Lipid peroxidation in cell death
By M. Gaschler, Brent R. Stockwell. Biochemical and Biophysical Research Communications - BBRC, 2017
1,598 citations recorded by the source corpus.
Disruption of redox homeostasis is a key phenotype of many pathological conditions. Though multiple oxidizing compounds such as hydrogen peroxide are widely recognized as mediators and inducers of oxidative stress, increasingly, attention is focused on the role of lipid hydroperoxides as critical mediators of death and disease. As the main component of cellular membranes, lipids have an indispensible role in maintaining the structural integrity of cells. Excessive oxidation of lipids alters the physical properties of cellular membranes and can cause covalent modification of proteins and nucleic acids. This review discusses the synthesis, toxicity, degradation, and detection of lipid peroxides in biological systems. Additionally, the role of lipid peroxidation is highlighted in disease and death, and strategies to control the accumulation of lipid peroxides are discussed.
Subfields: Biochemistry, Computational Theory and Mathematics, Organic Chemistry
View Paper: https://www.semanticscholar.org/paper/5d817cedaf5aee754f6bb18e7fa21be21ff1d7a5
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In Organic Chemistry
Citations in the corpus
- On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death (2017, neutral): “9,12,13 The accumulation of cellular LOOH occurs by two primary mechanisms: an iron-catalyzed spontaneous peroxyl radical-mediated process called autoxidation 14,15 and enzyme-mediated processes catalyzed by (non-heme) iron-dependent lipoxyge-nases (LOXs).”
- Neuronal Cell Death. (2018, neutral): “The hydroxyl radical can react with membrane lipids and, via a chain reaction, generate multiple lipid peroxides that can be neurotoxic (123, 237).”
- Antioxidative and Anti-Inflammatory Properties of Cannabidiol (2019, background): “In this situation, one of the most important processes is lipid peroxidation, which results in the oxidation of polyunsaturated fatty acids (PUFA), such as arachidonic, linoleic, linolenic, eicosapentaenoic, and docosahexaenoic acids [42].”
- Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases (2018, background): “These compounds help in scavenging the species that initiate the peroxidation, breaking the autoxidative chain reaction, quenching •O−2 , and preventing the formation of peroxides (Gaschler and Stockwell, 2017).”
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “237,239‐241 Unlike saturated fatty acids and monounsaturated fatty acids, PUFAs have bis‐allylic hydrogen atoms that are prone to free radical‐ as well as enzyme‐mediated oxidation.(242) PUFA oxidation is a critical step in ferroptosis during cellular response to diverse stimuli.”
- Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “72,81 In this process, once the initial phospholipid hydroperoxides (PLOOHs) are generated (via enzymatic reactions or other cellular metabolic processes) and are not promptly reduced by GPX4, they can interact with ferrous iron to yield alkoxyl and peroxyl radicals (Fenton reaction), initiating…”
- Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, neutral): “Lipid peroxides decompose into reactive derivatives, including aldehydes and Michael acceptors, which can react with proteins and nucleic acids (Gaschler and Stockwell, 2017).”
- Imidazole ketone erastin induces ferroptosis and slows tumor growth in a mouse lymphoma model (2019, background): “Most free fatty acids (10 mM) sensitized cells to ferroptosis, while oleic acid and palmitoleic acid (10 mM) protected against ferroptosis, which might be due to the fact that these two fatty acids lack bis-allylic sites, which are the sites for lipid peroxidation initiation (Gaschler and Stockwell,”