Demonstration of Rapid Onset Vascular Endothelial Dysfunction After Hyperhomocysteinemia

Chambers, John C.; McGregor, Andrew; Jean-Marie, Jeff; Obeid, Omar; Kooner, Jaspal S.

doi:10.1161/01.cir.99.9.1156

Cited by 404 publications

(284 citation statements)

References 27 publications

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“…The modest nature of the increase in plasma antoxidant activity associated with homocysteinelowering may reflect the relatively low plasma mean tHcy concentration in the cohort at baseline. It has been argued that an impaired endothelial function associated with transient elevation in plasma tHcy is mediated by oxidative mechanisms (Kanani et al, 1999;Chambers et al, 1999). The fall in plasma tHcy in response to folate intervention in the study reported here, did not elicit any improvement in endothelial function (to be reported elsewhere) which is consistent with the failure to observe any convincing effects of homocysteine-lowering on antioxidant activity or oxidative damage.…”

Section: Effect On Antioxidant Activitysupporting

confidence: 90%

Reduction in plasma total homocysteine through increasing folate intake in healthy individuals is not associated with changes in measures of antioxidant activity or oxidant damage

et al. 2003

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Background: Various mechanisms have been proposed to explain the association between plasma total homocysteine (tHcy) and risk of cardiovascular disease, including oxidative activity of homocysteine. Objective: To explore the putative role of reactive oxygen species in the association between plasma tHcy and risk of cardiovascular disease in healthy individuals. Design: A double-blind, placebo-controlled crossover intervention to increase folate intake through diet (increased consumption of folate-rich foods) and supplement (400 mg folic acid) was carried out in 126 healthy men and women. Measurements were made of antioxidant activity in red blood cells and plasma, and products of oxidant damage in plasma. Results: Diet and supplement-based interventions led to an increase in measures of folate status and a reduction in plasma tHcy. This was not associated with any significant change in measures of antioxidant activity (plasma and red blood cell glutathione peroxidase activity and red blood cell superoxide dismutase activity) or oxidant damage (plasma malondialdehyde), although an improvement in plasma total antioxidant capacity just failed to reach significance. Conclusions: In healthy individuals lowering plasma tHcy does not have any functional implications regarding oxidative damage.

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Section: Effect On Antioxidant Activitysupporting

confidence: 90%

Reduction in plasma total homocysteine through increasing folate intake in healthy individuals is not associated with changes in measures of antioxidant activity or oxidant damage

et al. 2003

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“…13 In cell culture studies, Hcy induced oxidative stress to endothelium 14 and reduced available nitric oxide, a potent vasodilator. 15 Confirming these observations in humans, endothelium-dependent vasodilatation was impaired in temporary 16,17 or chronic 18,19 HHcy.…”

supporting

confidence: 55%

Plasma homocysteine concentration and blood pressure in healthy Iranian adults: the Tehran Homocysteine Survey (2003–2004)

et al. 2005

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“…2) % in subjects with coronary artery disease (38) . In healthy subjects in whom hyperhomocysteinaemia has been induced with an oral methionine load the reduction in flow-mediated dilation can be ameliorated by pre-treatment with vitamin C supplementation of 1000 mg/d for 1 week (15) . In smokers supplemented with vitamin E (545 mg all-racemic a-tocopherol/d) there is an improvement in flow-mediated vasodilation of 5 .…”

Section: Carotenoids: Flavonoids: Cvd: Laser Doppler Imagingmentioning

confidence: 99%

Effects of chronic and acute consumption of fruit- and vegetable-puree-based drinks on vasodilation, risk factors for CVD and the response as a result of theeNOSG298T polymorphism

et al. 2009

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The average UK adult consumes less than three portions of fruit and vegetables daily, despite evidence to suggest that consuming five portions daily could help prevent chronic diseases. It is recommended that fruit juice should only count as one of these portions, as juicing removes fibre and releases sugars. However, fruit juices contain beneficial compounds such as vitamin C and flavonoids and could be a useful source of dietary phytochemicals. Two randomised controlled cross-over intervention studies investigating the effects of chronic and acute consumption of commercially-available fruit-and vegetable-puree-based drinks (FVPD) on bioavailability, antioxidant status and CVD risk factors are described. Blood and urine samples were collected during both studies and vascular tone was measured using laser Doppler imaging. In the chronic intervention study FVPD consumption was found to significantly increase dietary carotenoids (P = 0 . 001) and vitamin C (P = 0 . 003). Plasma carotenoids were increased (P = 0 . 001), but the increase in plasma vitamin C was not significant. There were no significant effects on oxidative stress, antioxidant status and other CVD risk factors. In the acute intervention study FVPD were found to increase total plasma nitrate and nitrite (P = 0 . 001) and plasma vitamin C (P = 0 . 002). There was no effect on plasma lipids or uric acid, but there was a lower glucose and insulin peak concentration after consumption of the FVPD compared with the sugar-matched control. There was a trend towards increased vasodilation following both chronic and acute FVPD consumption. All volunteers were retrospectively genotyped for the eNOS G298T polymorphism and the effect of genotype on the measurements is discussed. Overall, there was a non-significant trend towards increased endothelium-dependent vasodilation following both acute and chronic FVPD consumption. However, there was a significant time · treatment effect (P < 0 . 05) of acute FVPD consumption in individuals with the GG variant of the eNOS gene. Carotenoids: Flavonoids: CVD: Laser Doppler imagingCVD is one of the major causes of death in Europe and is responsible for 4 . 3 · 10 6 deaths each year across the continent (1) . One of the emerging risk factors for CVD is dysfunction of the endothelium (2,3) , which is characterised by a reduction in the bioavailability of vasodilators, predominantly NO, endothelium-derived hyperpolarizing factor and prostacyclin, and an increase in endothelium-derived vasoconstrictors, e.g. thromboxane A 2 , PGH 2 and endothelin 1 (2) . Endothelial dysfunction can be assessed by measuring enhanced and maintained endothelial activation and impaired endothelium-dependent vasodilation (4) .Endothelial activation is determined by an increase in the plasma concentrations of soluble cell adhesion molecules, such as intercellular adhesion molecule-1, vascularAbbreviations: atRA, all-trans-retinoic acid; eNOS, endothelial NO synthase; FVPD, fruit-and vegetable-puree-based drinks.

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Demonstration of Rapid Onset Vascular Endothelial Dysfunction After Hyperhomocysteinemia

Cited by 404 publications

References 27 publications

Reduction in plasma total homocysteine through increasing folate intake in healthy individuals is not associated with changes in measures of antioxidant activity or oxidant damage

Reduction in plasma total homocysteine through increasing folate intake in healthy individuals is not associated with changes in measures of antioxidant activity or oxidant damage

Plasma homocysteine concentration and blood pressure in healthy Iranian adults: the Tehran Homocysteine Survey (2003–2004)

Effects of chronic and acute consumption of fruit- and vegetable-puree-based drinks on vasodilation, risk factors for CVD and the response as a result of theeNOSG298T polymorphism

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