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Organelle-specific regulation of ferroptosis.
Chen, X, Kang, R, Kroemer, G, Tang, D
Cell death and differentiation. 2021;(10):2843-2856
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Abstract
Ferroptosis, a cell death modality characterized by iron-dependent lipid peroxidation, is involved in the development of multiple pathological conditions, including ischemic tissue damage, infection, neurodegeneration, and cancer. The cellular machinery responsible for the execution of ferroptosis integrates multiple pro-survival or pro-death signals from subcellular organelles and then 'decides' whether to engage the lethal process or not. Here, we outline the evidence implicating different organelles (including mitochondria, lysosomes, endoplasmic reticulum, lipid droplets, peroxisomes, Golgi apparatus, and nucleus) in the ignition or avoidance of ferroptosis, while emphasizing their potential relevance for human disease and their targetability for pharmacological interventions.
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Posttranslational Modifications in Ferroptosis.
Wei, X, Yi, X, Zhu, XH, Jiang, DS
Oxidative medicine and cellular longevity. 2020;:8832043
Abstract
Ferroptosis was first coined in 2012 to describe the form of regulated cell death (RCD) characterized by iron-dependent lipid peroxidation. To date, ferroptosis has been implicated in many diseases, such as carcinogenesis, degenerative diseases (e.g., Huntington's, Alzheimer's, and Parkinson's diseases), ischemia-reperfusion injury, and cardiovascular diseases. Previous studies have identified numerous targets involved in ferroptosis; for example, acyl-CoA synthetase long-chain family member 4 (ACSL4) and p53 induce while glutathione peroxidase 4 (GPX4) and apoptosis-inducing factor mitochondria-associated 2 (AIFM2, also known as FSP1) inhibit ferroptosis. At least three major pathways (the glutathione-GPX4, FSP1-coenzyme Q10 (CoQ10), and GTP cyclohydrolase-1- (GCH1-) tetrahydrobiopterin (BH4) pathways) have been identified to participate in ferroptosis regulation. Recent advances have also highlighted the crucial roles of posttranslational modifications (PTMs) of proteins in ferroptosis. Here, we summarize the recently discovered knowledge regarding the mechanisms underlying ferroptosis, particularly the roles of PTMs in ferroptosis regulation.
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Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: focusing on mitochondria.
Zhong, H, Yin, H
Redox biology. 2015;:193-9
Abstract
Oxidative stress-induced lipid peroxidation has been associated with human physiology and diseases including cancer. Overwhelming data suggest that reactive lipid mediators generated from this process, such as 4-hydroxynonenal (4-HNE), are biomarkers for oxidative stress and important players for mediating a number of signaling pathways. The biological effects of 4-HNE are primarily due to covalent modification of important biomolecules including proteins, DNA, and phospholipids containing amino group. In this review, we summarize recent progress on the role of 4-HNE in pathogenesis of cancer and focus on the involvement of mitochondria: generation of 4-HNE from oxidation of mitochondria-specific phospholipid cardiolipin; covalent modification of mitochondrial proteins, lipids, and DNA; potential therapeutic strategies for targeting mitochondrial ROS generation, lipid peroxidation, and 4-HNE.
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Lipids and proteins--major targets of oxidative modifications in abiotic stressed plants.
Anjum, NA, Sofo, A, Scopa, A, Roychoudhury, A, Gill, SS, Iqbal, M, Lukatkin, AS, Pereira, E, Duarte, AC, Ahmad, I
Environmental science and pollution research international. 2015;(6):4099-121
Abstract
Stress factors provoke enhanced production of reactive oxygen species (ROS) in plants. ROS that escape antioxidant-mediated scavenging/detoxification react with biomolecules such as cellular lipids and proteins and cause irreversible damage to the structure of these molecules, initiate their oxidation, and subsequently inactivate key cellular functions. The lipid- and protein-oxidation products are considered as the significant oxidative stress biomarkers in stressed plants. Also, there exists an abundance of information on the abiotic stress-mediated elevations in the generation of ROS, and the modulation of lipid and protein oxidation in abiotic stressed plants. However, the available literature reflects a wide information gap on the mechanisms underlying lipid- and protein-oxidation processes, major techniques for the determination of lipid- and protein-oxidation products, and on critical cross-talks among these aspects. Based on recent reports, this article (a) introduces ROS and highlights their relationship with abiotic stress-caused consequences in crop plants, (b) examines critically the various physiological/biochemical aspects of oxidative damage to lipids (membrane lipids) and proteins in stressed crop plants, (c) summarizes the principles of current technologies used to evaluate the extent of lipid and protein oxidation, (d) synthesizes major outcomes of studies on lipid and protein oxidation in plants under abiotic stress, and finally, (e) considers a brief cross-talk on the ROS-accrued lipid and protein oxidation, pointing to the aspects unexplored so far.
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The formation of lipid hydroperoxide-derived amide-type lysine adducts on proteins: a review of current knowledge.
Kato, Y
Sub-cellular biochemistry. 2014;:21-39
Abstract
Lipid peroxidation is an important biological reaction. In particular, polyunsaturated fatty acid (PUFA) can be oxidized easily. Peroxidized lipids often react with other amines accompanied by the formation of various covalent adducts. Novel amide-type lipid-lysine adducts have been identified from an in vitro reaction mixture of lipid hydroperoxide with a protein, biological tissues exposed to conditions of oxidative stress and human urine from a healthy person. In this chapter, the current knowledge of amide type adducts is reviewed with a focus on the evaluation of functional foods and diseases with a history of discovery of hexanoyl-lysine (HEL). Although there is extensive research on HEL and other amide-type adducts, the mechanism of generation of the amide bond remains unclear. We have found that the decomposed aldehyde plus peroxide combined with a lysine moiety does not fully explain the formation of the amide-type lipid-lysine adduct that is generated by lipid hydroperoxide. Singlet oxygen or an excited state of the ketone generated from the lipid hydroperoxide may also contribute to the formation of the amide linkage. The amide-adducts may prove useful not only for the detection of oxidative stress induced by disease but also for the estimation of damage caused by an excess intake of PUFA.
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Do n-3 polyunsaturated fatty acids increase or decrease lipid peroxidation in humans?
Kelley, NS, Yoshida, Y, Erickson, KL
Metabolic syndrome and related disorders. 2014;(8):403-15
Abstract
UNLABELLED Abstract Background: Despite many known health benefits of n-3 polyunsaturated fatty acids (PUFA), there is a concern that their high degree of unsaturation may actually increase oxidative stress, lipid peroxidation (LPO), and chronic inflammatory diseases. METHODS In this review, we have analyzed results from published human studies regarding the effects of n-3 PUFA supplementation on markers of lipid peroxidation. RESULTS Of the 22 published human studies, nine found no change, eight a decrease, and five an increase in markers of LPO. These inconsistencies may be due to methods, subject characteristics, dose, duration, fatty acid and antioxidant composition of supplements, and basal diets. METHODS used for analysis seem to be the most significant factor. Six of eight studies with a decrease in LPO determined F2-isoprostanes produced in vivo, and two determined plasma antioxidant capacity or hydroperoxides. n-3 PUFA can serve as scavengers for free radicals and also modulate expression of genes that determine the balance between oxidative and antioxidative status. Recent studies that monitored oxidation products of cholesterol and fatty acids support the hypothesis that n-3 PUFA decrease LPO. Most of the studies showing no change or increase in LPO determined markers that involved ex vivo sample preparation or oxidation (malondialdehyde, low-density lipoprotein oxidation, lipid hydroperoxides). CONCLUSION A majority of studies do not indicate that n-3 PUFA increased LPO. Future studies need to investigate the effects of dose, duration, and composition of n-3 PUFA with standardized diets and methods on concentrations and types of LPO products produced.
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Lipid hydroperoxide-derived adduction to amino-phospholipid in biomembrane.
Hisaka, S, Osawa, T
Sub-cellular biochemistry. 2014;:41-8
Abstract
Phospholipids such as phosphatidylethanolamine and phosphatidylcholine play crucial roles in the biological system to maintain the cellular environmental condition. Despite that, oxidative stress targets these phospholipids containing polyunsaturated fatty acids and accompanies the oxidized phospholipids. Recent studies have been suggested that oxidized phospholipids have the relationship with inflammation and might induce the atherosclerosis formation by uptake of oxidized LDL through scavenger receptor as ligands. Red blood cells, which have been studied the bilayer model, are also modified by oxidative stress because hemoglobin can mediate and produce the reactive oxygen species, which leads to lipid peroxidation of biomembrane. In these oxidation processes of biomolecules, hexanoylation against phosphatidylethanolamine and phosphatidylserine, which has the primary amine and is the target of this modification, generates the oxidized membrane such as erythrocyte ghosts. This unique structure of phosphatidylethanolamine and phosphatidylserine is possibly the useful biomarker to evaluate the oxidation of biomembrane in vivo using liquid chromatography tandem mass spectrometry and monoclonal antibody.
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Plasma lipoproteins as mediators of the oxidative stress induced by UV light in human skin: a review of biochemical and biophysical studies on mechanisms of apolipoprotein alteration, lipid peroxidation, and associated skin cell responses.
Filipe, P, Morlière, P, Silva, JN, Mazière, JC, Patterson, LK, Freitas, JP, Santus, R
Oxidative medicine and cellular longevity. 2013;:285825
Abstract
There are numerous studies concerning the effect of UVB light on skin cells but fewer on other skin components such as the interstitial fluid. This review highlights high-density lipoprotein (HDL) and low-density lipoprotein (LDL) as important targets of UVB in interstitial fluid. Tryptophan residues are the sole apolipoprotein residues absorbing solar UVB. The UVB-induced one-electron oxidation of Trp produces (•)Trp and (•)O2 (-) radicals which trigger lipid peroxidation. Immunoblots from buffered solutions or suction blister fluid reveal that propagation of photooxidative damage to other residues such as Tyr or disulfide bonds produces intra- and intermolecular bonds in apolipoproteins A-I, A-II, and B100. Partial repair of phenoxyl tyrosyl radicals (TyrO(•)) by α -tocopherol is observed with LDL and HDL on millisecond or second time scales, whereas limited repair of α -tocopherol by carotenoids occurs in only HDL. More effective repair of Tyr and α -tocopherol is observed with the flavonoid, quercetin, bound to serum albumin, but quercetin is less potent than new synthetic polyphenols in inhibiting LDL lipid peroxidation or restoring α -tocopherol. The systemic consequences of HDL and LDL oxidation and the activation and/or inhibition of signalling pathways by oxidized LDL and their ability to enhance transcription factor DNA binding activity are also reviewed.
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Berries: emerging impact on cardiovascular health.
Basu, A, Rhone, M, Lyons, TJ
Nutrition reviews. 2010;(3):168-77
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Abstract
Berries are a good source of polyphenols, especially anthocyanins, micronutrients, and fiber. In epidemiological and clinical studies, these constituents have been associated with improved cardiovascular risk profiles. Human intervention studies using chokeberries, cranberries, blueberries, and strawberries (either fresh, or as juice, or freeze-dried), or purified anthocyanin extracts have demonstrated significant improvements in LDL oxidation, lipid peroxidation, total plasma antioxidant capacity, dyslipidemia, and glucose metabolism. Benefits were seen in healthy subjects and in those with existing metabolic risk factors. Underlying mechanisms for these beneficial effects are believed to include upregulation of endothelial nitric oxide synthase, decreased activities of carbohydrate digestive enzymes, decreased oxidative stress, and inhibition of inflammatory gene expression and foam cell formation. Though limited, these data support the recommendation of berries as an essential fruit group in a heart-healthy diet.
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Lipid peroxidation in relation to ageing and the role of endogenous aldehydes in diabetes and other age-related diseases.
Dmitriev, LF, Titov, VN
Ageing research reviews. 2010;(2):200-10
Abstract
Lipid intermediates which are generated by ROS have drawn more attention after it was found that lipid peroxidation and lipid-radical cycles are two alternative processes. In biological membranes alpha-tocopherol and cytochrome b5, as known, act synergistically to overcome free radical injury and to form lipid-radical cycles. These cycles activate membrane proteins, protect membrane lipids from oxidation and prevent from formation of endogenous aldehydes. Experimental and clinical evidence accumulated for 5-6 years suggests that endogenous aldehydes, such as malonic dialdehyde (MDA) and methylglyoxal (MG), are the major initiators of the metabolic disorders. The age-related diseases emerge when cells cannot control formation of aldehydes and/or cannot abolish the negative effect of methylglyoxal on their metabolism. If the efficiency of the glyoxalase system is insufficient toxic aldehydes cause cumulative damage over a lifetime. In this paper, we provide evidence to consider ageing as a process in which lipid-radical cycles gradually substitute for lipid peroxidation. There are always two opposing tendencies or actions which counteract each other - actions of melatonin, lipid-radical cycles and the glyoxalase system (anti-ageing effect) and negative actions of the toxic aldehydes (pro-ageing effect). Life span is determined by the balance of two opposing processes.