The chemical properties of alicyclic heterocycles are similar to those of the corresponding chain compounds. Compound: 6-Aminonicotinamide, is researched, Molecular C6H7N3O, CAS is 329-89-5, about Metabolic interaction of hydrogen peroxide and hypoxia in zebrafish fibroblasts, the main research direction is hydrogen peroxide ROS PPP glycolysis hypoxia fibroblast zebrafish; Diphenyleneiodonium chloride; Glycolysis; Hydrogen peroxide; Hypoxia; Pentose phosphate pathway; Reactive oxygen species; Respiration; Zebrafish; roGFP2-Orp1.Recommanded Product: 329-89-5.
Cells require oxygen for aerobic metabolism, which may also result in the production of reactive oxygen species (ROS) as a byproduct. Under low oxygen conditions, ROS formation has been reported to either increase or decrease. We addressed this physiol. response for the first time in zebrafish embryonic fibroblasts (Z3) and used a hydrogen peroxide (H2O2)-specific fluorescent protein (roGFP2-Orp1) either targeted to the mitochondria or expressed in the cytosol. Microfluidic live-cell imaging measurements showed that oxygen deprivation in Z3 cells results in decreased or stable H2O2 levels within the mitochondria or the cytosol, resp., and that the reductive shift recorded in the mitochondrial matrix is directly dependent on oxygen concentration The response was accompanied by a transient increase in extracellular acidification rate (ECAR) and a lower cellular reducing potential as assessed by the viability stain alamarBlue. Complex I and III inhibition with Rotenone and Antimycin A led to H2O2 production under normoxia but these inhibitors were not able to avert the reductive shift under hypoxia. Only by system-wide inhibition of flavin-containing oxidases with Diphenyleneiodonium (DPI) were we able to decrease the reductive shift, while selective inhibition of NADPH oxidases with the inhibitor Apocynin had no effect on the hypoxia response. Since DPI also led to a strong increase in ECAR we found that, in order to keep the cytosolic H2O2 levels stable, glycolytic metabolism was of fundamental importance. According to our experiments with the glucose-6-phosphate dehydrogenase inhibitor 6-Aminonicotinamide, this was attributable to the pentose phosphate pathway producing reducing equivalent required for ROS degradation
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