L-ascorbic acid (vitamin C) is one of the well-known anti-viral agents, especially to influenza virus. Since the in vivo anti-viral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-α/β, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-α/β, were increased in the lung. Taken together, vitamin C shows in vivo anti-viral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-α/β.

Magnesia flue gas desulfurization is a promising process for small to medium scale industrial coal-fired boilers in order to reduce sulfur dioxide emissions, in which oxidation control of magnesium sulfite is of great importance for the recycling of products. Effects of four inhibitors were compared by kinetic experiments indicating that ascorbic acid is the best additive, which retards the oxidation process of magnesium sulfite in trace presence. The macrokinetics of magnesium sulfite oxidation inhibited by ascorbic acid were studied. Effects of the factors, including ascorbic acid concentration, magnesium sulfite concentration, oxygen partial pressure, pH, and temperature, were investigated in a stirred reactor with bubbling. The results show that the reaction rate is -0.55 order in ascorbic acid, 0.77 in oxygen partial pressure, and zero in magnesium sulfite concentration, respectively. The apparent activation energy is 88.0kJmol(-1). Integrated with the kinetic model, it is concluded that the oxidation rate of magnesium sulfite inhibited by ascorbic acid is controlled by the intrinsic chemical reaction. The result provides a useful reference for sulfite recovery in magnesia desulfurization.

Standard photolithographic techniques and a nitric oxide (NO) selective xerogel polymer were utilized to fabricate an amperometric NO microfluidic sensor with low background noise and the ability to analyze NO levels in small sample volumes (~250 µL). The sensor exhibited excellent analytical performance in phosphate buffered saline, including a NO sensitivity of 1.4 pA nM-1, a limit of detection (LOD) of 840 pM, and selectivity over nitrite, ascorbic acid, acetaminophen, uric acid, hydrogen sulfide, ammonium, ammonia, and both protonated and deprotonated peroxynitrite (selectivity coefficients of -5.3, -4.2, -4.0, -5.0, -6.0, -5.8, -3.8, -1.5, and -4.0 respectively). To demonstrate the utility of the microfluidic NO sensor for biomedical analysis, the device was used to monitor changes in blood NO levels during the onset of sepsis in a murine pneumonia model.

Abstract This study aimed to examine the protective effect of ascorbic acid against colistin-induced neurotoxicity mediated by oxidative stress, a potential mechanism. An in vitro neurotoxicity model was established with PC12 cells exposed to 125 µg/mL colistin sulfate for 24 h. PC12 cells were treated with colistin (125 µg/mL) in the absence and presence of ascorbic acid (0.1, 1.0 and 10µM/mL) for 24h. Both 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) assay were carried out to evaluated cell viability. The levels of intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione (GSH) levels were assessed. Moreover, we tested the level of DNA fragmentation, the release of cytochrome-c and the expressions of caspase-9 and -3 mRNA. The results showed that 1 and 10µM/mL ascorbic acid significantly increased the cell viability and the levels of SOD and GSH (both p<0.05), while 0.1,1 and 10µM/mL ascorbic acid significantly decreased generation of ROS, the release of cytochrome-c, formation of DNA fragmentation and the expressions of caspase-9 and -3 mRNA in colistin-treated PC12 cells, compared with the colistin model group. These results suggest that ascorbic acid could reduce colistin sulfate-induced neurotoxicity through the resistance of oxidative stress and the prevention of apoptosis mediated via mitochondoria pathway. They also highlight the potential of coadministering ascorbic acid to widen the therapeutic dose of colistin.

Copper(ii) is known to catalyze the generation of reactive nitrogen species in the presence of hydrogen peroxide, nitrite or nitric oxide, leading to tyrosine nitration, a biomarker for free radical species associated diseases. Here, we find that biological antioxidants such as ascorbic acid can promote tyrosine nitration in the presence of copper(ii) and nitrite under aerobic and weak acidic conditions. Tyrosine nitration is demonstrated on both the β-amyloid peptide and angiotensin I. These studies show that (i) ascorbic acid works as a pro-oxidant in the presence of copper(ii) to induce oxidation and nitration on peptides, (ii) both free and coordinated copper(ii) can catalyze peptide oxidation and nitration, (iii) nitration occurs under mild acidic conditions (pH = 6.0-6.5).

An interconversion between a binuclear Cu(I) double helicate and a tetranuclear Cu(II) grid is reported. The passage from the Cu(I) double helicate to the Cu(II) grid occurs through oxidation of Cu(I) into Cu(II) or through displacement of Cu(I) by Cu(II). The conversion of the Cu(II) grid into the Cu(I) double helicate occurs through treatment of the grid with triflic acid, reduction of Cu(II) with ascorbic acid, and neutralization with triethylamine. During the studies, in order to ascertain the structure of Cu(I) complexes, a heteroleptic binuclear Cu(I) double helicate was generated.

There is no study that assessed the effect of co-supplementation of iron and vitamin C on biomarkers of oxidative stress in non-anemic iron-deficient females. We investigated the effects of iron vs. iron + vitamin C co-supplementation on biomarkers of oxidative stress in iron-deficient girls. In a double-blind randomized controlled clinical trial, performed among 60 non-anemic iron-deficient girls, participants were randomly assigned to receive either 50 mg/day elemental iron supplements or 50 mg/day elemental iron + 500 mg/day ascorbic acid for 12 weeks. Fasting blood samples were taken at baseline, weeks 6 and 12 for assessment of biomarkers of oxidative stress. Compared with the baseline levels, both iron and iron + vitamin C supplementation resulted in a significant reduction in serum malondialdehyde (MDA) levels (P time < 0.001) and remarkable elevation in serum total antioxidant capacity (TAC; P time < 0.001) and vitamin C levels (P time = 0.001); however, comparing the two groups we failed to find an additional effect of iron + vitamin C supplementation to that of iron alone on serum TAC and MDA levels (P group was not statistically significant). Iron + vitamin C supplementation influenced serum vitamin C levels much more than that by iron alone (P group < 0.01). We also found a significant interaction term between time and group about serum vitamin C levels while this interaction was not significant about serum TAC and MDA levels. In conclusion, we found that iron supplementation with/without vitamin C improve biomarkers of oxidative stress among non-anemic iron-deficient females and may strengthen the antioxidant defense system by decreasing reactive oxygen species. Co-supplementation of iron + vitamin C has no further effect on oxidative stress compared with iron alone.

In this work, the subsite -3 of cyclodextrin glycosyltransferase (CGTase) from Paenibacillus maceras was engineered to improve maltodextrin specificity for 2-O-d-glucopyranosyl-l-ascorbic acid (AA-2G) synthesis. Specifically, the site-saturation mutagenesis of tyrosine 89, asparagine 94, aspartic acid 196, and aspartic acid 372 in subsite -3 was separately performed, and three mutants Y89F (tyrosine → phenylalanine), N94P (asparagine → proline), and D196Y (aspartic acid → tyrosine) produced higher AA-2G titer than the wild-type and the other mutants. Previously, we found the mutant K47L (lysine → leucine) also had a higher maltodextrin specificity. Therefore, the four mutants K47L, Y89F, N94P, and D196Y were further used to construct the double, triple, and quadruple mutations. Among the 11 combinational mutants, the quadruple mutant K47L/Y89F/N94P/D196Y produced the highest AA-2G titer of 2.23g/L, which was increased by 85.8% compared to that produced by the wild-type CGTase. The reaction kinetics of all the mutants were modeled, and the pH and thermal stabilities of all the mutants were analyzed. The structure modeling indicated that the enhanced maltodextrin specificity may be related with the changes of hydrogen bonding interactions between the side chain of residue at the four positions (47, 89, 94, and 196) and the substrate sugars.

The present research described the preparation, purification, and identification of antioxidant peptides from goat milk casein (GMC). Goat milk casein was hydrolyzed by using a combination of neutral and alkaline proteases to obtain goat milk casein hydrolysates (GMCH) with high antioxidant activity. After desalting by nonpolar macroporous absorption resin, GMCH was isolated and purified by gel filtration chromatography and reversed-phase HPLC, respectively, and further identified by nanoliter electrospray ionization-tandem mass spectrometry. Antioxidant activities of GMC, GMCH, and pure peptides were evaluated and compared using free radical scavenging activity, metal ion chelating ability, and anti-lipid peroxidation ability. Compared with GMC, the free radical-scavenging ability and ferrous ion-chelating ability of GMCH increased significantly. The inhibition effect of lipid peroxidation of GMCH was much stronger than that of tert-butylhydroquinone and phytogermine and a little lower than that of ascorbic acid. The antioxidant activity of GMCH could be attributed to the high antioxidant activity of oligopeptides, especially 5 novel oligopeptides: Val-Tyr-Pro-Phe, Phe-Gly-Gly-Met-Ala-His, Phe-Pro-Tyr-Cys-Ala-Pro, Tyr-Val-Pro-Glu-Pro-Phe, and Tyr-Pro-Pro-Tyr-Glu-Thr-Tyr, which were first observed in GMCH. The antioxidant activity of these 5 novel oligopeptides and GMCH increased 3.59 to 380 times compared with GMC, combining anti-lipid peroxidation ability of GMCH, which indicated that GMCH and its purified fractions in different stages could be used as functional food ingredients, food additives, and pharmaceutical agents in the future.