IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN: 2279-0853, p-ISSN: 2279-0861. Volume 8, Issue 6 (Jul.- Aug. 2013), PP 01-05 www.iosrjournals.org www.iosrjournals.org 1 | Page Antioxidant enzymes and antioxidants in children with Pneumonia NA Vaidya 1 , PM Bulakh 2 1, 2 Department of Biochemistry Bharati Vidyapeeth Deemed University Medical college, Pune, India Abstract : In children pneumonia is a leading cause of death which is characterized by inflammation of the parenchyma of the lung tissue due to infection. Additional risk factors being continuous exposure of lung epithelium to environmental pollutants, microorganisms, resulting into inflammation and increased oxidative stress .Lung tissue are protected from environmental oxidants by the endogenous antioxidants. A disruption in the fine balance between the antioxidants and oxidants leads to oxidative stress. The present study was conducted to study the oxidative stress in pneumonia by measuring the levels of lipid peroxidation in terms of malondialdehyde, enzymatic and non-enzymatic antioxidants as compared to control group. The study observed significantly lowered levels of antioxidant enzymes glutathione peroxidase, glutathione reductase and paraoxonase 1 along with lowered levels of non enzymatic antioxidants Vitamin C, vitamin E, and β carotene (p< 0.001) and an increased malondialdehyde levels among patients diagnosed with pneumonia when compared with the control group(p <0.001). Our observations are suggestive of an increased oxidative stress in cases of pneumonia in the pediatric age group. Key words: Antioxidants, Nrf2, Oxidative stress, Pneumonia ,Reactive oxygen species. I. Introduction Pneumonia is an acute respiratory disease affecting all age group persons characterized by inflammation of the parenchyma of the lung tissue due to infection by viruses, bacteria or fungi Among the respiratory diseases, pneumonia ranks first for the mortality and morbidity and kills an estimated 1.2 million children under the age of five years every year(WHO data) [1].Various risk factors such as environmental pollutants/irritants, compromised immune system, malnutrition play an important role in disease development. Microorganisms after infection produce edema in lung tissue proliferate there and invade adjacent tissue. This blocks the ciliary action of epithelial tissue resulting into increased cellular destruction and inflammation [2]. The childhood pulmonary susceptibility may be related to immature lung tissue. Lung development takes place in first 6 – 8 years of post natal period. During this period the lung undergoes alveolarization and continued morphogenesis with cell differentiation such as respiratory epithelial and critical immune effecter cell populations, specific cell-cell interaction. These developmental events are disrupted if the lungs are exposed to vast array of materials of undefined toxicity, and results into drastic long-term consequences. Early evaluation and management in the predisposed infants is necessary to avoid the irreversible loss of lung function and high morbidity [3]. Lungs are exposed to many unwanted events such as infection, exposure to toxicants, irritants which triggers the synthesis of cytokines and interleukins by initiating the inflammatory process in lung tissue ;a primary defense process against the pathogens .The inflammatory cells activates polymorphonuclear leucocytes, macrophages, monocytes, platelets and mast cells. All these inflammatory reactions are responsible for generation of free radicals and reactive oxygen species (ROS) such as hydroxyl, superoxide and peroxynitrite radicals [4]. Oxidative stress results from an imbalance between formation and neutralization of ROS which in excess, damage cell membranes and lipoproteins by a process called lipid peroxidation. Malondialdehyde (MDA) is a major aldehyde product of lipid peroxidation, believed to be responsible for cytopathological effects observed during lipid peroxidation induced oxidative stress [5] Al-Abdulla et al have found reduced ascorbic acid and alpha -tocopherol concentrations and increased MDA levels in the respiratory lining fluid of adults with asthma [6]. An imbalance between antioxidants and oxidants in the epithelial lining fluid of the lung is thought to contribute to oxidative stress in respiratory disease Lipid peroxidation occurs by a radical chain reaction, i.e. once started it spreads rapidly and affects a great number of lipid molecules generating excess free radicals and lipid hydroperoxides that can seriously alter the cell membranes, membrane fluidity and permeability. These hydroperoxides and ROS attack other cell structures such as proteins, lipids, lipoproteins, and deoxyribonucleic acid (DNA) [7]. Oxidative damage to DNA leads to the formation of oxidative DNA lesions which can cause mutations and cytotoxicity. The body has several mechanisms to counteract these attacks by using endogenous antioxidant system consisting of antioxidant enzymes such as glutathione reductase , glutathione peroxidase , paraoxonase , super oxide dismutase, catalase, and non enzymatic antioxidant molecules like ascorbic acid , alpha tocopherol, beta