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Ferroptosis is biochemically, genetically, and morphologically distinct from other forms of regulated cell death such as apoptosis and necroptosis. [1] Oxytosis/ferroptosis can be initiated by the failure of the glutathione-dependent antioxidant defenses, resulting in unchecked lipid peroxidation and eventual cell death. [2]
Lipid peroxidation, or lipid oxidation, is a complex chemical process that leads to oxidative degradation of lipids, [1] resulting in the formation of peroxide and hydroperoxide derivatives. [2] It occurs when free radicals , specifically reactive oxygen species (ROS), interact with lipids within cell membranes , typically polyunsaturated fatty ...
The damage is largely due to iron-catalyzed oxidative reactions. Iron can exchange electrons with a variety of substrates, which can lead to generation of reactive oxygen species. This can lead to oxidative stress, lipid peroxidation, and DNA damage, which may result in cell death. [4]
The antioxidant enzyme glutathione peroxidase 4 (GPX4) belongs to the family of glutathione peroxidases, which consists of 8 known mammalian isoenzymes (GPX1–8).GPX4 catalyzes the reduction of hydrogen peroxide, organic hydroperoxides, and lipid peroxides at the expense of reduced glutathione and functions in the protection of cells against oxidative stress.
These compounds affect cellular membrane function, in part by inducing lipid peroxidation and by causing lipid damage. [9] The alteration of ion components in the cell and the breakdown of cellular components in the presence of ROS result in the death of affected cells, as well as the formation of local lesions.
Another method of termination is the reaction between a lipid radical and a lipid peroxide, or the combination of two lipid peroxide molecules, resulting in stable nonreactive molecules. [4] [5] Reinforced lipids that become part of the membrane if consumed with heavy isotope diet also inhibit peroxidation. [6]
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
Cells treated with erastin are deprived of cysteine and are unable to synthesize the antioxidant glutathione. Depletion of glutathione eventually leads to excessive lipid peroxidation and cell death. Erastin was first described in 2003. Its name is short for "eradicator of RAS and ST-expressing cells". [4]