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Vitamins.

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Usha Sethuraman. 2006. Vitamins.. https://doi.org/10.1542/pir.27-2-44

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Effect of light on ascorbic acid biosynthesis and bioinformatics analysis of related genes in Chinese chives.

Ascorbic acid (AsA) is an essential nutritional component and powerful antioxidant in vegetables, and in plants, AsA levels are regulated by light. AsA levels in the leaves of Chinese chive (Allium tuberosum Rottler ex Spr), a popular vegetable, are poorly understood. Thus, this study was performed to assess the influence of light on AsA biosynthesis in chive and select related genes (AtuGGP1 and AtuGME1); in addition, bioinformatic analyses and gene expression level assays were performed. The biological information obtained for AtuGGP1 and AtuGME1 was analysed with several tools, including NCBI, DNAMAN, and MEGA11. After different light treatments were performed, the Chive AsA content and AtuGGP1 and AtuGME1 expression levels were determined. These results suggest that 1) compared with natural light, continuous darkness inhibited AsA synthesis in chives. 2) The amino acid sequences of AtuGGP1 and AtuGME1 are very similar to those of other plants. 3) The trends observed for the expression levels of AtuGGP1 and AtuGME1 were consistent with the AsA content observed in chives. Hence, we speculated that light controls AsA biosynthesis in chives by regulating AtuGGP1 and AtuGME1 expression. This study provided impactful and informative evidence regarding the functions of GGP and GME in chives.

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Application of far-infrared irradiation in the manufacturing process of green tea.

Seven kinds of green tea leaves were manufactured with far-infrared (FIR) irradiation, and the physicochemical characteristics of the green tea were determined. Appropriate FIR irradiation during the manufacturing process significantly increased the polyphenolic content of green tea. FIR irradiation at 90 degrees C for 10 min, replacing the roasting step, and of the fully processed green tea leaves (GTP3) increased the total phenol content of green tea from 475.6 to 811.1 mg/g and the total flavanol content from 175.7 to 208.7 mg/g, as compared to the control. Epigallocatechin and epigallocatechin gallate increased from 57.68 and 9.60 mg/g in a nonirradiated control to 89.88 and 16.33 mg/g in GTP3, respectively. Ascorbic acid, caffeine, and nitrite scavenging activities were also increased in GTP3. However, the overall color change of GTP3 was negligible. These results indicate that the chemical properties of green tea are significantly affected by FIR irradiation at specific stages of the manufacturing process of green tea leaves and that this FIR irradiation results in high-quality green tea.

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Ascorbate acts as a highly potent inducer of chromate mutagenesis and clastogenesis: linkage to DNA breaks in G2 phase by mismatch repair.

Here we examined the role of cellular vitamin C in genotoxicity of carcinogenic chromium(VI) that requires reduction to induce DNA damage. In the presence of ascorbate (Asc), low 0.2-2 microM doses of Cr(VI) caused 10-15 times more chromosomal breakage in primary human bronchial epithelial cells or lung fibroblasts. DNA double-strand breaks (DSB) were preferentially generated in G2 phase as detected by colocalization of H2AX and 53BP1 foci in cyclin B1-expressing cells. Asc dramatically increased the formation of centromere-negative micronuclei, demonstrating that induced DSB were inefficiently repaired. DSB in G2 cells were caused by aberrant mismatch repair of Cr damage in replicated DNA, as DNA polymerase inhibitor aphidicolin and silencing of MSH2 or MLH1 by shRNA suppressed induction of H2AX and micronuclei. Cr(VI) was also up to 10 times more mutagenic in cells containing Asc. Increasing Asc concentrations generated progressively more mutations and DSB, revealing the genotoxic potential of otherwise nontoxic Cr(VI) doses. Asc amplified genotoxicity of Cr(VI) by altering the spectrum of DNA damage, as total Cr-DNA binding was unchanged and post-Cr loading of Asc exhibited no effects. Collectively, these studies demonstrated that Asc-dependent metabolism is the main source of genotoxic and mutagenic damage in Cr(VI)-exposed cells.

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