma lipid peroxide (MDA) levels were high antioxidant (alpha- tocopherol, SOD) and thiol proteins were low in patients with COPD. Exogenous supplementation with vitamin E increases slightly thiol proteins levels and brings down the levels of MDA showing attenuation of further damage. Conclusion: Our study confirmed the existence of oxidative stress and and the augmentation of antioxidant defenses as shown by slight increase in thiol proteins level. The antioxidant therapy is adjunct in lung disease patients and opens a promising field in prevention of oxidative stress related complications in these patients. Keywords: Vitamin E, Malondialdehyde, Superoxide Dismutase, Antioxidants, Chronic Obstructive Pulmonary disease, thiol proteins. Introduction Lung disease is a global health concern and is a major cause of chronic morbidity and mortality. It reduces quality of life causes frequent hospital admission and carries an increase risk of prevalence death for those affected [1]. Lung is an organ which is constantly exposed to many atmospheric pollutants such as cigarette smoke, ozone and nitrogen dioxide and is also at risk from oxidant injury by inhalation [2]. Since lung contains the largest endothelial surface area than any other organ, it makes the lung a major target site for circulating oxidants and xenobiotics. Chronic obstructive pulmonary disease (COPD) a chronic slowly progressive disorder is characterized by airflow obstruction. Chronic inflammation by cigarette smoke was associated with a dramatic depletion of thiol proteins. Vitamin E is the most important lipohilic antioxidant in humans. It contributes to membrane stability and protects critical cell structures against harmful effects from oxygen free radicals and reactive lipoperoxides, which is relevant for several human pathological states, including lung diseases. The oxidative stress is believed to play a vital role in the pathogenesis of COPD being responsible for a series of events including recruitment of neutrophils and macrophages, increased mucus secretion, vascular permea- bility, airway inflammation, bronchospasm and inhibition of protease inhibitors [3]. The oxidative stress and protease antiprotease imbalance promote alveolar damage and chronic airway inflammation which are pathophysiologic hallmarks of COPD [4]. While oxidative stress has been well