Oxidative stress causes increased production of ROS like superoxide anion and hydroxyl radical during pathophysiological conditions and lowers generation of antioxidant resources which imbalances and injures healthy tissues followed by lipid peroxidation and alteration at cellular level. ROS stress is concerned in a wide spectrum of diseases, including chronic inflammation and in a wide variety of cancers. Body also reverts to this reaction by stimulating inflammatory response by means of generating proinflammatory chemokines, enhancing infiltration of macrophage, neutrophils, abnormal proliferation of T and B lymphocytes further aggravating apoptosis, release of oxidants, nitrates, halogens and inflammatory interleukins.  In an oxidative stress, reactive oxygen species generally provoke the series of oxidation at cellular level.  The buildup of free radicals in turn triggers various inflammatory cells causing release of various inflammatory interleukins, cytokines, chemokines, and tumor necrosis factors which mediate signal transduction and transcription pathways as nuclear factor- kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), hypoxia-inducible factor-1 (HIF-1α) and nuclear factor-erythroid 2-related factor (Nrf2). <br />
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<strong>References</strong><br />
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1.Srivastava S, et al. Int J Biol Macromol. 2017;101:502–517.