cell biochemistry and function Cell Biochem Funct 2006; 24: 269–273. Published online 22 March 2005 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1027/cbf.1220 Oxidative stress and enzymic–non-enzymic antioxidant responses in children with acute pneumonia Mustafa Cemek* 1 , Hu¨seyin C¸ aksen 2 , Fahri Bayirog˘lu 3 , Fatma Cemek 2 and Semiha Dede 4 1 Department of Chemistry (Biochemistry Division), Faculty of Science, Afyon Kocatepe University, Afyon, Turkey 2 Department of Pediatrics, Faculty of Medicine, Yu¨zu¨ncu¨ Yıl University, Van, Turkey 3 Department of Physiology, Faculty of Veterinary Medicine, Yu¨zu¨ncu¨ Yıl University, Van, Turkey 4 Department of Biochemistry, Faculty of Veterinary Medicine, Yu¨zu¨ncu¨ Yıl University, Van, Turkey In this article, oxidative stress and enzymic–non-enzymic antioxidants status were investigated in children with acute pneu- monia. Our study included 28 children with acute pneumonia and 29 control subjects. The age ranged from 2 to 11 years (4.57  2.13 years) and 2 to 12 years (4.89  2.22 years) in the study and control groups, respectively. Whole blood mal- ondialdehyde (MDA) and reduced glutathione (GSH), serum -carotene, retinol, vitamin C, vitamin E, catalase (CAT), cer- uloplasmin (CLP), total bilirubin, erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were studied in all subjects. There was a statistically significant difference between the groups for all parameters except for serum CAT. Whole blood MDA, serum CLP and total bilirubin levels were higher in the study group than those of the control group. However, SOD, GPx, -carotene, retinol, vitamin C, vitamin E and GSH levels were lower in the study group com- pared with the control group. All antioxidant vitamin activities were decreased in children with acute pneumonia. Our study demonstrated that oxidative stress was increased whereas enzymic and non-enzymic antioxidant activities were significantly decreased in children with acute pneumonia. Copyright # 2005 John Wiley & Sons, Ltd. key words — antioxidant; oxidative stress; pneumonia; child; reactive oxygen species INTRODUCTION Toxicity from oxygen metabolites released by stimu- lated neutrophils, macrophages, and other cells has been proposed as one of the significant mechanisms of lung injury. 1 Reactive oxygen species (ROS) in the form of the O 2  ,H 2 O 2 and the hydroxyl radical (OH  ) cause damage to DNA, lipids and proteins. These species are produced by bacteria during aerobic respiration and by phagocytic cells when they encoun- ter bacteria as part of the host defence against infec- tion. It is known that the development of many inflammatory processes is accompanied by an increased activity of free radicals. 2 Oxidative stress results from an oxidant/antioxidant imbalance, an excess of oxidants or a depletion of antioxidants. Oxi- dative stress is thought to play an important role in the pathogenesis of a number of lung diseases, not only through direct injurious effects, but by involvement in the molecular mechanisms that control lung inflam- mation. 1,3 By-products of lipid peroxidation (LPO) formed in various biochemical reactions are normally scavenged by antioxidants. Antioxidants are com- pounds that are involved in effective scavenging of free radicals and in suppressing the actions of reactive oxygen substances. 4 Pulmonary antioxidant defences are widely distributed and include both enzymic and non-enzymic systems. The major enzymic antioxi- dants are superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). -Carotene, vitamin C, vitamin E, reduced glutathione (GSH), cer- uloplasmin (CLP), and bilirubin are some of the non- enzymic factors that may function as antioxidants. 5 Acute lower respiratory tract infections (ALRI) pre- sent as important public health problems in many developing countries. In these countries, ALRI are among the most important causes of morbidity and Received 9 August 2002 Revised 28 October 2004 Copyright # 2005 John Wiley & Sons, Ltd. Accepted 10 November 2004 * Correspondence to: Dr Mustafa Cemek, Afyon Kocatepe U ¨ niversitesi, Fen Edebiyat Faku¨ltesi, Kimya Bo¨lu¨mu¨, Biyokimya AD, ANS Kampu¨su¨, Afyon, Turkey. Tel: 0 þ90-(272) 228 13 12. Fax: 0 þ90-(272) 228 12 35. E-mail: mcemek@yahoo.com