High impact information on Acon

• We also find that exposure of adults to paraquat converts cytosolic aconitase to IRP1 but has no affect on mitochondrial aconitase, indicating that paraquat generates superoxide in the cytosol but not in mitochondria [1].
• Furthermore, Drosophila SDHb represents the second example, after porcine mitochondrial aconitase, of an enzyme of the citric acid cycle whose mRNA possesses all necessary features for translational regulation by cellular iron levels [2].
• Administration of fluoroacetate, a competitive inhibitor of aconitase activity, resulted in a dose-dependent decrease in the life span of the flies [3].
• Exposure to 100% ambient oxygen showed that aconitase was highly susceptible to undergo oxidative damage and loss of activity under oxidative stress [3].
• Under hyperoxia, fh-RNAi flies also showed a dramatic reduction of aconitase activity that seriously impairs the mitochondrial respiration while the activities of succinate dehydrogenase, respiratory complex I and II, and indirectly complex III and IV are normal [4].

Associations of Acon with chemical compounds

• Aconitase inactivation was calibrated using the known rate of matrix superoxide production from complex I. Glycerol phosphate dehydrogenase generated superoxide about equally to each side of the membrane, whereas centre o of complex III in the presence of antimycin A generated superoxide about 30% on the cytosolic side and 70% on the matrix side [5].

References