Biochemistry of fluoroacetate poisoning. Isolation of an active tricarboxylic acid fraction from poisoned kidney homogenates

Buffa, P.; Peters, Rudolph; Wakelin, R. W.

doi:10.1042/bj0480467

Cited by 57 publications

(33 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, Buffa & Peters (1949) have shown that animals poisoned with fluoroacetate show large accumulations of citrate in many of their tissues (their paper may be consulted for references to the earlier literature). This observation has been confirmed by Potter & Busch (1950), Lindenbaum, White & Schubert (1951 and Kandel, Johnson & Chenoweth (1951).…”

Section: Discussionmentioning

confidence: 99%

“…This and other work has led to the hypothesis, originally proposed to explain in vitro experiments by Li6becq & Peters (1948) and Martius (1949), that fluoroacetate is metabolized in a similar manner to ordinary acetate via the tricarboxylic acid cycle to a fluorotricarboxylic acid which then inhibits one of the enzymes necessary for citrate oxidation. In a test of this hypothesis by Buffa, Peters & Wakelin (1951), tricarboxylic acid fractions containing fluorine have been isolated from poisoned kidney tissue. These fractions are potent inhibitors of citrate metabolism in kidney homogenates.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

1952

Biochemical Journal

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

1952

Biochemical Journal

View full text Add to dashboard Cite

“…Unfortunately this is not very helpful since it is well known that at least two key enzymes in oxidative catabolism -pyruvic and alpha-ketoglutaric dehydrogenasehave such a grouping and are inhibited by these compounds (12). The inhibition by fluoroacetate also points to the involvement of the tricarboxylic acid cycle (5). The carbonyl reagents, bisulfite.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of stimulation of respiration by purines: I. Inhibitor studies

Bach¹

1961

Plant Physiol.

View full text Add to dashboard Cite

A previous publication (1) reported a striking stinmulation of the endogenous respiration of nitrogenstarved Chlorella cells by low concentrations of various purines and purine analogs. This stimulation has sinice been shown in a large variety of nitrogenstarved nmicroorganisms as well as in some higher plants (2).Because of the widespread occurrence of this effect an(l the possibility that a novel regulatory functiotn of intracellular purines might be involved, the nmodle of action of the purines was further investigatedl. One mleanis of gaining insight into the possible metabolic pathways which nmight be involved is by means of imietabolic inhibitors with known sites of action. Thus it miight be possible to locate the purine effect in reactions involving the cytochrome system, oxidative phosplhorylation, amino acid metabolism, or glvcolvsis, for example. if it could be shown that known specific inhibitors of these systems inhibited the purine effect. This paper discusses the results fronm such studies andl points to the involvement of flavoprotein enzymes and cellular lipids in the respiration wlhiclh is causedt by purines. Further direct evidence for the existence of an electron transport system Nwhichl is mle(liated by free purines and is active in the oxi(lation of storage fat will be presented in future papers (3,4 (13). Total radioactivity was leternlinedl by plating the BaCOŵhich was recovered from the center wells of the Warburg oxygen flasks. The center wells wvere rinsed three tinmes into a centrifuge tube with distilled water an(d the trapped C'40., precipitate(l by the addition of a few drops of 12 % BaCI.2. The precipitate was washed with methanol and plate(d as previously dlescribe(l (1). Duplicate flasks were used in all cases. All radioactivities were corrected for self absorption and are expressed for infinite thickness.In the tinme course experimielnts 5 mll cells were suspen(le(l with or without 6-mercaptopurine in 25 nl Frlenmileyer flasks and shaken at 250 C in the (lark. At given intervals flasks were removedl. 3 ml of the contents pipette(l into Warburg flasks and the respirometric expel-imiients con(lucte(l.Although results from (luplicate flasks in these experiments always agreed to within less than 10 % there was consi(derable dlay to (lay variation (1). As a result, all experiments were con(lucted at least at two separate occasions and the results thus obtained were average(l after adjustnment of the uninhibited controls to the same level (1). Furthermore

show abstract

“…found (Table 2). These observations areconsistent with the view that in Gloeocapsa sp., as in many other organisms, fluoroacetate undergoes 'lethal synthesis' to fluorocitrate, which inhibits aconitate hydratase and blocks the metabolism of citrateito isocitrate, 2-oxoglutarate and glutamate (Buffa et al, 1951). In addition, the NADP+-dependent isocitrate dehydrogenase of Gloeocapsa sp.…”

Section: Fluoroacetate and Carbon Metabolismmentioning

confidence: 99%

“…Ethanol-soluble radioactive products were isolated, separated and identified as above or by chromatography in propanol/ammonia/water (6 : 3 : 1, by vol.) according to the method of Buffa, Peters & Wakelin (1951). Lipids were extracted as described by Folch, Lees & Sloane-Stanley (1957) after termination of the incubation by adding excess (6 ml) methanol or 2-propanol.…”

Section: Growth Of Cultures Gloeocapsa Sp ~~7 9mentioning

confidence: 99%

Fluoroacetate Metabolism in Gloeocapsa sp. LB795 and its Relationship to Acetylene Reduction (Nitrogen Fixation)

Gallon

Ul-Haque

Chaplin

1978

Journal of General Microbiology

View full text Add to dashboard Cite

Sodium fluoroacetate (1 mM) caused an accumulation of citrate and altered the lipid composition in cells of Gloeocapsa sp. ~~7 9 5 .It also inhibited acetylene reduction (nitrogen fixation) by the alga -markedly under aerobic conditions, but much less so in the absence of oxygen. This inhibition is largely the result of the conversion of fluoroacetate to fluorocitrate which, by inhibiting aconitate hydratase (EC 4.2.1 .3), interrupts the synthesis of the 2-oxoglutarate required for the assimilation of NH,+. The consequent accumulation of NH,+ within the cells of Gloeocapsa sp. inhibits nitrogenase synthesis and, since oxygen rapidly inactivates pre-existing nitrogenase, nitrogen fixation by Gloeocapsa sp. decreases under aerobic conditions.

show abstract

Biochemistry of fluoroacetate poisoning. Isolation of an active tricarboxylic acid fraction from poisoned kidney homogenates

Cited by 57 publications

References 5 publications

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

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

Mechanism of stimulation of respiration by purines: I. Inhibitor studies

Fluoroacetate Metabolism in Gloeocapsa sp. LB795 and its Relationship to Acetylene Reduction (Nitrogen Fixation)

Contact Info

Product

Resources

About