LDL and HDL Oxidation and Fatty Acid Composition in Vegetarians

Nagyová, A; Krajcovicová-Kudlácková, M; Klvanová, J

doi:10.1159/000046722

Cited by 20 publications

(15 citation statements)

References 12 publications

(10 reference statements)

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“…This finding supports the hypothesis that HDL is more susceptible to oxidation than LDL (43,44). This may relate to the higher antioxidant content of LDL (7,45), which delays lipid peroxide formation.…”

Section: Discussionsupporting

confidence: 87%

HDL is the major lipoprotein carrier of plasma F2-isoprostanes

Proudfoot

Barden

Loke

et al. 2009

Journal of Lipid Research

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Section: Discussionsupporting

confidence: 87%

HDL is the major lipoprotein carrier of plasma F2-isoprostanes

Proudfoot

Barden

Loke

et al. 2009

Journal of Lipid Research

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“…Such a relation has been already shown in humans fed sunflower oil (38). It was then related to the value of the PI: This latter parameter indeed accurately reflects the degree of unsaturation of FA and estimates the concentration of bisallylic hydrogen atoms able to interact with free radicals (23). This could explain why the production of CD in lipoproteins tended to be higher in steers given linseed oil (18:3n-3) than in steers given sunflower oil (18:2n-6).…”

Section: Discussionmentioning

confidence: 54%

Effect of dietary n−6 and n−3 polyunsaturated fatty acids on peroxidizability of lipoproteins in steers

Scislowski¹,

Bauchart²,

Gruffat³

et al. 2005

Lipids

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The susceptibility of major plasma lipoproteins to lipoperoxidation was studied in relation to the FA composition of their neutral and polar lipids in steers given PUFA-rich diets. Two trials used, respectively, 18 ("sunflower" experiment, S) or 24 ("linseed" experiment, L) crossbred Salers x Charolais steers. Each involved three dietary treatments over a 70-d period: a control diet (CS or CL diets) consisting of hay and concentrate, or the same diet supplemented with oilseeds (4% diet dry matter) fed either as seeds (SS or LS diets) or continuously infused into the duodenum (ISO or ILO diets). Compared with control diets, ISO and ILO treatments tended to decrease the resistance time of LDL and HDL classes to peroxidation, mainly owing to the enrichment of their polar and neutral lipids with PUFA. With diets SS and LS, sensitivity of major lipoprotein classes (LDL, light and heavy HDL) was not affected because ruminal hydrogenation of dietary PUFA decreased their incorporation into lipoparticles. ISO and ILO treatments induced a more important production of conjugated dienes and hydroperoxides generated by peroxidation in the three lipoprotein classes due to the higher amounts of PUFA esterified in lipids of the core and the hydrophilic envelope of particles. The production of malondialdehyde (MDA) increased in steers fed linseed supplements, indicating that MDA production did not occur with linoleic acid provided by sunflower oil supplements. Thus, plasma peroxidation of PUFA generates toxic products in steers fed diets supplemented with PUFA and can be deleterious for the health of the animal during long-term treatment.

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“…This is primarily because IsoP is a primary measure of lipid peroxidation. Specifically, HDL is the major lipoprotein carrier for IsoP (Proudfoot et al, 2009) and is more susceptible to oxidation than LDL (Raveh et al, 2000;Nagyova et al, 2001), which is consistent with the observed positive correlation with IsoP in the standard care patient group over 12 months. Blood lipids may present a biological influence on plasma IsoP concentration, and therefore may need to be considered for the interpretation of oxidative stress.…”

Section: Discussionsupporting

confidence: 82%

Identification of potential mediators of oxidative damage and targets for novel treatments for chronic kidney disease

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Chronic kidney disease (CKD) is a common and serious problem causing a significant burden to healthcare systems and, most importantly, the affected individual. Despite this, few successful treatments exist for CKD. Understanding the pathophysiological features that are common to chronic kidney pathologies is vital to identify targets for treatment. Oxidative stress has been implicated in all chronic diseases, acting via highly conserved pathways of disease progression.However, evidence to date shows limited benefit of antioxidants as therapies for CKD patients, suggesting a need to better identify the pathways that are stimulated.This thesis focuses on the role of oxidative stress, the regulation of mitochondrial homeostasis, the action of antioxidant compounds, and the disruption of oxidant signalling networks in chronic kidney pathologies (reviewed in Chapter 1). The aims of this project were to: (1) to use an in vitro model of oxidative stress-induced kidney injury to determine how a failure in balance between oxidative stress and oxidant control causes the cellular characteristics of CKD, then to determine whether exogenous antioxidants can prevent and restore renal cell bioenergetics and reduce cell injury; (2) to use an in vivo model of oxidative stress-induced kidney injury with molecular and metabolic imaging to measure potential biomarkers identified in Aim 1, in association with changes in kidney structure and function, and determine whether treatment with an antioxidant therapy modulates kidney disease pathology; and (3) to explore the links between biomarkers of oxidative stress and clinical characteristics of CKD in patients to determine whether a lifestyle intervention in conjunction with standard nephrology care improve systemic oxidative stress and whether this influences kidney function. The renal specific in vitro, in vivo, and clinical models and the methods used are explained in Chapter 2.Chapter 3 reports the separate and cumulative effects of oxidative stress, mitochondrial dysfunction and cell senescence in promoting loss of renal cells in an in vitro model of kidney disease. The results demonstrate that oxidative stress and cell senescence cause mitochondrial destabilization and kidney tubular epithelial cell loss. This may contribute to the development of cellular and tissue atrophy seen in CKD.Chapter 4 further defines the role of mitochondrial alterations as a consequence of a specificallyimpaired oxidant signalling regulatory mechanism, namely, peroxisome proliferator-activated receptor-gamma (PPARγ)-regulated mitochondrial biogenesis. Oxidative stress promoted mitochondrial destabilisation in kidney proximal tubular epithelial cells, in association with ii increased PPARγ Serine 112 phosphorylation. Despite their positive effects in other tissues, PPARγ agonists failed to protect proximal tubular epithelial (PTE) cells, and appear to be detrimental to kidney PTE cell health when oxidative stress induces the cell damage.Chapter 5 examined mediators of oxidative stress in an in...

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LDL and HDL Oxidation and Fatty Acid Composition in Vegetarians

Cited by 20 publications

References 12 publications

HDL is the major lipoprotein carrier of plasma F2-isoprostanes

HDL is the major lipoprotein carrier of plasma F2-isoprostanes

Effect of dietary n−6 and n−3 polyunsaturated fatty acids on peroxidizability of lipoproteins in steers

Identification of potential mediators of oxidative damage and targets for novel treatments for chronic kidney disease

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