12/4/2023 0 Comments Ros reactive oxygenin the presence of reduced transition metals such as iron.− and H 2O 2 can facilitate the formation of the more toxic and reactive HO.Activity of multiple enzyme systems, such as the cytochrome P 450 monoxygenase system, xanthine oxidoreductase, nitric oxide synthases, and several others involved in the inflammatory process (cyclooxygenase and lipoxygenase), can also increase the generation of ROS. However, other cellular components, such as endoplasmic reticulum-bound enzymes, cytoplasmic enzyme systems, and the surface of the plasma membrane, also contribute ( 5, 6). Processes causing uncoupling of electron transport can enhance the production of ROS, with mitochondria being a major source ( 4). It readily accepts free electrons generated by normal oxidative metabolism within the cell, producing ROS, such as O 2 Oxygen has a unique molecular structure and is abundant within cells. Finally, antioxidant defenses that scavenge ROS and mitigate associated toxicities will be presented, with a discussion of potential therapeutic approaches for the prevention and/or treatment of human diseases using enzymatic and nonenzymatic antioxidants. The molecular, cellular, pathologic, and physiologic targets will then be discussed with a particular emphasis on aspects relevant to child development. This review will outline the origins of endogenous and exogenously generated ROS. The nature of the injury will ultimately depend on specific molecular interactions, cellular locations, and timing of the insult. An imbalance between the production of ROS and the antioxidant defenses that protect cells has been implicated in the pathogenesis of a variety of diseases, such as cancer, asthma, pulmonary hypertension, and retinopathy. However, the generation of ROS can also provoke damage to multiple cellular organelles and processes, which can ultimately disrupt normal physiology. Reactive oxygen species (ROS) serve as cell signaling molecules for normal biologic processes.
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