Antihistamine Effect of Supplemental Ascorbic Acid and Neutrophil Chemotaxis

Johnston, Carol S.; Martin, Linda J.; Cai, Xi

doi:10.1080/07315724.1992.12098241

Cited by 73 publications

(15 citation statements)

References 26 publications

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“…Beside its antioxidant properties and its role in collagen synthesis, vitamin C has been shown to improve phagocytic function and has an immunomodulatory effect on lymphocyte cells (Anderson et al 1980 ). It also has been shown that large doses of vitamin C might markedly lower blood histamine concentrations, which is inversely associated with leukocyte chemotaxis (Johnston et al 1994 ). Vitamin C deficiency is associated with a decreased resistance to diseases and some evidence suggests that it might have antiviral activity in humans (Mortola et al 1998 ) (Jariwalla and Harakeh 1998 ).…”

Section: Discussionmentioning

confidence: 99%

Vitamin C supplementation modulates gene expression in peripheral blood mononuclear cells specifically upon an inflammatory stimulus: a pilot study in healthy subjects

Canali¹,

Natarelli²,

Leoni³

et al. 2014

Genes Nutr

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In order to study the effects of vitamin C supplementation on gene expression and compare its action between physiological and inflammatory conditions, a pilot study was set up utilizing microarray and qPCR technologies. Five healthy volunteers were supplemented with 1 g vitamin C (Redoxon®) per day for five consecutive days. Peripheral blood mononuclear cells (PBMNC) were isolated before and just after the last supplementation, and RNA was isolated for the Affymetrix gene 1.0 ST chip analysis. PBMNC were also, ex vivo, treated with LPS, and gene expression was quantified by means of a “Human NFkB Signaling” qPCR array. Only a very moderate effect on the baseline gene expression modulation was associated with vitamin C supplementation. However, in spite of the limited number of subjects analyzed, vitamin C supplementation resulted in a markedly different modulation of gene expression upon the inflammatory stimulus, specifically at the level of the MyD88-dependent pathway and of the anti-inflammatory cytokine IL-10 synthesis. This study suggests that vitamin C supplementation in healthy subjects, not selected according to a specific genetic profile, consuming an adequate amount of vitamin C, and having a satisfactory vitamin C plasma concentration at the baseline, does not result in a significant modification of gene expression profile. Under this satisfactory micronutrient status, supplementation of vitamin C is “buffered” within a homeostatic physiological equilibrium. Differently, following a second “hit” constituted of an inflammatory stimulus such as LPS, able to trigger a critical burst to the normal physiological state, the higher availability of ascorbic acid emerges, and results in a significant modulation of cell response.

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Section: Discussionmentioning

confidence: 99%

Vitamin C supplementation modulates gene expression in peripheral blood mononuclear cells specifically upon an inflammatory stimulus: a pilot study in healthy subjects

Canali¹,

Natarelli²,

Leoni³

et al. 2014

Genes Nutr

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“…[ 7 8 ] Aspirin is a classic nonsteroidal anti-inflammatory drug and has obvious anti-inflammatory effects as well as antioxidant effects demonstrated experimentally in both animals and humans. [ 9 10 ] Vitamin C (ascorbic acid) is an essential water-soluble vitamin in the human body, which is not only an effective antioxidant[ 11 ] but also can both prevent histamine release and increase the detoxification of histamine,[ 12 ] thus essentially acting as an anti-inflammatory agent. Vitamin E is an essential lipid-soluble vitamin in the human body, which is an effective antioxidant.…”

Section: Introductionmentioning

confidence: 99%

Ovarian Damages Produced by Aerosolized Fine Particulate Matter (PM2.5) Pollution in Mice

Gai

Qian

et al. 2017

Chinese Medical Journal

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Background:Ambient aerosol fine particulate matter (PM2.5) is associated with male reproductive toxicity in experiments and may have adverse effects in the female. However, studies evaluating the protective effects and precise mechanisms of aspirin, Vitamin C, Vitamin E, or ozone against toxic effects of PM2.5 are sparse. This study was conducted to investigate the possible protective effects and mechanisms of aspirin, Vitamin C, Vitamin E, or ozone on fertility in female mice treated with PM2.5.Methods:Eighty-four ICR mice were divided into six groups: control group, PM2.5 group, PM2.5 + aspirin group, PM2.5 + Vitamin C group, PM2.5 + Vitamin E group, and PM2.5 + ozone group. PM2.5 was given by intratracheal instillation every 2 days for 3 weeks. Aspirin, Vitamin C, and Vitamin E were given once a day by oral gavage for 3 weeks, and ozone was administered by intraperitoneal injection once a day for 3 weeks. The levels of anti-Müllerian hormone (AMH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were measured using enzyme-linked immunosorbent assay. Western blotting analysis was used to analyze the expressions of Bcl-2, Bax, and caspase-3 in ovaries. Changes in histological structure were examined by light microscope and electron microscopy was used to detect ultramicrostructure.Results:The results demonstrated that PM2.5 decreased AMH levels (P < 0.001); however, aspirin (P < 0.001), Vitamin C (P < 0.001), Vitamin E (P = 0.001), and ozone (P = 0.002) alleviated the decrease. Changes of IL-6, TNF-α, 8-OHdG, Bax/Bcl-2, and caspase-3 in PM2.5 group were increased compared to control group (P < 0.001), while in PM2.5 + aspirin, PM2.5 + Vitamin C, PM2.5 + Vitamin E, and PM2.5 + ozone groups, they were statistically decreased compared to PM2.5 group (P < 0.001 or P < 0.05).Conclusions:PM2.5 cause the damage of ovaries, and aspirin, Vitamin C, Vitamin E, and ozone antagonizes the damage. The protective mechanism is probably due to its ability to blunt the inflammatory and oxidative stress caused by PM2.5, which subsequently suppressing the expression of apoptotic regulatory protein and reducing the incidence of ovary apoptosis.

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“…Previously, vitamin C has been shown to act not only as a potent reducing agent but also to play a role (currently not yet clearly understood) in modulating the production of lymphocytes and cytokines, the activity of phagocytes, and the expression of a number of cell adhesion molecules in monocytes [ 57 ]. Furthermore, vitamin C seems to prevents histamine release and increases the detoxification of histamine [ 58 ], thus acting as an anti-inflammatory agent as well as a potent antioxidant. Considering the major role played by ROS in the pathogenesis of BBB impairment as well as that of neurological disorders [ 21 - 23 , 32 , 59 ] we evaluated the independent and complementary effectiveness of antioxidants vitamins supplementation, such as vitamin C (protection against protein oxidation [ 60 - 62 ] and vitamin E (counteract lipid peroxidation [ 63 - 65 ]), in shielding the BBB from the chronic exposure to TS-generated oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

In Vitro Assessment of Tobacco Smoke Toxicity at the BBB: Do Antioxidant Supplements Have a Protective Role?

et al. 2011

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BackgroundTobacco smoke (TS) contains highly reactive oxygen species (such as hydrogen peroxide, peroxynitrite, etc), which cause oxidative damage in vascular tissue and may exacerbate inflammatory events leading to the blood-brain barrier damage (BBBD) which accompanies the development of a variety of neurological disorders. Smokers often have elevated leukocyte counts (primarily neutrophils and monocytes), and significant decreases in plasma alpha-tocopherol (vitamin E) and ascorbic acid (vitamin C) levels due to increased anti-oxidative mobilization in response to oxidative stress evoked by TS. For this purpose, using static culture systems and a well-established dynamic in vitro BBB model (DIV-BBB) we tested the hypothesis that antioxidant vitamin supplementation (E and/or C) can protect the BBB during exposure to whole soluble TS.ResultsTS exacerbates inflammatory events and leads to endothelial overexpression of vascular adhesion molecules (VCAM-1, P-selectin and E-selectin), release of pro-inflammatory cytokines (TNF-α and IL-6) and nitric oxide (NO), release and activation of matrix metalloproteinases (MMP-2 and MMP-9), monocytic maturation into macrophages, and adhesion to the vascular endothelium. Furthermore, TS altered the normal glucose metabolic behaviour of in vitro BBB capillaries and caused a period of transient anaerobic respiration to meet the cellular bioenergetic demand. Pre-treatment with antioxidant vitamins (C and/or E) effectively reduced the pro-inflammatory activity associated with TS, protecting the viability and functions of the BBB.ConclusionOur results have shown that loss of endothelial viability as well as BBB function and integrity caused by TS exposure can be prevented or at least reduced by normal physiologic concentrations of antioxidant vitamins in vitro.

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Antihistamine Effect of Supplemental Ascorbic Acid and Neutrophil Chemotaxis

Cited by 73 publications

References 26 publications

Vitamin C supplementation modulates gene expression in peripheral blood mononuclear cells specifically upon an inflammatory stimulus: a pilot study in healthy subjects

Vitamin C supplementation modulates gene expression in peripheral blood mononuclear cells specifically upon an inflammatory stimulus: a pilot study in healthy subjects

Ovarian Damages Produced by Aerosolized Fine Particulate Matter (PM2.5) Pollution in Mice

In Vitro Assessment of Tobacco Smoke Toxicity at the BBB: Do Antioxidant Supplements Have a Protective Role?

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