The antioxidant role of vitamin C

Bendich, Adrianne; Machlin, L. J.; Scandurra, O.; Burton, Graham W.; Wayner, Danial D. M.

doi:10.1016/s8755-9668(86)80021-7

Cited by 606 publications

(262 citation statements)

References 61 publications

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“…Like dietary vitamin C, a single intravenous injection of vitamin C just 5 min prior to CS exposure resulted in a similar protection from CS-induced leukocyte/platelet/endothelium interaction, suggesting that vitamin C does not need to be incorporated into cells in order to be effective, but that it merely needs to be circulating in the bloodstream in order to neutralize aqueous-phase ROS (14)(15)(16). This result is of interest with respect to a proposed pro-rather than antioxidant effect of vitamin C, as can be observed in vitro in the presence oftransition metals (32). However, plasma contains no free redox-active transition metal ions, leaving the ROS scavenging (antioxidant) action of vitamin C prevailing in the in vivo situation (33).…”

Section: Resultsmentioning

confidence: 82%

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Lehr¹,

Frei²,

Arfors³

1994

Proc. Natl. Acad. Sci. U.S.A.

153

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A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro-and macrovascular endothelium. A previous study, using a skinfold chamber model for intravial fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro-and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 ± 11.0 vs. 149.6 ± 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 ± 4.2 vs. 54.3 ± 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 ± 0.4 vs. 12.4 ± 5.6 leukocytes per mm2 P < 0.01; means ± SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CSinduced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 ± 22.2 spM, n 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.Cigarette smoke (CS) has been identified as an independent major risk factor for the development of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease, emphysema, atherosclerosis, and coronary artery disease (1). Although the spectrum of adverse effects of CS involves multiple tissue and organ systems, a feature common to the pathomechanism of most CS-associated diseases is the activation and adhesion of circulating leukocytes to micro-and/or macrovascular endothelium (2-4), followed by acute and/or chronic leukocyte-mediated tissue damage (5, 6). In agreement with earlier reports on the sequestration and activation of leukocytes in the pulmonary microcirculation in rabbits (7), hamsters (8, 9), and humans (10), intravital microscopy in a skinfold chamber model in hamsters revealed that the exposure of hamsters to the smoke of one cigarette elicits the rolling and adhesion of fluorescently labeled leukocytes to the endothelium of small venules and arterioles in striated muscle (11). Leukocyte adhesion was significantly reduced by pretreatment of the animals with superoxide dismutase, implying a key mediator role for superoxide radicals in CS-induced leu...

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Section: Resultsmentioning

confidence: 82%

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Lehr¹,

Frei²,

Arfors³

1994

Proc. Natl. Acad. Sci. U.S.A.

153

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“…However, what is unknown from the present research is the specific site of free radical scavenging. It is plausible, since plasma is saturated at doses of 1,000 mg, that the ascorbic acid scavenged bloodborne free radicals, thus inhibiting the propagation of lipid peroxidation [38]. In support of this idea, Frei et al [39] have shown that ascorbic acid protects plasma lipids against peroxidative damage induced by aqueous lipid-derived peroxyl radicals and that ascorbic acid is the only plasma antioxidant capable of doing so.…”

Section: Discussionmentioning

confidence: 99%

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

et al. 2008

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Aims/hypothesis Patients with type 1 diabetes mellitus are more susceptible than healthy individuals to exercise-induced oxidative stress and vascular endothelial dysfunction, which has important implications for the progression of disease. Thus, in the present study, we designed a randomised doubleblind, placebo-controlled trial to test the original hypothesis that oral prophylaxis with vitamin C attenuates rest and exercise-induced free radical-mediated lipid peroxidation in type 1 diabetes mellitus. Methods All data were collected from hospitalised diabetic patients. The electron paramagnetic resonance spectroscopic detection of spin-trapped α-phenyl-tert-butylnitrone (PBN) adducts was combined with the use of supporting markers of lipid peroxidation and non-enzymatic antioxidants to assess exercise-induced oxidative stress in male patients with type 1 diabetes (HbA 1c 7.9±1%, n=12) and healthy controls (HbA 1c 4.6±0.5%, n=14). Following participant randomisation using numbers in a sealed envelope, venous blood samples were obtained at rest, after a maximal exercise challenge and before and 2 h after oral ingestion of 1 g ascorbate or placebo. Participants and lead investigators were blinded to the administration of either placebo or ascorbate treatments. Primary outcome was the difference in changes in free radicals following ascorbate ingestion. Results Six diabetic patients and seven healthy control participants were randomised to each of the placebo and ascorbate groups. Diabetic patients (n=12) exhibited an elevated concentration of PBN adducts (p<0.05 vs healthy, n=14), which were confirmed as secondary, lipid-derived oxygen-centred alkoxyl (RO·) radicals (a nitrogen =1.37 mT and aβ hydrogen =0.18 mT). Lipid hydroperoxides were also selectively elevated and associated with a depression of retinol and lycopene (p<0.05 vs healthy). Vitamin C supplementation increased plasma vitamin C concentration to a similar degree in both groups (p<0.05 vs presupplementation) and attenuated the exercise-induced oxidative stress response (p<0.05 vs healthy).There were no selective treatment differences between groups in the primary outcome variable. Conclusions/interpretation These findings are the first to suggest that oral vitamin C supplementation provides an Diabetologia

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“…5, the increase in metal ion concentration in the examined concentration range causes a linear decrease in the estimated inhibition percent (negative D). According to Bendich, Machalin, Scandura, Burton and Wayner [20], the presence of some transition metal ions results in autoxidative destruction of vitamin C, which promotes and accelerates the autoxidation of polyunsaturated lipid material. It is difficult to explain the inhibition percent decline of BHT resulting from the presence of metal ions in the system by the destruction of the antioxidant (BHT) used in the experiments.…”

Section: Methodsmentioning

confidence: 99%

Influence of some experimental variables and matrix components in the determination of antioxidant properties by β-carotene bleaching assay: experiments with BHT used as standard antioxidant

Dawidowicz

Olszowy

2010

Eur Food Res Technol

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The b-carotene bleaching assay belongs to the oldest and continuously commonly applied methods of estimating the antioxidant activity of compounds and mixtures. In this method, the antioxidant activity of the examined substance is evaluated by the spectrophotometric measurement of b-carotene concentration changes in bcarotene/peroxyl radicals (LOO • ) systems with and without antioxidant. Yet a little is known about factors influencing the value of inhibition percent of the investigated antioxidant, estimated by this method. The paper shows that both the antioxidant solvent type and the amount of the antioxidant solvent in the measuring system significantly influence the inhibition percent value for butylohydroxytoluene (BHT), used as standard antioxidant in the performed experiments. Moreover, the results shown in the paper prove the essential influence of hydrogen and metal ions on the results of antioxidant assay. The relationships discussed in this paper indicate the necessity of standardizing b-carotene method and reveal the complexity of the problem of estimation of adequate antioxidant activity of examined substances.

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The antioxidant role of vitamin C

Cited by 606 publications

References 61 publications

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

Influence of some experimental variables and matrix components in the determination of antioxidant properties by β-carotene bleaching assay: experiments with BHT used as standard antioxidant

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