Abstract
Reactive oxygen species (ROS) are chemical molecules with one unpaired electron and mostly derived from molecular oxygen. It is produced in all the mammalian system by various exogenous and endogenous sources. Mitochondria are major sources of ROS production and they are produced as a respiratory by-product. The main sites of superoxide radical production in the respiratory chain are complexes III and I; however, other mitochondrial enzymes are also involved in the production of ROS. Because of the presence of one unpaired electron, ROS is highly reactive, and it may cause oxidative damage to the biomolecules and cell organelles and hence may affect the cellular physiology and their survivability.
A variety of diseases have been associated with excessive ROS production leading to mitochondrial damage, apoptosis, and necrosis. The interrelationship between ROS and mitochondria suggests shared pathogenic mechanisms in mitochondrial and ROS-related diseases. Some common diseases, known to be caused by ROS and mitochondrial damages, are several mitochondrial diseases, neurodegenerative diseases, and aging. In the present chapter, we have summarized the molecular mechanisms of ROS production, its damaging effect on cellular physiology, as well as the existing evidence of mitochondrial ROS involvement in human diseases.
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Author wishes to acknowledge Nancy Taneja, Arshpreet Kalsi, and Alok Tandon for their contribution in editing the manuscript.
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Mani, S. (2015). Production of Reactive Oxygen Species and Its Implication in Human Diseases. In: Rani, V., Yadav, U. (eds) Free Radicals in Human Health and Disease. Springer, New Delhi. https://doi.org/10.1007/978-81-322-2035-0_1
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DOI: https://doi.org/10.1007/978-81-322-2035-0_1
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