Abstract
Superoxide is a primary oxygen radical that is produced when an oxygen molecule receives one electron. Superoxide dismutase (SOD) plays a primary role in the cellular defense against an oxidative insult by ROS. However, the resulting hydrogen peroxide is still reactive and, in the presence of free ferrous iron, may produce hydroxyl radicals and exacerbate diseases. Polyunsaturated fatty acids are the preferred target of hydroxyl radicals. Ferroptosis, a type of necrotic cell death induced by lipid peroxides in the presence of free iron, has attracted considerable interest because of its role in the pathogenesis of many diseases. Radical electrons, namely those released from mitochondrial electron transfer complexes, and those produced by enzymatic reactions, such as lipoxygenases, appear to cause lipid peroxidation. While GPX4 is the most potent anti-ferroptotic enzyme that is known to reduce lipid peroxides to alcohols, other antioxidative enzymes are also indirectly involved in protection against ferroptosis. Moreover, several low molecular weight compounds that include α-tocopherol, ascorbate, and nitric oxide also efficiently neutralize radical electrons, thereby suppressing ferroptosis. The removal of radical electrons in the early stages is of primary importance in protecting against ferroptosis and other diseases that are related to oxidative stress.
Highlights
The liver is the main organ for the detoxification of drugs or xenobiotics and is prone to damage due to them being present in excess, which may be associated with non-alcoholic liver diseases [40]
Because lipid peroxidation occurs in a variety of pathogenic conditions with elevated reactive oxygen species (ROS) production, it is conceivable that ferroptosis could be involved in a variety of diseases that include the aggravation of ischemic diseases and neurodegenerative diseases [153]
We found that a long-lasting Nitric oxide (NO) donor effectively suppressed the ferroptosis that is induced in mouse hepatoma-derived Hepa16 cells under Cys deprivation cultures, xCT inhibition, and GPX4 inhibition [244]
Summary
The free energy that is released from organic compounds by oxidation supports animal life. While antioxidant compounds or enzymes can protect against oxidative damage, the excessive elimination of ROS may impair cellular functions via disrupting redox signaling [4]. For these reasons, high levels of ROS and an imbalance between. Our body is protected by a wide range of antioxidative enzymes and compounds that of coordinately act in antioxidation reactions, and their insufficiency enhances the toxic effects of ROS. Superoxide by the action of antioxidative compounds, notably NO and ascorbate (Asc) to maintain redox homeostasis in the mammalian body
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