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Reactive oxygen species are implicated in cellular activity to a variety of inflammatory responses including cardiovascular disease. They may also be involved in hearing impairment via cochlear damage induced by elevated sound levels , in ototoxicity of drugs such as cisplatin , and in congenital deafness in both animals and humans.
Termination can occur when two lipid hydroperoxyl radicals (LOO•) react to form peroxide and oxygen (O 2). [3] [clarification needed] Termination can also occur when the concentration of radical species is high. [citation needed] The primary products of lipid peroxidation are lipid hydroperoxides (LOOH). [3]
After being carried in blood to a body tissue in need of oxygen, O 2 is handed off from the heme group to monooxygenase, an enzyme that also has an active site with an atom of iron. [9] Monooxygenase uses oxygen for many oxidation reactions in the body. Oxygen that is suspended in the blood plasma equalizes into the tissue according to Henry's law.
Pro-oxidants are chemicals that induce oxidative stress, either by generating reactive oxygen species or by inhibiting antioxidant systems. [1] The oxidative stress produced by these chemicals can damage cells and tissues, for example, an overdose of the analgesic paracetamol (acetaminophen) can fatally damage the liver, partly through its production of reactive oxygen species.
Production of mitochondrial ROS, mitochondrial ROS. Mitochondrial ROS (mtROS or mROS) are reactive oxygen species (ROS) that are produced by mitochondria. [1] [2] [3] Generation of mitochondrial ROS mainly takes place at the electron transport chain located on the inner mitochondrial membrane during the process of oxidative phosphorylation.
The enzymatic components may directly scavenge active oxygen species or may act by producing the nonenzymatic antioxidants. There are four enzymes that provide the bulk of protection against deleterious reactions involving active oxygen in bacteria: SODs (superoxide dismutases encoded by sodA and sodB ), catalases ( katE and katG ), glutathione ...
The antioxidants catalase, superoxide dismutase, mannitol, and sodium azide in combination with Cu 2+ increased the DNA degradation activity of myricetin. Myricetin was shown to create reactive oxygen species that caused the DNA damage. [1]
Although oxidative phosphorylation is a vital part of metabolism, it produces reactive oxygen species such as superoxide and hydrogen peroxide, which lead to propagation of free radicals, damaging cells and contributing to disease and, possibly, aging and senescence.