PubMed · 13633101
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
1959. ASCORBIC acid in serum.. https://doi.org/10.1111/j.1753-4887.1959.tb06400.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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.
A short-term pre-exposure to dehydroascorbic acid (DHA) promotes U937 cell death upon exposure to otherwise non-toxic levels of peroxynitrite (ONOO-). Toxicity is mediated by a saturable mechanism and cell death takes place as a consequence of mitochondrial permeability transition. The following lines of evidence are consistent with the notion that the enhancing effects of DHA were related to mitochondrial events resulting in inhibition of complex III upon exposure to otherwise inactive concentrations of ONOO-. First, DHA, as well as bona fide complex III inhibitors, similarly enhanced toxicity and subsequent formation of H2O2 induced by ONOO- via a rotenone- or catalase-sensitive mechanism. Secondly, bona fide complex III inhibitors were ineffective in DHA-pre-loaded cells. In addition, respiration-deficient cells were resistant to toxicity elicited by ONOO- and their supplementation with increasing concentrations of DHA, although resulting in the accumulation of vitamin C levels identical with those observed in respiration-proficient cells, failed to affect ONOO- toxicity. Finally, oxygen-consumption experiments demonstrated that pre-exposure to DHA promotes the ONOO--dependent inhibition of complex III. In conclusion, the above results collectively demonstrate that increasing the intracellular accumulation of vitamin C promotes mitochondrial events leading to ONOO--dependent formation of H2O2 and resulting in a rapid necrotic response.
A novel approach potentially useful for the development of more thromboresistant polymeric materials is examined. The method is based on the catalytic generation of nitric oxide (NO) via Cu(I) mediated reduction of nitrite ions. Preliminary solution phase studies demonstrate that ascorbate or thiolate anions can generate Cu(I) from Cu(II) with subsequent catalytic conversion of any nitrite ions present to NO by the unstable Cu(I) species. Incorporation of this same chemistry within a hydrophobic polymeric material requires immobilizing Cu(II) ions into a polymeric phase via use of a lipophilic Cu(II) chelating ligand (dibenzo [e,k]-2,3,8,9-tetraphenyl-1,4,7,10-tetraaza-cyclododeca-1,3,7,9-tetraene (DTTCT)). It is shown that this complex can be reduced to its Cu(I) form by appropriate reducing equivalents present in the bathing solution. The resulting Cu(I) complex can then reduce nitrite to NO with the NO generation occurring at the polymer/solution interface at physiological pH. Data from chemiluminescence experiments indicate that the flux of NO at the polymer surface is comparable to that of endothelial cells (>/=1x10(-10)mol/cm(2)min) when 0.5mM nitrite/1mM ascorbate are present in the bathing solution. Potentially more useful NO generation can be achieved by doping the polymer film with the Cu(II) complex along with a lipophilic quaternary ammonium nitrite salt. In this case reducing equivalents within the aqueous phase enable the nitrite derived from the polymer to be converted into NO by the Cu(II/I) ligand complex. Films of this type are shown to generate NO for at least 6h in PBS buffer with fluxes on the order of 1.5x10(-10)mol/cm(2)min. Physiologically relevant levels of NO release are also shown to exist at the polymer interface when films are soaked in fresh plasma as well as undiluted whole blood, indicating that endogenous reducing equivalents present in blood can efficiently reduce the Cu(II)-ligand within the polymer film. The prospects of using these new NO releasing films to devise more biocompatible polymeric coatings for biomedical applications are discussed.