Lipid Peroxidation in Neurodegeneration

Cháfer-Pericás, Consuelo

doi:10.3390/antiox10030484

Cited by 7 publications

(9 citation statements)

References 7 publications

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“…However, the later products of lipoperoxidation, 8-IsoP-U, was significantly increased in our patients compared to the healthy group. A direct comparison between the levels of the oxidative stress markers analysed in biological fluids and in the CNS was, however, not reliable, as a correlation between the plasma and cerebrospinal fluid has not been confirmed [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…However, our conclusions need to be considered with caution, as correlations between markers of lipid peroxidation in the plasma and cerebrospinal fluid have not been confirmed [ 21 , 40 ]. Markers of oxidative stress are age-dependent, and therefore, the findings in adults may not be confirmed in children and adolescents and vice versa [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…Despite the inconsistency in the results regarding markers of oxidative stress, especially oxidative damage to lipids, the inhibition of oxidative damage to biologically important molecules may reduce disorder progression and severity [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress Markers and Antioxidant Enzymes in Children and Adolescents with Depressive Disorder and Impact of Omega-3 Fatty Acids in Randomised Clinical Trial

et al. 2021

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Oxidative stress (OS) is thought to play a role in mental disorders. However, it is not clear whether the OS is the cause or consequence of the disorder. We investigated markers of oxidative stress (8-isoprostane (8-IsoP-U), lipoperoxides (LP), advanced oxidation protein products (AOPP) and nitrotyrosine (NT)) and antioxidant protection (Trolox equivalent antioxidant capacity (TEAC), activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in 60 paediatric and adolescent patients with depressive disorder (DD) compared to healthy controls. The patients were divided into two groups (1:1). One group received an emulsion of omega-3 fatty acid (FA), and the other group an emulsion of sunflower oil with omega-6 FA for 12 weeks. The levels of 8-IsoP-U, AOPP and NT were increased, and GPx activity was decreased in patients compared to the controls. We found a significant positive correlation of the Children’s Depression Inventory score with NT and a negative correlation with TEAC, SOD and GPx. NT correlated positively with the baseline omega-6/omega-3 FA ratio and a negatively with SOD. A supplementation with omega-3 FA, but not with omega-6 FA, decreased 8-IsoP-U, AOPP, NT levels and increased TEAC and SOD activity. Our results suggest that NT may play a role in the pathophysiology of DD, while elevated isoprostane is likely caused by the high omega-6/omega-3 FA ratio. Omega-3 FA supplementation reduces oxidative stress in patients with DD. This study was registered with the ISRCTN registry (ISRCTN81655012).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Oxidative Stress Markers and Antioxidant Enzymes in Children and Adolescents with Depressive Disorder and Impact of Omega-3 Fatty Acids in Randomised Clinical Trial

et al. 2021

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“…Moreover, lipid peroxidation is a common oxidation reaction of polyunsaturated FA in living organisms. Excessive oxidation products are harmful to proteins, lipids, and nucleic acids, leading to the damage to cellular structure and function (Cháfer-Pericás, 2021). Thereby, reactive oxygen species-induced lipid peroxidation could contribute to chronic diseases, such as cardiovascular disease, diabetes, cancer, and senescence (Clemente et al, 2020;Gianazza et al, 2020;Kuzgun et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Ellagic Acid on Hepatic Lipid Metabolism and Antioxidant Activity in Mice

Tang

et al. 2021

Front. Physiol.

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Accumulating evidence has demonstrated that the imbalance of lipid metabolism and antioxidant capacity leads to damage to liver. The present study aimed to investigate the effects of ellagic acid (EA), a phenolic compound, on hepatic lipid metabolism and antioxidant activity in mice. In our study, 24 C57BL/6J mice were divided into three groups: (1) control (CON); (2) basal diet+0.1% EA (EA1); and (3) basal diet+0.3% EA (EA2). After the 14-day experiment, the liver was sampled for analysis. The results showed that 0.3% EA administration increased the liver weight. Total cholesterol and low-density lipoprotein cholesterol activities decreased and high-density lipoprotein cholesterol activity increased by EA supplementation. Meanwhile, dietary supplementation with EA dose-dependently decreased the acetyl-CoA carboxylase protein abundance and increased the phospho-hormone-sensitive lipase, carnitine palmitoyltransferase 1B, and peroxisome proliferator-activated receptor alpha protein abundances. Moreover, EA supplementation reduced the malonaldehyde concentration and increased the superoxide dismutase and catalase concentrations. The protein abundances of phospho-nuclear factor-E2-related factor 2, heme oxygenase-1, and NAD(P)H: quinone oxidoreductase 1 increased by EA supplementation in a dose-dependent manner. Taken together, EA supplementation promoted the lipid metabolism and antioxidant capacity to maintain the liver health in mice.

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“…Mitochondrial dysfunction with excessive ROS production, autophagy disruption, lipofuscin accumulation, and lipid peroxidation are common pathomechanisms in these disorders. 34,55,115,116,118,119 Indirect evidence of ferroptosis include abnormal levels of iron import, storage, and export proteins indicating iron dyshomeostasis, reduced expression of GSH and other antioxidants, upregulation of the NRF2, and accumulation of products from lipid peroxidation, such as malonyldialdehyde and 4-hydroxynonenal. [16][17][18][19][20][21] A set of iron-responsive elements in 59untranslated regions of mRNA can bind excessive iron and fold mRNA into loops that affect transcription of proteins such as amyloid precursor protein (APP), α-synuclein, and prion protein; many of these proteins interact with iron, which may initiate a potential feedback to accelerate ferroptosis.…”

Section: Role Of Ferroptosis In Neurologic Diseasementioning

confidence: 99%

What Is the Role of Ferroptosis in Neurodegeneration?

Benarroch

2023

Neurology

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Ferroptosis is a unique form of programmed cell death pathway that is mechanistically different from necrosis, apoptosis, or autophagy.1 Ferroptosis is induced by reactive oxygen species (ROS) originating from multiple sources, especially accumulation of free intracellular divalent iron (Fe2+), leading to peroxidation of polyunsaturated fatty acids (PUFAs) and resulting in membrane damage (Figure). One major trigger of ferroptosis is decreased availability of intracellular antioxidant enzymes, particularly glutathione peroxidases (GPXs).1-7 Because of its high lipid concentration and oxygen consumption rate, the nervous tissue is extremely vulnerable to oxidative damage and ferroptosis. With aging, iron accumulates in the brain, which predisposes to and exacerbates these processes.8 Iron promotes ferroptosis both directly and as a cofactor required for the activity of enzymes mediating redox reactions and lipid peroxidation.9,10 Epigenetic regulation can determine cell sensitivity to ferroptosis by affecting intracellular iron levels, oxidative stress, and lipid metabolism.11 Ferroptosis affects all cell types in the nervous system, including neurons, glial cells, and pericytes.12 Microglia are the primary iron-accumulating cells in disease.13,14 Recent evidence indicates that iron-laden microglia have a critical role in ferroptosis associated with neurodegeneration.15 Studies in vitro, in experimental disease models, and in human brain tissue indicate that iron accumulation, oxidative stress, and lipid peroxidation are major disease mechanisms in a wide range of neurologic disorders. These studies also suggest that the different components of the ferroptosis pathway are potential targets for therapeutic intervention. The mechanisms of ferroptosis and its role in neurologic disorders have been the subject of several recent comprehensive reviews.7,8,16-21 Some of these concepts pertinent to neurodegeneration will be emphasized in this study.

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Lipid Peroxidation in Neurodegeneration

Abstract: Neurodegenerative diseases have multiple social and economic impacts on society, and they are the cause of millions of deaths every year [...]

Cited by 7 publications

References 7 publications

Oxidative Stress Markers and Antioxidant Enzymes in Children and Adolescents with Depressive Disorder and Impact of Omega-3 Fatty Acids in Randomised Clinical Trial

Oxidative Stress Markers and Antioxidant Enzymes in Children and Adolescents with Depressive Disorder and Impact of Omega-3 Fatty Acids in Randomised Clinical Trial

The Effect of Ellagic Acid on Hepatic Lipid Metabolism and Antioxidant Activity in Mice

What Is the Role of Ferroptosis in Neurodegeneration?

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