Vitamin C

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Vitamin C revisited

Vitamin C revisited

This narrative review summarizes the role of vitamin C in mitigating oxidative injury-induced microcirculatory impairment and associated organ failure in ischemia/reperfusion or sepsis. Preclinical studies show that high-dose vitamin C can prevent or restore microcirculatory flow impairment by inhibiting activation of nicotinamide adenine dinucleotide phosphate-oxidase and inducible nitric oxide synthase, augmenting tetrahydrobiopterin, preventing uncoupling of oxidative phosphorylation, and decreasing the formation of superoxide and peroxynitrite, and by directly scavenging superoxide. Vitamin C can additionally restore vascular responsiveness to vasoconstrictors, preserve endothelial barrier by maintaining cyclic guanylate phosphatase and occludin phosphorylation and preventing apoptosis. Finally, high-dose vitamin C can augment antibacterial defense. These protective effects against overwhelming oxidative stress due to ischemia/reperfusion, sepsis or burn seems to mitigate organ injury and dysfunction, and promote recovery after cardiac revascularization and in critically ill patients, in the latter partially in combination with other antioxidants. Of note, several questions remain to be solved, including optimal dose, timing and combination of vitamin C with other antioxidants. The combination obviously offers a synergistic effect and seems reasonable during sustained critical illness. High-dose vitamin C, however, provides a cheap, strong and multifaceted antioxidant, especially robust for resuscitation of the circulation. Vitamin C given as early as possible after the injurious event, or before if feasible, seems most effective. The latter could be considered at the start of cardiac surgery, organ transplant or major gastrointestinal surgery. Preoperative supplementation should consider the inhibiting effect of vitamin C on ischemic preconditioning. In critically ill patients, future research should focus on the use of short-term high-dose intravenous vitamin C as a resuscitation drug, to intervene as early as possible in the oxidant cascade in order to optimize macrocirculation and microcirculation and limit cellular injury.
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Prevention of Hepato-renal toxicity with Vitamin E, Vitamin C and their combination in Gentamicin treated rats

Prevention of Hepato-renal toxicity with Vitamin E, Vitamin C and their combination in Gentamicin treated rats

I/P prior to gentamicin administration for 3 days and simultaneously with it for 10 days results in a significant increase in the activities of renal and hepatic antioxidant enzymes (GPx, SOD and CAT) and significant decrease in MDA levels when compared with the gentamicin administered group. The best obtained results were in the group treated with the combination of vitamin E and vitamin C with their respective doses. Kadkhodaee et al., [37] reported that antioxidants reduced gentamicin –induced oxidative stress and so, has nephroprotective and hepatoprotective effect against gentamicin toxicity.
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Modulation of Oxidative Stress Responses by Vitamin E, or Vitamin A plus Vitamin C Treatment in Human Retinal Pigment Epithelial Cells

Modulation of Oxidative Stress Responses by Vitamin E, or Vitamin A plus Vitamin C Treatment in Human Retinal Pigment Epithelial Cells

levels on AP1 expression. This analysis indicates if there is a protective effect (vitamin pretreatments lower AP1 expression), an additive effect (meaning the decrease in AP1 expression is equal to the sum of the effect of ex- posure to only vitamin C or only vitamin A), a synergistic effect (meaning the decrease in AP1 expression is greater than the sum of individual treatment with vitamin C or vitamin A), or an antagonistic effect (meaning combined treatment is less effective than treatment with either vitamin alone). The fitted linear models for each gene with ∆Ct as the dependent outcome, as a function of the respective “low” and “high” values for vitamin A and C (including any possible interactions), resulted in the following findings within the range of administered vitamin A and C levels: For FOSB at 4 h, (time point of maximal OS response transcription) we conclude that there is an additive protective effect of pretreatment with vitamin A and C with respect to transcription levels but no evidence for a synergistic effect (no interaction-term in the model). For CFOS at 1 h, (time point of maximal OS response transcription) we conclude that there is a substantial interaction between vitamin A and C (statistically, i.e., as related to the transcription level, not necessarily in terms of chemical/biological interaction between these agents) that modulates the effect of each vitamin on AP1 expression levels depending on whether the other vitamin is administered in its respective “low” or “high” dose. A potentially protective effect is only achieved when 100 µM vitamin C are concurrently administered with 15 µM vitamin A, and is not observed when a lower dose of either vitamin is delivered. For ATF3 at 4 h, (time point of maximal OS response tran- scription) we conclude that there is a potentially protective effect of a pretreatment with the higher dose of vita- min A, but no statistically significant change in transcription level could be found when changing vitamin C from 50 to 100 µM, at least when 10 or 15 µM vitamin A are concurrently administered.
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Estimation of Plasma Antioxidants – Vitamin E and Vitamin C in Oral Pre-Cancer and Cancer Patients

Estimation of Plasma Antioxidants – Vitamin E and Vitamin C in Oral Pre-Cancer and Cancer Patients

becomes dissociated over the scavenger and the resulting product will not readil y accept an electron from or donate an electron to another molecule, preventing the further propagation of the chain reaction. 3. Transition metal binding proteins: Transition metal binding proteins (ferritin, transferring, lactoferrin and cerruloplasmin) act by sequestering iron and copper so that the y are not available to drive the formation of the h ydrox yl radical. In this stud y we have estimated the levels of Vitamin-E and Vitamin-C – Chain breaking antioxidants in plasma of individuals with tobacco habits with various mucosal changes.
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Epigenetic reprogramming of melanoma cells by vitamin C treatment

Epigenetic reprogramming of melanoma cells by vitamin C treatment

A2058 cells cultured in 6-well plates were treated with or without vitamin C (0.1 mM) for 48 h. Medium was chan- ged daily before each treatment to avoid the accumulation of vitamin C in the medium. Total RNA was then ex- tracted from these cells. A Bioanalyzer 2000 (Agilent, Palo Alto, CA, USA) was used to monitor the quality of RNA. All samples ’ RNA integrity numbers (RIN) were above nine (data not shown). The whole transcriptome sequencing was carried out at the Sequencing Core of John P. Hussman Institute of Human Genomics at the University of Miami. Briefly, after ribosome RNA (rRNA) was de- pleted, sequencing libraries were constructed following the standard Illumina protocols and were subsequently processed by a Hiseq2500 (Illumina, San Diego, CA, USA) sequencing system (200 bp paired-end reads, four samples per lane). Raw read data was first run through quality con- trol metrics using FastQC (http: //www.bioinformatics.bab raham.ac.uk/projects/fastqc/). After quality control was checked, sequence reads were aligned using the STAR aligner [37]. The aligned reads from the STAR aligner was then run through HTseq for transcript quantification against the GENCODE v19.gtf file [38]. After all features were quantified, the data was then run through three dif- ferent differential expression calculators in EdgeR, DESeq, and BaySeq [39-41]. The intersection of the three methods were taken and transformed into a list of the final differen- tially expressed features. Differentially expressed features were determined by cutoff adjusted P values of 0.05 across all three methods. That final list was then put through gene ontology annotation using the BiNGO added into Cytos- cape v 3.1.1 [42]. The list was also run through GeneGO for pathway enrichment (https://www.portal.genego.com).
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Stability of vitamin C in broccoli at different storage conditions

Stability of vitamin C in broccoli at different storage conditions

stant observed in this study was similar to ear- lier reported values. The degradation of ascorbic acid in broccoli could be mainly due to the oxida- tion of ascorbic acid by oxidizing enzymes, e.g. ascorbic acid oxidase, peroxidase, catalase, and polyphenol oxidase (Mapson, 1970; Venkatesh & Park, 2014). Two types of vitamin C degrada- tion could occur: aerobic and anaerobic degrada- tion. In aerobic degradation, the AA is oxidised to L-dehydro-ascorbic acid (L-DA) followed by hydrolysis and further oxidation, whereas anaer- obic degradation has not been clearly studied and reported (Wang, Law, Mujumdar, & Xiao, 2017). During processing, matrix disruption could oc- cur thus facilitating the oxidation of L-AA to L- DA by the enzyme AAO. The L-DA can then be further hydrolysed to 2,3-diketogulonic acid, thus losing its antiscorbutic activity. Other pos- sible chemical reactions associated with changes in flavour, colour, and odour could have oc- curred with time due to interactions among the components and this resulted in changes in pH (El-Ishaq & Obirinakem, 2015; Munyaka et al., 2010). In this study, low temperature likely caused minimal destruction of structure, thus en- zymatic degradation reaction was observed at a slower rate as compared to high temperature. At high temperature, structural damage could en- hance enzymatic degradation as well as increase interaction with other released components. Figure 3 shows the Arrhenius plot of Ln (k 1 ) ver-
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Oral vitamin C supplementation to patients with myeloid cancer on azacitidine treatment: Normalization of plasma vitamin C induces epigenetic changes

Oral vitamin C supplementation to patients with myeloid cancer on azacitidine treatment: Normalization of plasma vitamin C induces epigenetic changes

Linear mixed-effects models with random intercepts and false discovery rate adjusted contrasts were used to ana- lyse plasma levels of vitamin C, ferritin, iron, and trans- ferrin measured over time. Because some patients took a dietary supplement before study inclusion, we used the lowest vitamin C concentration from blood samples C1D1, C1D5, or C2D1 as the baseline level of vitamin C. Standard linear regression was used to assess associa- tions between vitamin C and each of IPSS-R score, haemoglobin, blast percentage, number of blood transfu- sions, and WHO diagnosis; all models were adjusted for age and sex. Differences in baseline vitamin C, ferritin, iron, and transferrin were analysed via Student ’ s t test with Box-Cox transformations as needed when signifi- cant outliers (via Grubb ’ s test and/or Cook ’ s distance) or non-normality (via Shapiro-Wilks test) were detected; all assumptions were met after transformation. Differences in 5mC and 5hmC/5mC levels between groups were analysed with Welch ’ s two-sample t tests, and two add- itional models were used to assess the sensitivity of these results to baseline vitamin C levels. The first was a linear ridge regression fit via the R package ridge [24], adjusted for baseline vitamin C levels, both with and without an interaction term. The second was a weighted linear re- gression, with weights estimated via the genetic match- ing algorithm from the R package MatchIt [25], which seeks to non-parametrically balance the baseline vitamin C levels between the two groups. Standard linear regres- sion models were used to test for associations between baseline levels and continuous clinical variables. Normal- ity of residuals for all linear models was assessed visually using qq-plots; no extreme deviations were found. All hypothesis tests were two-sided, except for a t test to de- termine if the change in 5hmC/5mC was greater than 0 for the vitamin C group. The significance level for all tests was 0.05. All analyses were performed using R v3.4.4 (https://cran.r-project.org/).
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Synthesis and evaluation of chitosan-Vitamin C complex

Synthesis and evaluation of chitosan-Vitamin C complex

Chitosan is a biocompatible, biodegradable and non-toxic polysaccharide polymer. It dissolves in water only if the pH is lower than 6.5. To extend its range of application, many water-soluble derivatives have therefore been prepared. In this research, chitosan-vitamin C complex was synthesized and characterized with Fourier transformed infrared spectroscopy, differential scanning calorimetry and 1 H-NMR. The solubility of chitosan-vitamin C complex in

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AMELIORATING EFFECT OF VITAMIN E AND VITAMIN C ON CADMIUM INDUCED HEPATOTOXICITY IN LABORATORY CHICKS

AMELIORATING EFFECT OF VITAMIN E AND VITAMIN C ON CADMIUM INDUCED HEPATOTOXICITY IN LABORATORY CHICKS

Vitamins are essential to maintain normal metabolic processes and homeostasis within the body. Vitamin C (Vit C) and vitamin E (Vit E) are low molecular mass antioxidants that scavenge or quench free radicals (Janisch et al., 2005). These findings suggest potential role of antioxidants to ameliorate cadmium toxicity. Both Vit C and Vit E alleviate oxidative stress associated with a variety of pollutants. Vit C and Vit E reduced lipid peroxidation and oxidative stress result from arsenic (Kannan and Flora, 2004), Ozone (Sienra-Monge et al., 2004) and cadmium toxicity (Grosicki, 2004).Vitamin C and vitamin E are recognized as essential nutrients for all species of animals. In other words, these vitamins have been shown to have protective effect against metal induced toxicity (Rao and Sharma, 2001; Jiraungkoorskul et al., 2007) Therefore, the present study was designed to evaluate the effect of vitamin E and vitamin C separately and in combined form against cadmium chloride induced liver hepatotoxicity in chicks.
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Vitamin C transporter gene (SLC23A1 and SLC23A2) polymorphisms, plasma vitamin C levels, and gastric cancer risk in the EPIC cohort

Vitamin C transporter gene (SLC23A1 and SLC23A2) polymorphisms, plasma vitamin C levels, and gastric cancer risk in the EPIC cohort

Follow-up for these analyses was through 2003–2006, depending upon the study center. In general, case identi- fication was based upon information available from popu- lation cancer registries except in France, Greece, Germany, and Naples (Italy) where a combination of methods including health insurance records, hospital-based cancer and pathology registries, and active participant tracking was used. GC for these analyses included diagnoses coded as C16 according to the 10th revision of the International Classification of Disease (ICD-10). A total of 665 GC cases were observed (487 adenocarcinomas, 145 non-adenocar- cinomas, 7 stump tumors and 26 not specified) of which a total of 444 were first, incident, primary gastric adenocarcinomas (hereafter referred to as gastric cancer or GC). Cases were validated for histologic (diffuse, intestinal, mixed, or not specified using Lauren’s classification) and anatomic sub- types (cardia C16.0, non-cardia C16.1-9, mixed, or not spec- ified) by a panel of pathologists who reviewed original pathology reports, tumor slides, and paraffin blocks obtained on GC cases from EPIC centers (Carneiro et al. 2007). Nested case–control study of gastric adenocarcinoma A nested case–control study of primary incident gastric adenocarcinoma (Eurgast) was designed to efficiently study biomarkers and genetic susceptibility in relation to GC risk in the EPIC cohort (Sala et al. 2012). Each incident primary GC case with an available blood sample was matched by study center, sex, age group (±2.5 years), and date of blood collection (±45 days) to four control participants randomly selected from the cohort at risk at the time of diagnosis of the index case. There were 365 GC cases (181 non-cardias, 107 cardias, and 77 with mixed or unspecified anatomic subsite; and 126 intestinal, 128 dif- fuse, and 111 with mixed or unspecified histologic subtype) and 1,284 controls with complete genetic information. There were 172 GC cases and 311 controls with both genetic and plasma vitamin C information. Helicobacter
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Effect of Vitamin C on Styrene Induced Respiratory Toxicity

Effect of Vitamin C on Styrene Induced Respiratory Toxicity

Administration of ST caused depletion of GSH and induced toxicity in mice lung [ 23]. In vitro study has been shown that Clara cells are the main target cells for ST-induced pulmonary toxicity in human [ 22]. Antioxidant agents such as N-acetylcysteine (NAC) and glutathione protected liver cells against ST metabolite induced toxicity in mice [ 16]. Cruzan et al. observed that inhalation of ST by mice results cytotoxicity in terminal bronchioles [ 24]. Thus, it appears that ST produced toxicity in respiratory epithelial cells following metabolic activation and generation of reactive toxic metabolites. Acute exposure to ST caused an increased in lipid peroxidation and decreased glutathione level in mice. These authors suggested that enhancement of lipid peroxidation in lung is a consequence of depletion of glutathione on certain critical levels [ 20]. Occupational exposure to ST- induced inflammatory response in respiratory system [ 11, 12]. We observed that vitamin C protected lung and respiratory epithelial cells against ST induced toxicity. On the basis of these results, we conclude that vitamin C may prevent the occurrence of ST induced adverse effect in humans respiratory system. The mechanism by which vitamin C protected cells against ST toxicity may be related to vitamin C is able to reduce reactive metabolites and/or supporting glutathione biosynthesis that serves directly as an antioxidant. Asthma associated with occupational exposure to ST was reported by several investigators [ 7, 8, 25]. Hays et al. described occupational asthma in ST exposure workers [ 8]. Roder- Stolinski et al. reported that ST-induced release of the inflammatory mediators by the human airway epithelial cells. These authors found that NAC inhibited the release of mediators [ 12]. Morbet et al. concluded that oxidative stress act as a primary molecular response mechanism of human lung epithelial cells to ST exposure [ 22]. Mogel et al. observed ST induced inflammatory reactions in human lung epithelial cells and NAC was capable to prevent the cells against ST toxicity. These authors suggested that generation of oxidative stress was responsible for ST–produced lung injury [ 11]. Result of our study along with others support the view that generation of oxidative stress is likely involved in ST–induced toxicity in humans and experimental animals. These data also support the use of antioxidants in order to ameliorate the adverse effects of ST in respiratory system.
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High-dose intravenous vitamin C as an Antican...

High-dose intravenous vitamin C as an Antican...

Intravenous administration was found to increase plasma ascorbate concentrations by an order of magnitude compared to what may be achieved orally 15 . This may explain the discrepancy between Cameron and Pauling‘s success and the negative results observed at the Mayo Clinic. To date, no randomized controlled clinical trial with high-dose intravenous vitamin C has been published. A limited number of Phase I clinical trials confirm the non-toxic character of the treatment, and give some indications that the treatment may improve quality of life, but do not suggest distinct anti-cancer effects. Several case reports argue for a positive effect on survival time, even reporting cancer remission, and improved quality of life. This article presents a literature review of the role of high dose intravenous vitamin C as an anticancer agent.
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Nephrotoxicity in Recipients of Vancomycin vs. Vancomycin with Vitamin C

Nephrotoxicity in Recipients of Vancomycin vs. Vancomycin with Vitamin C

Current literature points to a potentialrenal-protective benefit associated with vitamin C.Ocak et al. tested the use of vitamin E, vitamin C (concentration of 200 mg/dl), n-acetylcysteine (NAC) and caffeic acid phenethyl ester (CAPE) in a rat model to prevent VIN. In this study, vitamin E was found to be most effective for preventing renal tubular damage, followed by vitamin C, NAC, and CAPE. Blood urea nitrogen (BUN), renal malondialdehyde, and nitric oxide levels were used to assess renal dysfunction. BUN changes were statistically significant within the vitamin E and C groups (p < 0.05). However, renal malondialdehyde and nitric oxide levels were significantly suppressed by all of the agents used in the study (p < 0.05) (Ocak et al., 2007).
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ANTIOXIDANT VITAMIN C: LUNG FUNCTION; LUNG CANCER

ANTIOXIDANT VITAMIN C: LUNG FUNCTION; LUNG CANCER

The utilization of vitamin C in surgical repair and lymphocyte-related host resistance [147]: Plasma and buffy-coat vitamin C were estimated in 158 samples from 139 lung cancer patients, at all stages of the disease. Most samples showed hypovitaminosis C in both estimations: 64% had plasma, and 25% buffy-coat values below the thresholds for incipient clinical scurvy (0.3 mg% and 10 jg/108 cells, respectively). Levels were diet-dependent and could be increased by oral supplements. Levels were low both in tumor-bearing patients and in those clinically free of disease after resection. The latter had particularly low values during the first 6 months, indicating the utilization of vitamin C in surgical repair. The vitamin C content of 13 primary lung tumors was assayed: Tumors had higher vitamin C content (mean 1116+551, ug/g tissue) than normal lung (58.5 + 20-4, ug/g). Mononuclear cells from normal individuals show a higher vitamin C content than polymorphs, but in lung cancer patients, the expected correlation of buffy-coat vitamin C with the proportion of lymphocytes in peripheral blood was obscured by an inverse correlation in patients with relative lymphocytosis (25% lymphocytes), confirmed by an inverse correlation of the proportion of lymphocytes in peripheral blood with mononuclear-cell vitamin C in 14 patients in whom this was measured. These correlations were unaffected by controlling for plasma values and indicate the utilization of vitamin C in lymphocyte-related antitumor mechanisms. Vitamin C is necessary for phagocytosis and for the expression of cell-mediated immunity. In view of the increasing circumstantial evidence that immune mechanisms exert some measure of control on tumor extension and metastasis in man, the effect of supplementation with vitamin C in lung cancer patients on survival should be tested in a clinical trial. The results, over several years this laboratory has measured plasma and
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The effect of heating on the vitamin C content of selected vegetables

The effect of heating on the vitamin C content of selected vegetables

Vegetables have a special place in human nutrition. They are one of the food groups recognized as a leader in healthy eating. Food specialists recommend three or more servings of a variety of vegetables per day. Vegetables supply carbohydrates that are important for the body, taking part in maintaining the optimal humoral environment and the functioning of all cells in the body. Vitamins and minerals contained in vegetables are a source of health and vitality for the body [6]. Vegetables are rich in various phytochemicals, and biologically active substances with beneficial health effects. They promote optimal health by reducing the risk of a number of chronic diseases. Vegetables are consumed both fresh and processed. It has to be noted that much of the vitamin C is destroyed by heat treatment, freezing and even longer storage [7].
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Kinetic and Energetic Correlations in the Reaction of Vitamin-C Tablets

Kinetic and Energetic Correlations in the Reaction of Vitamin-C Tablets

Ascorbic acid is a white crystalline and odourless substance. Due to its polar characteristics, it is easily soluble in water and its solubility in nonaqueous media, such as ethanol and acetonitrile, is quite limited. The crystalline and pure ascorbic acid is stable when exposed to air, light, and ambient temperature for a long period [1]. Vitamin C is the generic kind of all compounds exhibiting qualitatively the biological activity of ascorbic acid. It suffices as a water- soluble antioxidant by reacting with free radicals and reducing reactive oxygen species to protect against the oxidation of lipids, proteins, and DNA [2]. The non-isothermal aerobic degradation of ascorbic acid (AA), and the organization and subsequent degradation of the dehydroascorbic acid (DHAA) are distinguished by two simultaneous rate equations. Also accepted is that the temperature-dependence of these three reactions' rate-constants follows the exponential model, a simpler substitute for the traditional Arrhenius equation [3]. Vitamin C and its degradation products participate in chemical modifications of proteins in vivo through non- enzymatic glycation (Maillard reaction) and formation of different products called advanced glycation end products. The identification of 3- deoxythreosone as the major degradation product bound to human lens proteins provides in vivo evidence for the non-oxidative pathway of dehydroascorbate degradation into erythrulose as a major pathway for vitamin C degradation in vivo [4]. Matei et al. [5] determinate the rate constant, the half-time and the activation energy for vitamin C. It can take note that the rate constants depend strongly on temperature, typically increasing rapidly with increasing T. It can take note that the values of the activation energy, analytical and graphical determined are in good agreement. The dynamics of vitamin C have been examined extensively in model systems with exceptional care to intermediate moisture foods and during storage studies. Hence, it is necessary to study the subject of different processing temperatures on the retention of vitamin C in the product and kinetic modelling to anticipate the losses during processing by different heating methods [6]. Cyclic Voltammetry was used to examine the kinetics of degradation of ascorbic acid (AA) at different temperatures. It has been shown that the reduction of the concentration of AA in all temperatures follows the dynamics of the first order reaction. The kinetics of degradation of vitamin C was also studied using titrimetric and
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Periodontitis Is Associated with a Low Concentration of Vitamin C in Plasma

Periodontitis Is Associated with a Low Concentration of Vitamin C in Plasma

Although gingival bleeding is a clinical symptom of both scurvy and periodontitis, the two conditions are distinct disease entities. Unlike for scurvy, which is caused by vitamin C defi- ciency, the etiological agents in periodontitis are dental plaque bacteria, especially gram-negative microorganisms, including Actinobacillus actinomycetemcomitans and Porphyromonas gin- givalis. An inflammatory response to the overgrowth of peri- odontal bacteria in general, and to certain species in particular, leads to microulceration in the epithelium-facing tooth surface in periodontal pockets, opening a route for the bacteria to the circulation. In periodontitis, bacteria and their components are commonly spread in circulating blood (7). The continued local or systemic bacterial stimulus causes release of proinflamma- tory mediators, which may have a role in the pathogenesis of atherosclerosis and stroke (14, 28, 35). Accordingly, findings suggesting a role of periodontitis in cardiovascular diseases (CVD) add a new perspective to the importance of oral status for systemic health (8).
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Vitamin C supplementation for the primary prevention of cardiovascular disease

Vitamin C supplementation for the primary prevention of cardiovascular disease

A systematic review of the effects of individual vitamins and min- erals, and multivitamins, on clinical endpoints has been conducted (Fortmann 2013). This review was conducted for the US Task Force for Preventative Services. The authors found two trials of vitamin C supplementation reporting clinical endpoints relevant for CVD prevention, where no effect of the intervention was found. In terms of effects on CVD risk factors, from preliminary searching of the Cochrane Library, we identified five systematic reviews in the Database of Abstracts of Reviews of Effects (DARE), which assessed the effects of vitamin C supplementation on blood pressure (Juraschek 2012; McRae 2006a; Ness 1997), low-density lipid (LDL) cholesterol and triglycerides (McRae 2008), and to- tal cholesterol (McRae 2006b). Only two of these included only RCTs (Juraschek 2012; McRae 2008), the reminder include also non-randomised experimental studies and observational studies. The first review of RCTs covered both primary and secondary prevention and the effects of vitamin C supplementation alone and in combination with other agents (such as vitamin E, mag- nesium, zinc, selenium) in trials between two and 26 weeks du- ration (Juraschek 2012). The authors concluded that vitamin C supplementation reduced systolic and diastolic blood pressure in short-term trials. The second review concluded that supplemen- tation with at least 500 mg/day of vitamin C, for a minimum of four weeks, can result in a significant decrease in serum LDL cholesterol and triglyceride concentrations. However, the lack of
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Influence of processing on vitamin C content of rosehip fruits

Influence of processing on vitamin C content of rosehip fruits

Tests carried out on rosehip tea, respectively syrup and jam have aimed at assessing quality of products processed by drying and pasteurization. For investigation of the contents of ascorbic acid, total soluble solids, pH values and the antioxidant capacity, samples were taken after different stages of production to determine the effects of processing. Vitamin C content was determined by separating samples of rose-hip and dosage in a HPLC SHMADZU system coupled with UV–VIS detector (DAD).

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Dietary supplement with vitamin C prevents nitrate tolerance

Dietary supplement with vitamin C prevents nitrate tolerance

Enhanced formation of superoxide radicals has been pro- posed to play a major role in the development of nitrate tol- erance in humans. We tested the effects of vitamin C (Vit-C) supplementation on glyceroltrinitrate (GTN)-induced hemo- dynamic effects during 3-d nonintermittent transdermal ad- ministration of GTN (0.4 mg/h) in nine healthy subjects. Tolerance development was monitored by changes in arte- rial pressure, dicrotic digital pulse pressure, and heart rate. Studies with GTN, Vit-C, or GTN/Vit-C were successively carried out at random in three different series in the same subjects. GTN treatment caused an immediate rise in arte- rial conductivity (a/b ratio of dicrotic pulse), but within 2 d of initiating GTN, the a/b ratio progressively decreased and reached basal levels. In addition, there was a progressive loss of the orthostatic decrease in blood pressure. However, coadministration of Vit-C and GTN fully maintained the GTN-induced changes in the orthostatic blood pressure, and the rise of a/b ratio was augmented by 310% for the du- ration of the test period. Changes in vascular tolerance in GTN-treated subjects were paralleled by upregulation of the activity of isolated platelets, which was also reversed by Vit-C administration. These findings demonstrate that di- etary supplementation with Vit-C eliminates vascular tol- erance and concomitant upregulation of ex vivo–washed platelet activity during long-term nonintermittent adminis- tration of GTN in humans. ( J. Clin. Invest. 1998. 102:67– 71.) Key words: arterial conductivity • soluble guanylyl cyclase activity • platelet aggregation • membrane micro-
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