Dynamics of oxidation of LDL and its inhibition by antioxidants

Niki, Etsuo; Noguchi, Noriko

doi:10.1002/biof.5520060214

Cited by 5 publications

(4 citation statements)

References 79 publications

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“…MDA, a secondary product of lipid peroxidation, is used as an indicator of tissue damage [53]. Aging has been reported to be associated with increased disruption of membrane lipids leading to subsequent formation of peroxide radicals [54]. A higher plasma lipid peroxidation was found in aged rats when compared to the younger ones [55].…”

Section: Discussionmentioning

confidence: 99%

The effects of caffeic acid phenethyl ester and melatonin on age‐related vascular remodeling and cardiac damage

Eşrefoğlu¹,

Gül²,

Ateş³

et al. 2010

Fundamemntal Clinical Pharma

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Oxidative stress has been implicated with cardiovascular aging. Most antioxidant intervention studies have involved long-term treatments as a potential means to eliminate age-related oxidative damage in many systems. In the present study, not only light and electron microscopic pictures of the heart and thoracic aorta of young and aged and, caffeic acid phenethyl ester (CAPE) and melatonin and administered aged Sprague Dawley rats, but also antioxidant system status was evaluated. Significantly elevated levels of malondialdehyde (MDA) were observed in the heart and thoracic aorta of aged rats (P<0.05 and P<0.001, respectively). Chronic melatonin and CAPE administration significantly reduced the levels of MDA in the heart (P=0.005 and P=0.05, respectively) and thoracic aorta (P<0.001 and P<0.05, respectively) of aged animals. Additionally, melatonin and CAPE were efficient in stimulating the activities and increasing the levels of the antioxidant enzymes in the heart and aorta. Prominent electron microscopic alterations in cardiac myocytes such as nuclear irregularity, mitochondrial degeneration, myofilament disorganization and disruption, and lipofuscin accumulation were observed in aged rats. The main age-related histologic modifications observed in aorta were irregularity in endothelial cells and their nuclei, divergence of endothelial cells from basement membrane and neighboring cells, and elastic fibril fragmentation and reduction. Melatonin and CAPE obviously reduced these alterations in both heart and aorta of aged rats. Taking the results together, we suggest that supplemental administration of CAPE and melatonin is beneficial in delaying age-related cellular damage in cardiovascular system.

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Section: Discussionmentioning

confidence: 99%

The effects of caffeic acid phenethyl ester and melatonin on age‐related vascular remodeling and cardiac damage

Eşrefoğlu¹,

Gül²,

Ateş³

et al. 2010

Fundamemntal Clinical Pharma

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“…Lipid peroxidation includes peroxidation of phospholipid and CE at the polyunsaturated fatty acid moieties. This process generates more reactive aldehyde products and metabolites including malondialdehyde and 4-hydroxynoneal which are linked to ApoB, phosphatidylserine, and phosphatidylethanolamine, through building adduct with Schiff-base lysine residue ( Niki and Noguchi, 1997 ; Khatana et al, 2020 ). In general, CE 18:2 hydroperoxide, CE 18:2 hydroxide, phosphatidylcholine hyderoperoxide, ketone, oxidized ApoB, oxidized sphingomyelin, and 7-ketocholesterol are major oxidized components of ox-LDL ( Yoshida and Kisugi, 2010 ; Khatana et al, 2020 ).…”

Section: Atherogenic Mechanisms Of Ldlmentioning

confidence: 99%

Low-density lipoprotein particles in atherosclerosis

2022

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Among the diseases causing human death, cardiovascular disease (CVD) remains number one according to the World Health Organization report in 2021. It is known that atherosclerosis is the pathological basis of CVD. Low-density lipoprotein (LDL) plays a pivotal role in the initiation and progression of atherosclerotic CVD (ASCVD). LDL cholesterol (LDL-C) is the traditional biological marker of LDL. However, large numbers of patients who have achieved the recommended LDL-C goals still have ASCVD risk. In multiple prospective studies, LDL particle (LDL-P) is reported to be more accurate in predicting CVD risk than LDL-C. LDL-Ps differ in size, density and chemical composition. Numerous clinical studies have proved that the atherogenic mechanisms of LDL-Ps are determined not only by LDL number and size but also by LDL modifications. Of note, small dense LDL (sdLDL) particles possess stronger atherogenic ability compared with large and intermediate LDL subfractions. Besides, oxidized LDL (ox-LDL) is another risk factor in atherosclerosis. Among the traditional lipid-lowering drugs, statins induce dramatic reductions in LDL-C and LDL-P to a lesser extend. Recently, proprotein convertase subtilsin/kexin type 9 inhibitors (PCSK9i) have been demonstrated to be effective in lowering the levels of LDL-C, LDL-P, as well as CVD events. In this article, we will make a short review of LDL metabolism, discuss the discordance between LDL-C and LDL-P, outline the atherogenic mechanisms of action of LDL by focusing on sdLDL and ox-LDL, summarize the methods used for measurement of LDL subclasses, and conclude the advances in LDL-lowering therapies using statins and PCSK9i.

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“…The protein moiety of LDL may be directly oxidized at tyrosine residues, e.g., by PMN-derived hypochlorous acid [24], or by peroxynitrite [38]. More importantly, free radical intermediates of lipid peroxidation [58], malondialdehyde [3,15] and the reactive alkenals [25], form adducts with the protein moiety of LDL, as inter alia evident from the loss of lysine residues in apolipoprotein B100 [58].…”

Section: Introductionmentioning

confidence: 99%

13‐HPODE and 13‐HODE modulate cytokine‐induced expression of endothelial cell adhesion molecules differently

et al. 1999

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Expression of cellular adhesion molecules (CAMs) at endothelial surfaces represents a physiological response to vascular damage and mediates the initiation of inflammation and possibly of atherogenesis. The cytokines TNF alpha and IL-1 are potent inducers of CAMs in endothelial cells. Reactive oxygen species comprising lipid oxidation products have been implicated in the signaling pathways of both TNF alpha and IL-1 and accordingly could modulate atherogenic events. We, therefore, investigated the potential role of the lipoxygenase product, 13-hydroperoxyoctadecadienoic acid (13-HPODE), which has also been identified in oxidized low density lipoproteins on CAM expression in HUVEC. 13-HPODE induced the expression of ICAM-1 in a concentration dependent manner up to 75 microM. Higher concentrations were toxic. Similar effects were observed with H2O2 and phosphatidylcholine hydroperoxide. VCAM-1 and E-selectin were not induced by 13-HPODE. 13-HPODE administered simultaneously with IL-1 or TNF alpha induced ICAM-1 additively, suggesting that hydroperoxides and cytokines act on the same signaling pathways. In contrast, pretreatment of cells with 50 microM 13-HPODE for 1 hour rather inhibited subsequent cytokine-induced ICAM-1 and E-selectin expression. Surprisingly, the reduction product of 13-HPODE, 13-hydroxyoctadecadienoic acid (13-HODE) proved to be an even better inducer of ICAM-1 than 13-HPODE. Pretreatment with 13-HODE did not show any inhibitory effect on ICAM-1 expression. Our data show that lipoxygenase products differentially affect CAM expression. 13-HPODE is stimulatory by itself and can positively or negatively affect cytokine signaling depending on time of exposure. 13-HODE induces CAM expression by itself but does not inhibit cytokine signaling. Thus, the interplay of lipoxygenase products with proinflammatory cytokines can not simply be explained by an oxidant-mediated facilitation of cytokine signaling.

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Dynamics of oxidation of LDL and its inhibition by antioxidants

Cited by 5 publications

References 79 publications

The effects of caffeic acid phenethyl ester and melatonin on age‐related vascular remodeling and cardiac damage

The effects of caffeic acid phenethyl ester and melatonin on age‐related vascular remodeling and cardiac damage

Low-density lipoprotein particles in atherosclerosis

13‐HPODE and 13‐HODE modulate cytokine‐induced expression of endothelial cell adhesion molecules differently

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