Disease relevance of Pterin-6-aldehyde

• Radiation-induced apoptosis and its possible enhancement in the presence of 6-formylpterin (6-FP), a metabolite of folic acid, were examined in human myelomonocytic lymphoma U937 cells [1].
• However, the killing rate of the DPI-treated neutrophils against E. coli and S. aureus significantly increased when 6-formylpterin was administered [2].
• In order to apply this potential to anti-cancer photodynamic therapy (PDT), we prepared a novel variant of 6FP, 2-(N,N-dimethylaminomethyleneamino)-6-formyl-3-pivaloylpteridine-4-one (6FP-tBu-DMF), and examined its photodynamic effects on a pancreatic cancer cell line, Panc-1 cells [3].
• 6-Formylpterin protects retinal neurons from transient ischemia-reperfusion injury in rats: a morphological and immunohistochemical study [4].

High impact information on Pterin-6-aldehyde

• 6-Formylpterin was purified by paper chromatography, and bovine pineal hydroxyindole-O-methyltransferase (S-adenosyl-L-methionine:N-acetylserotonin O-methyl-transferase; EC 2.1.1.4) was purified by flat-bed gel electrofocusing [5].
• 6-formylpterin suppressed cell proliferation in PanC-1 cells and inhibited Fas-mediated apoptosis in Jurkat cells [6].
• The intracellular ROS generation by 6-formylpterin was observed in other cells, such as PanC-1 cells and Jurkat cells [6].
• When 6-formylpterin was administered to HL-60 cells, intracellular ROS generation was observed and apoptosis was induced [6].
• In the T cells stimulated with mitogenic lectin phytohemagglutinin (PHA) in conjunction with phorbol myristate acetate (PMA), 6-formylpterin suppressed the NF-kappaB-dependent transcription, the production of cytokines (IFN-gamma and IL-2) and the cell proliferation [7].

Chemical compound and disease context of Pterin-6-aldehyde

• The enhancement of heat-induced apoptosis by 6-formylpterin, an intra-cellular generator of hydrogen peroxide (H2O2), was examined in human myelomonocytic lymphoma U937 cells [8].

Biological context of Pterin-6-aldehyde

• The incubation of T cells with 50-500microM 6-formylpterin for 24hr brought about the elevation of intracellular ROS without inducing cell death [7].
• When T cells isolated from fresh blood were incubated with 6-formylpterin for 1hr, the oxygen consumption and concomitant ROS generation were observed [7].
• The induction of heat-induced apoptosis evaluated by morphological observation and DNA fragmentation were promoted by the addition of 6-formylpterin [8].

Anatomical context of Pterin-6-aldehyde

• Effects of intracellular reactive oxygen species generated by 6-formylpterin on T cell functions [7].
• The effects of 6-formylpterin on the impaired bactericidal activity of human neutrophils were examined ex vivo [2].
• After iodine oxidation, biopterin, 6-hydroxymethylpterin, and 6-formylpterin were identified in mouse spleen lymphocytes by means of reverse-phase HPLC, Crithidia assay, and oxidative degradation [9].
• Protective effects of intracellular reactive oxygen species generated by 6-formylpterin on tumor necrosis factor-alpha-induced apoptotic cell injury in cultured rat hepatocytes [10].
• Effects of 6-formylpterin as an internal source of hydrogen peroxide on cell death of human peripheral blood leukocytes [11].

Associations of Pterin-6-aldehyde with other chemical compounds

• When neutrophils isolated from fresh blood were incubated with 6-formylpterin, the intracellular production of hydrogen peroxide (H(2)O(2)) occurred [2].
• The superoxide (O2.-) scavenging activity and the neuroprotective effects of pterin-6-aldehyde (P6A), a xanthine oxidase inhibitor, were examined and compared with those of alpha-phenyl-N-tert-butyl nitrone (PBN), a spin trapping agent [12].
• NP did not affect O2.- release in hypoxanthine/xanthine oxidase (HPX/XOD) reaction system, but pterin-6-aldehyde (P6A), one of photodegraded products of NP, suppressed it [13].
• A detailed analysis utilising UV/visible spectrophotometry, HPLC, TLC, and mass spectroscopy showed for sepiapterin direct oxidation to P-6-COOH, whereas 6-biopterin formed the intermediate 6-formylpterin (P-6-CHO) which is then further photo-oxidised to P-6-COOH [14].
• The results presented in this paper, however, demonstrate that normal human skin fibroblasts in culture readily degrade folic acid to pterin-6-aldehyde or a closely-related substance [15].

Gene context of Pterin-6-aldehyde

• 6-Formylpterin suppressed the expression of iNOS, and it also inhibited the catalytic activity of iNOS, which collectively resulted in the inhibition of NO production in the stimulated macrophages [16].
• The co-incubation of the TNF-alpha/ActD-treated hepatocytes with 100-500 microM 6-formylpterin attenuated the TNF-alpha/ActD-induced apoptotic cell injury [10].
• Therefore, our findings suggest that intracellular ROS generated by 6-formylpterin decline the intracellular redox state to an oxidant state, which suppresses the caspase activity and prevents the apoptotic cell injury of hepatocytes [10].
• Furthermore, both the release of cytochrome c from mitochondria to cytosol and the translocation of PKCd from cytosol to mitochondria, which were induced by heat shock, were enhanced by the addition of 6-formylpterin [8].
• Novel 6-formylpterin derivatives: chemical synthesis and O(2) to ROS conversion activities [17].

Analytical, diagnostic and therapeutic context of Pterin-6-aldehyde

• Twenty-nine patients whose diagnoses were not revealed until after the test of their first morning urine for pterin-6-aldehyde was completed were studied for the presence or absence of pterin-6-aldehyde by thin-layer chromatography [18].
• The production analysis using high-performance liquid chromatography documented that 6-formylpterin catalyzes the conversion from NADH to NAD [6].
• The study using laser scanning confocal microscopy showed that the drug uptake, the 1O2 generation, and cell death were observed in the 6FP-tBu-DMF-treated cells, while these phenomena were not observed in the 6FP-treated cells [3].

References