Vitamin C-lipid metabolites: Uptake and retention and effect on plasma C-reactive protein and oxidized LDL levels in healthy volunteers
Previously, a novel formulation of vitamin C-lipid metabolites (PureWay-C) was shown to be more rapidly taken-up by human T-lymphocytes and more rapidly stimulate neurite outgrowth, fibroblast adhesion and inhibition of xenobiotic-induced T-cell hyperactivation. Here, PureWay-C serum levels were measured in healthy volunteers after oral supplementation. Plasma C-reactive protein and oxidized low density lipoprotein levels (LDL) were also measured.
Healthy volunteers maintained a low vitamin C diet for 14 days and, following an overnight fast, received a single oral dose of (vitamin C) 1000 mg of either ascorbic acid (AA), calcium ascorbate (CaA), vitamin C-lipid metabolites (PureWay-C), or calcium ascorbate-calcium threonate-dehydroascorbate (Ester-C). Blood samples were collected immediately prior to the oral dose administration and at various times post ingestion. Twenty-four-hour urine collections were saved for oxalate and uric acid assays.
PureWay-C supplementation leads to the highest absolute serum vitamin C levels when compared to AA, CaA and Ester-C. PureWay-C provides a statistically significant greater serum level than calcium ascorbate at 1, 2, 4, and 6 hours post oral supplementation whereas Ester-C shows a less but slightly statistically significant increase at only 1 and 4 hours. Oral supplementation with PureWay-C also led to a greater reduction in plasma C-reactive protein and oxidized LDL levels compared to the other vitamin C formulations.
PureWay-C is more rapidly absorbed and leads to higher serum vitamin C levels and greater reduction of plasma levels of inflammatory and oxidative stress markers than other forms of vitamin C, including Ester-C.
Available from: Takahiro Ueno
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ABSTRACT: Previous studies have shown that oxidative stress plays an important role in coronary heart disease. Polymorphisms in key enzymes that regulate oxidative stress may play a role in atherogenicity and were investigated in this study.
One hundred and forty-three patients with angiographically proven coronary artery disease were studied. The effect of the C242T polymorphism of the p22phox gene, an essential component of the NADH/NADPH oxidase, and glutathione-S-transferase T1, M1 and P1 polymorphisms on plasma MDA-LDL, soluble CD40 ligand, E-selectin and soluble ICAM1 levels was determined. Genotyping of the p22 phox C242T polymorphism was performed by RFLP analysis, and GSTT1, GSTM1 and GSTP1 genotypes were determined using a multiplex PCR assay. The MDA-LDL, sCD40L, E-selectin and sICAM1 levels were determined using ELISA.
Patients with the TT or TC genotype of the p22 phox C242T polymorphism had significantly higher plasma MDA-LDL levels compared to those of the CC genotype. Plasma E-selectin and soluble ICAM1 levels were significantly higher in the TT or TC genotype compared to that of the CC genotype. In GSTT1+ patients, plasma MDA-LDL levels were significantly higher than those of GSTT1- patients.
Genetic polymorphism of the p22 phox gene had a significant effect on plasma lipid peroxidation and endothelial function through oxidative stress. The results of this study confirm the effect of NADH/NADPH oxidase on atherogenecity.
Available from: Colleen G Le Prell
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ABSTRACT: Hearing loss encompasses both temporary and permanent deficits. If temporary threshold shift (TTS) and permanent threshold shift (PTS) share common pathological mechanisms, then agents that reduce PTS also should reduce TTS. Several antioxidant agents have reduced PTS in rodent models; however, reductions in TTS have been inconsistent. This study first determined whether dietary antioxidants (beta-carotene and vitamins C and E) delivered in combination with magnesium (Mg) reliably increase plasma concentrations of the active agents. Then, additional manipulations tested the hypothesis that these nutrients reduce acute TTS insult in the first 24 h after loud sound as well as longer lasting changes in hearing measured up to 7 days postnoise. Saline or nutrients were administered to guinea pigs prior to and after noise exposure. Sound-evoked electrophysiological responses were measured before noise, with tests repeated 1-h postnoise, as well as 1-day, 3-days, 5-days, and 7-days postnoise. All subjects showed significant functional recovery; subjects treated with nutrients recovered more rapidly and had better hearing outcomes at early postnoise times as well as the final test time. Thus, this combination of nutrients, which produced significant increases in plasma concentrations of vitamins C and E and Mg, effectively reduced hearing loss at multiple postnoise times. These data suggest that free radical formation contributes to TTS as well as PTS insults and suggest a potential opportunity to prevent TTS in human populations.
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ABSTRACT: Noise-induced hearing loss (NIHL) is a significant clinical, social, and economic issue. The development of novel therapeutic agents to reduce NIHL will potentially benefit multiple very large noise-exposed populations. Oxidative stress has been identified as a significant contributor to noise-induced sensory cell death and NIHL, and several antioxidant strategies have now been suggested for potential translation to human subjects. One such strategy is a combination of beta-carotene, vitamins C and E, and magnesium, which has shown promise for protection against NIHL in rodent models, and is being evaluated in a series of international human clinical trials using temporary (military gunfire, audio player use) and permanent (stamping factory, military airbase) threshold shift models (NCT00808470). The noise exposures used in the recently completed Swedish military gunfire study described in this report did not, on average, result in measurable changes in auditory function using conventional pure-tone thresholds and distortion product otoacoustic emission (DPOAE) amplitudes as metrics. However, analysis of the plasma samples confirmed significant elevations in the bloodstream 2 hours after oral consumption of active clinical supplies, indicating the dose is realistic. The plasma outcomes are encouraging, but clinical acceptance of any novel therapeutic critically depends on demonstration that the agent reduces noise-induced threshold shift in randomized, placebo-controlled, prospective human clinical trials. Although this noise insult did not induce hearing loss, the trial design and study protocol can be applied to other populations exposed to different noise insults.
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