Cholesterol is more readily oxidized than phospholipid linoleates in cell membranes to produce cholesterol hydroperoxides

Saito, Yoshiro; Noguchi, Noriko; Niki, Etsuo

doi:10.1016/j.freeradbiomed.2023.12.011

Cited by 3 publications

(1 citation statement)

References 104 publications

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“…Like the proliferation of nuclear fission in an atomic reactor, after absorbing a free radical, PUFAs release more free radicals and propagate oxidation [ 152 ]. By absorbing a free radical without propagation, antioxidants, such as glutathione peroxidase, superoxide dismutase, coenzyme Q10, selenium, vitamin C, Vitamin E, and cholesterol [ 153 , 154 , 155 ], slow the production of reactive species.…”

Section: Dietary Lipids and Oxidative Stressmentioning

confidence: 99%

Paradoxes: Cholesterol and Hypoxia in Preeclampsia

Hart

2024

Biomolecules

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Preeclampsia, a hypertensive disease of pregnancy of unknown etiology, is intensely studied as a model of cardiovascular disease (CVD) not only due to multiple shared pathologic elements but also because changes that develop over decades in CVD appear and resolve within days in preeclampsia. Those affected by preeclampsia and their offspring experience increased lifetime risks of CVD. At the systemic level, preeclampsia is characterized by increased cellular, membrane, and blood levels of cholesterol; however, cholesterol-dependent signaling, such as canonical Wnt/βcatenin, Hedgehog, and endothelial nitric oxide synthase, is downregulated indicating a cholesterol deficit with the upregulation of cholesterol synthesis and efflux. Hypoxia-related signaling in preeclampsia also appears to be paradoxical with increased Hypoxia-Inducible Factors in the placenta but measurably increased oxygen in maternal blood in placental villous spaces. This review addresses the molecular mechanisms by which excessive systemic cholesterol and deficient cholesterol-dependent signaling may arise from the effects of dietary lipid variance and environmental membrane modifiers causing the cellular hypoxia that characterizes preeclampsia.

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Section: Dietary Lipids and Oxidative Stressmentioning

confidence: 99%

Paradoxes: Cholesterol and Hypoxia in Preeclampsia

Hart

2024

Biomolecules

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Vitamin E nomenclature. Is RRR-α-tocopherol the only vitamin E?

Noguchi,

Niki

2024

Free Radical Biology and Medicine

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Iron associated lipid peroxidation in Alzheimer’s disease is increased in lipid rafts with decreased ferroptosis suppressors, tested by chelation in mice

Thorwald

Godoy‐Lugo

Silva

et al. 2023

Preprint

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The role of reactive iron in Alzheimer's Disease (AD) has major gaps. Little is known of AD changes in iron transport, glutathione-mediated oxidative repair, and associations with ApoE alleles. Intravascular blood was minimized by washing minced postmortem brains. HNE from iron-associated lipid peroxidation was increased in AD prefrontal cortex by 50% for whole tissue and subcellular lipid rafts, where Aβ-peptides are produced. Proteins mediating iron deposition and oxidative repair were extensively altered by AD. Protein oxidation was proportionate to the iron storage protein ferritin light chain (FTL); both higher in ApoE4. Loss of neurons and synapses in AD was proportionate to FTL. Iron transport was impaired with lower transferrin, transferrin receptor, and ferroportin. AD decreased Ferroptosis suppressor protein 1 and glutamate cysteine ligase modulator subunit (GCLM), which regulates glutathione synthesis. These findings provide a mechanistic framework for iron-associated neurodegeneration during AD through impairment of lipid peroxidation repair mechanisms involving glutathione.

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Cholesterol is more readily oxidized than phospholipid linoleates in cell membranes to produce cholesterol hydroperoxides

Cited by 3 publications

References 104 publications

Paradoxes: Cholesterol and Hypoxia in Preeclampsia

Paradoxes: Cholesterol and Hypoxia in Preeclampsia

Vitamin E nomenclature. Is RRR-α-tocopherol the only vitamin E?

Iron associated lipid peroxidation in Alzheimer’s disease is increased in lipid rafts with decreased ferroptosis suppressors, tested by chelation in mice

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