Trace amounts of Triton X-100 modify the inhibitor sensitivity of the mitochondrial porin.
Transport properties of mitochondrial porin were investigated on the basis of changes in the activity of hexokinase utilizing external ATP. Production of glucose 6-phosphate is inhibited by polyanion both in intact brain mitochondria and in contact point vesicles. Hexokinase activity is restored by solubilization of the enzyme by high ionic strength or 0.5-1% Triton X-100. In very low concentrations (0.001-0.005%) Triton does not mobilize hexokinase from its binding sites but it is able to release polyanion-inhibition completely. This finding provides an explanation for the discrepancy observed in the transport properties of porin when studied 'in situ' or in artificial lipid membranes.
Báthori
G
G
Department of Physiology, Semmelweis Medical University, Budapest, Hungary.
Fonyó
A
A
Ligeti
E
E
D000818:Animals; D001921:Brain / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D006593:Hexokinase / Q000378:metabolism; D007700:Kinetics; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009245:NADH Dehydrogenase / Q000378:metabolism; D017830:Octoxynol / Q000494:pharmacology*; D018272:Porins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D012680:Sensitivity and Specificity; D013385:Succinate Dehydrogenase / Q000378:metabolism
D018272:Porins; D017830:Octoxynol; D013385:Succinate Dehydrogenase; D009245:NADH Dehydrogenase; D006593:Hexokinase; D003402:Creatine Kinase