الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Asthma is the most frequent chronic disease in childhood; both the prevalence and mortality from asthma have increased during the last four decades. Asthma is a chronic inflammatory airway disorder associated with recruitment of inflammatory cells. It is characterized by reversible and variable recurrent episodes of airway obstruction that resolve spontaneously or as a result of treatment (Sayyah, 2011).
Airways are exposed to high level of environmental oxidants and the inflammatory cells infiltrating the airways produce several inflammatory mediators including a range of toxic reactive oxygen species (ROS) (Dut et al., 2008). The mechanism by which oxygen radicals cause asthma pathology is oxidation or nitration of proteins, lipids, or DNA to cause dysfunction of these molecules. In addition, physiological antioxidant system is impaired in asthma, possibly because of inflammation. Thus, the imbalance between oxidant and antioxidant that is called oxidant stress is critical in asthma pathogenesis (Babusikova et al., 2012).
Malondialdehyde (MDA), is a marker of lipid peroxidation, it has a strong correlation with asthmatic children suggesting that oxidative stress occurs simultaneously on lipid peroxidation (Sharma et al., 2003). Oxidative stress can have many effects on airway function, including airway smooth muscle contraction, induction of airway hyperresponsiveness, mucous hypersecretion, epithelial shedding and vascular exudation. Further more, ROS and lipid peroxidation products can influence the inflammatory response at many levels through its impact on.