The inhibition of aconitase by ‘inhibitor fractions’ isolated from tissues poisoned with fluoroacetate

Abstract

second, increased deposition of muscle glycogen; third, increased glucose use in the tissues; and fourth, conversion to fat.In the non-diabetic rat salicylate caused no change in blood glucose, but a significant reduction of liver glycogen and similar mechanis may be involved. The possibility that the glucose may be converted to glucuronic acid which is used for conjugation with salicylate is unlikely because of Lutwak-Mann's (1942) conclusion that the ability of rat liver to form a conjugated glucuronide from salicylate was negligible.It is proposed to extend this work to investigate the possibilities discussed above. SUMMARY 1. The effect of salicylate on the glycosuria, blood glucose and liver-glycogen content of the alloxan-diabetic rat and on the blood glucose and liver glycogen of the normal rat have been studied.2. Salicylate reduces the glycosuria and blood glucose in the diabetic rat, but causes no change in the liver-glycogen content. In the normal rat salicylate causes no alteration in the blood glucose, but a depression of the liver-glycogen content. 3. Possible mechanisms of these changes are discussed.We wish to express our thanks to Miss M. Sandiford and Miss E. Quilley for able technical assistance. One of us (M.J.H.S.) is indebted to the Board of Governors of King's College Hospital for a grant towards the cost of the work.

Abundance and ecophysiology of Defluviicoccus spp., glycogen-accumulating organisms in full-scale wastewater treatment processes

“…Accumulation of polyP was also determined in biomass sampled directly from the aerobic zone of full-scale plants. The glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase was inhibited using sodium iodoacetate (Bickis & Quastel, 1965) at final concentrations of 0.5, 1.0 or 2.0 mM, and aconitase, which catalyses conversion of citrate to isocitrate in the tricarboxylic acid (TCA) cycle, was inhibited using sodium fluoroacetate (Lotspeich et al, 1952) at final concentrations of 0.5, 1.0 or 2.0 mM.…”

The Role of the Krebs Cycle in Conjugation in Escherichia coli K-12

“…Fluoroacetic acid acts as a poison by first being converted to ff uorocitric acid which then competitively inhibits the metabolism of citric acid by the tricarboxylic acid cycle (Buffa & Peters, 1949;LiCbecq & Peters, 1949;Lotspeich, Peters & Wilson, 1952). The ability of this inhibitor to stop zygote formation was accordingly investigated.…”

Aconitase is a sensitive and critical target of oxygen poisoning in cultured mammalian cells and in rat lungs.

“…We now report that aconitase is a sensitive target of hyperoxic damage in vitro and in vivo and demonstrate that inhibition of aconitase with fluoroacetate (or fluorocitrate) (29)(30)(31)(32)(33)(34) dehydrogenase, and porcine heart isocitrate dehydrogenase were from Sigma. Sodium (+)-fluorocitrate was prepared by titrating barium fluorocitrate with a slight excess of sulfuric acid, centrifuging to remove BaSO4, and then neutralizing the supernatant with NaOH.…”

“…We now report that aconitase is a sensitive target of hyperoxic damage in vitro and in vivo and demonstrate that inhibition of aconitase with fluoroacetate (or fluorocitrate) (29)(30)(31)(32)(33)(34) (and growth) were assessed by the neutral red dye-retention assay (35). To prepare cell extracts, the growth medium was aspirated from the adherent A549 cell cultures, and the cells (=5 x 106 per dish) were chilled and washed with 5 ml of ice-cold Dulbecco's phosphate-buffered saline (PBS) (1.1 mM KH2PO4/8.1 mM Na2HPO4/138 mM NaCl/2.7 mM KCI/0.5 mM MgCl2/0.9 mM CaCl2).…”