Lack of effect of acute oral ingestion of vitamin C on oxidative stress, arterial stiffness or blood pressure in healthy subjects

Kelly, Raymond P.; Yeo, Kwee Poo; Isaac, Helen B.; Lee, Jetty Chung‐Yung; Huang, Shan; Teng, Leyan; Halliwell, Barry; Wise, Stephen D.

doi:10.1080/10715760802087431

Cited by 40 publications

(32 citation statements)

References 36 publications

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“…32 However, interestingly, an acute intake of vitamin C appears to have no effect on oxidative stress, arterial stiffness, or BP in human subjects. 33 The study examining the effect of a single large dose of vitamin C was tested in 26 healthy volunteers, and vitamin C showed no effect on vasodilatation measured by augmentation index, forearm blood flow, or several markers of oxidative stress compared with placebo. 33 However, there has been recent evidence of an association between vitamin C and BP in a longitudinal study of young black and white women aged 18 to 21 years (nϭ242) at baseline (with 10-year follow-up), 34 as well as in a clinical trial setting involving 110 hypertensive men with a mean age of 46 years (range: 35 to 60 years).…”

Section: Discussionmentioning

confidence: 99%

Association Between Plasma Vitamin C Concentrations and Blood Pressure in the European Prospective Investigation Into Cancer-Norfolk Population-Based Study

Myint

Luben

Wareham³

et al. 2011

Hypertension

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Abstract-The effect of fruit and vegetable consumption and blood pressure is unclear. A population-based cross-sectional study was conducted in 20 926 men and women aged 40 to 79 years participating in the European Prospective Investigation Into Cancer-Norfolk who completed a health questionnaire and attended a clinic from 1993 to 1997. The relationship between plasma vitamin C concentrations, as an indicator of fruit and vegetable intake, and systolic BP was examined. Key Words: blood pressure Ⅲ hypertension Ⅲ ascorbic acid Ⅲ diet Ⅲ antioxidant H ypertension is one of the major risk factors for cardiovascular disease (CVD), 1 which is responsible for a third of global deaths with increasing disease burden attributed to increasing aging of populations across the world. 2 Hypertension has been well recognized as a major risk factor for CVD. The World Health Organization defines hypertension as blood pressure Ն140/90 mm Hg regardless of age or sex. 3 There also appears to be a linear and direct relationship between blood pressure and CVD incidence, as well as mortality. 4 -6 Fresh fruits and vegetables are a richer source of ascorbic acid compared with cooked/boiled fruit and vegetables. Ascorbic acid in the food is also easily destroyed (eg, cooking in water, roasting, or grilling). 7 and has a short half-life (Ϸ30 minutes) in the blood. 8,9 Furthermore, the main source of vitamin C (ascorbic acid) in humans is from food consumption, predominantly fruits and vegetables, because they cannot synthesize ascorbic acid in the body. 7 Therefore, plasma concentration of vitamin C is highly related to the individual's habitual dietary pattern and method of food preparation. Although randomized trials indicate that supplementation with antioxidant vitamins including ␤-carotene, vitamin E, or vitamin C does not reduce cardiovascular risk, 10,11 prospective studies indicate that high fruit and vegetable intake, of which plasma vitamin C is a good biomarker, is inversely related to mortality and incident CVD, especially stroke. [12][13][14] The association between fruit and vegetable intake and blood pressure is less well known. Because hypertension is the major risk factor for stroke, we hypothesize that plasma vitamin C concentrations, which are derived from fruit and vegetable intake, may reduce stroke incidence through blood pressure-lowering effect. Therefore, in this study, we explored the cross-sectional association between plasma vitamin C concentrations and blood pressure using a large United

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Section: Discussionmentioning

confidence: 99%

Association Between Plasma Vitamin C Concentrations and Blood Pressure in the European Prospective Investigation Into Cancer-Norfolk Population-Based Study

Myint

Luben

Wareham³

et al. 2011

Hypertension

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“…Reasons for this have been extensively reviewed. [166][167][168][169] Harrison and colleagues 170 proposed a new strategy to increase antioxidant capacity without the use of exogenous antioxidants. They suggest that drugs that selectively inhibit multidrug resistant protein 1 would prevent cellular glutathione loss and thereby protect against oxidative damage, endothelial dysfunction and hypertension.…”

Section: Therapeutic Potential Of Ros Modulators In Hypertensionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

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“…In this sense, it is important to mention that the type, dosage and matrix of exogenous antioxidants seem to be determinant in the balance between beneficial or deleterious effects of vit. C. Briefly, the antioxidants in fruit and vegetables may be tightly bound within the tough fibrous material of these foodstuffs and may exert their antioxidant activity not in the blood or tissues but in the gastrointestinal tract where free radicals are constantly generated from food (Kelly et al, 2008) and on the contrary, vitamins ingested as food supplements are probably digested too quickly to replicate these effects. Moreover, in many cases, the equivalent serum levels of vitamin C cannot be achieved if the supplement is given orally since there is an upper limit for absorption of vitamin C of about 500 mg, which is why this is normally the highest dose given (Monsen, 2000).…”

Section: Vitamins E and Cmentioning

confidence: 99%

Compounds with Antioxidant Capacity as Potential Tools Against Several Oxidative Stress Related Disorders: Fact or Artifact?

Pérez-Matute¹,

Crujeiras²,

Fernández‐Galilea³

et al. 2012

Oxidative Stress and Diseases

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Oxidative Stress and Diseases 544 reactive species: reactive oxygen species (ROS, thus, oxygen-containing molecules that are highly reactive), reactive chlorine species (RCN) and reactive nitrogen species (RNS). All these reactants contain free radicals as well as nonradicals. Low concentrations of these reactive species are necessary for normal cell redox status, cell function and intracellular signalling (Droge, 2002;Valko et al., 2007;Perez-Matute et al., 2009). However, in some disease states, free radicals are produced in excess and can damage DNA, proteins, carbohydrates and lipid constituents and compromise cell function leading to the development of type 2 diabetes, atherosclerosis, obesity, arthritis etc. Thus, it is clear that excessive production of free radicals causes damage to biological material and is an essential event in the aetiopathogenesis of various diseases. However, the question that has risen in the past years is whether uncontrolled formation of ROS is a primary cause or a downstream consequence of the pathological processes. In other words, it is still not clear what comes first, the chicken or the egg. However, what is clear is that there must be a balance between these reactive species and the antioxidants, whose main function is to counteract the deleterious effects of these reactive species. In fact, antioxidant is defined as any substance that when present at low concentrations compared with those of an oxidizable substrate, significantly delays or prevents oxidation of that substrate (Halliwell & Gutteridge, 1999). These defences include both enzymatic (superoxide dismutases, glutathione peroxidase, catalase, thioredoxin) and non-enzimatic systems (vitamins such as vitamin C, E, A, minerals such as selenium, zinc, cooper, bilirrubine, uric acid, some aminoacids etc).Several studies have demonstrated an increased oxidative state (either caused by an increased ROS production or diminished levels of antioxidants) in serious pathologies such as obesity, cardiovascular diseases, metabolic syndrome, cancer etc. Thus, oxidative stress actually may be related with the mentioned processes. In this context, it is tempting to suggest that if oxidative damage significantly contributes to disease pathology, then, actions that decrease it (via decreasing ROS production or increasing endogenous levels of antioxidants) might be therapeutically beneficial. In fact, attenuation or complete suppression of oxidative stress as a way to improve several diseases has flourished as one of the main challenges of research in the last years. Thus, several approaches have been carried out in order to either decrease the high levels of ROS generated or boost the endogenous levels of antioxiants. Inhibition of ROS production through the development of inhibitors (natural or chemical) against the main sources of ROS generation offers an interesting approach. Thus, NADPH oxidase and mitochondria have been postulated as the main targets to reduce ROS production (reviewed by Pérez-Matute et al., 2009). Another str...

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Lack of effect of acute oral ingestion of vitamin C on oxidative stress, arterial stiffness or blood pressure in healthy subjects

Cited by 40 publications

References 36 publications

Association Between Plasma Vitamin C Concentrations and Blood Pressure in the European Prospective Investigation Into Cancer-Norfolk Population-Based Study

Association Between Plasma Vitamin C Concentrations and Blood Pressure in the European Prospective Investigation Into Cancer-Norfolk Population-Based Study

Reactive oxygen species and vascular biology: implications in human hypertension

Compounds with Antioxidant Capacity as Potential Tools Against Several Oxidative Stress Related Disorders: Fact or Artifact?

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