Cellular antioxidant enzymes such as catalase and superoxide dismutase are naturally occurring mechanisms to regulate ROS levels. ĭisruption of the antioxidant system can promote the development of chronic inflammation. Previous evidence established that the mitochondrial DNA (mtDNA) leakage could activate Toll-like receptor 9 (TLR9) in the endosome, leading to an inflammatory response via the initiation of myeloid differentiation primary response 88 (MYD88) adaptor protein. Moreover, ROS-induced mitochondrial damage promotes the release of double stranded double stranded DNA (dsDNA) to the cytosol and becomes a crucial driver of inflammation via DNA sensor pathways, leading to the inflammatory response. However, mitochondrial oxidative metabolism is a major source of ROS production. It is well-established that ROS are produced by various cellular compartments, including mitochondria, the cytosol, the cell membrane, the endoplasmic reticulum and peroxisomes. Furthermore, a decrease in the antioxidant system leads to increased cellular and molecular damage, resulting in tissue injury. Oxidative stress is generated by the elevated exhibition of reactive oxygen species (ROS), including hydrogen peroxide, superoxide radicals, peroxynitrite and hydroxyl radicals.
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