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Citric acid cycle citrate

Aconitase (citric acid cycle) Citrate/isocitrate... [Pg.213]

In the Calvin cycle, COg is converted into hexose or fructose. 3-Phosphoglycerate is the key catalytic molecule that is consumed and generated in this cycle. In the citric acid cycle, citrate is the intermediate species in the sequence of oxidation steps that lead to CO2. [Pg.315]

These considerations are supported by the observation that the active oxidation of some member of the citric acid cycle (citrate) is necessary for the maximum incorporation of formate into serine by the cyclo-phorase system of Green. ... [Pg.116]

Glycolysis and the citric acid cycle (to be discussed in Chapter 20) are coupled via phosphofructokinase, because citrate, an intermediate in the citric acid cycle, is an allosteric inhibitor of phosphofructokinase. When the citric acid cycle reaches saturation, glycolysis (which feeds the citric acid cycle under aerobic conditions) slows down. The citric acid cycle directs electrons into the electron transport chain (for the purpose of ATP synthesis in oxidative phosphorylation) and also provides precursor molecules for biosynthetic pathways. Inhibition of glycolysis by citrate ensures that glucose will not be committed to these activities if the citric acid cycle is already saturated. [Pg.619]

Aconitase catalyzes the citric acid cycle reaction citrate isocitrate... [Pg.672]

Elucidating the stereochemistry of reaction at prochirality centers is a powerful method for studying detailed mechanisms in biochemical reactions. As just one example, the conversion of citrate to (ds)-aconitate in the citric acid cycle has been shown to occur with loss of a pro-R hydrogen, implying that the reaction takes place by an anti elimination mechanism. That is, the OH and H groups leave from opposite sides of the molecule. [Pg.317]

The dehydration of citrate to yield c/s-aconitate, a step jn the citric acid cycle, involves the pro-R "arm" of citrate rather than the pio-S arm. Which of the following two products is formed ... [Pg.329]

The first step in the citric acid cycle is reaction of oxaloacetate with acetyl CoA to give citrate. Propose a mechanism, using acid or base catalysis as needed. [Pg.911]

Enzymes work by bringing reactant molecules together, holding them, in the orientation necessary for reaction, and providing any necessary acidic or basic sites to catalyze specific steps. As an example, let s look at citrate synthase, an enzyme that catalyzes the aldol-like addition of acetyl CoA to oxaloacetate to give citrate. The reaction is the first step in the citric acid cycle, in which acetyl groups produced by degradation of food molecules are metabolized to yield C02 and H20. We ll look at the details of the citric acid cycle in Section 29.7. [Pg.1043]

Step 1 of Figure 29.12 Addition to Oxaloacetate Acetyl CoA enters the citric acid cycle in step 1 by nucleophilic addition to the oxaloacetate carbonyl group, to give (S)-citryl CoA. The addition is an aldol reaction and is catalyzed by citrate synthase, as discussed in Section 26.11. (S)-Citryl CoA is then hydrolyzed to citrate by a typical nucleophilic acyl substitution reaction, catalyzed by the same citrate synthase enzyme. [Pg.1156]

Problem 29.11 Write mechanisms for step 2 of the citric acid cycle, the dehj dration of citrate and the addition of water to aconitate. [Pg.1159]

Problem 29.12 ls the pro-R or pro-5 hydrogen removed from citrate during the dehydration in step 2 of the citric acid cycle Does the elimination reaction occur with syn or anti geometry ... [Pg.1159]

Citrate is isomerized to isocitrate by the enzyme aconitase (aconitate hydratase) the reaction occurs in two steps dehydration to r-aconitate, some of which remains bound to the enzyme and rehydration to isocitrate. Although citrate is a symmetric molecule, aconitase reacts with citrate asymmetrically, so that the two carbon atoms that are lost in subsequent reactions of the cycle are not those that were added from acetyl-CoA. This asymmetric behavior is due to channeling— transfer of the product of citrate synthase directly onto the active site of aconitase without entering free solution. This provides integration of citric acid cycle activity and the provision of citrate in the cytosol as a source of acetyl-CoA for fatty acid synthesis. The poison fluo-roacetate is toxic because fluoroacetyl-CoA condenses with oxaloacetate to form fluorocitrate, which inhibits aconitase, causing citrate to accumulate. [Pg.130]

The citric acid cycle is the final pathway for the oxidation of carbohydrate, Upid, and protein whose common end-metabolite, acetyl-CoA, reacts with oxaloacetate to form citrate. By a series of dehydrogenations and decarboxylations, citrate is degraded, releasing reduced coenzymes and 2CO2 and regenerating oxaloacetate. [Pg.135]

Chenoweth believes that an explanation of the above results may lie in the reactions occurring before the entrance of fatty acid metabolites into the citric acid cycle. Activated acetate, i.e. acetyl coenzyme A (AcCoA) is the end-product of fatty acid metabolism prior to its condensation with oxalacetate to form citrate. Possibly fluoro-fatty acids behave like non-fluorinated fatty acids. The end-product before the oxalacetate condensation could be the same for all three fluorinated inhibitors, viz. fluoroacetyl coenzyme A (FAcCoA). Fluorocitrate could then be formed by the condensation of oxalacetate with FAcCoA, thereby blocking the citric acid cycle. The specificity of antagonisms must therefore occur before entrance of the metabolites into the citric acid cycle. [Pg.180]

The key to unraveling the toxicity of fluoracetate came from observations of Buffa and Peters (1949) that in animals treated with FAc, considerable quantities of citrate accumulated in some tissues. Oxygen uptake was also diminished. The citric acid cycle was thus implicated as the site of inhibition. Fluorcitrate was then isolated from the affected tissues. It was found to be a powerful competitive inhibitor of aconitase, thus blocking citrate oxidation. The suggestion was therefore made that fluoracetate was toxic not in itself, but because it was metabolized in cells via fluoracetyl CoA to give a toxic derivative, an example of lethal synthesis —the capacity of organisms to metabolize nontoxic compounds and convert them to potentially lethal products. [Pg.80]

This diagram shows the citric acid cycle. For simplicity, the molecules in the citric acid cycle are represented here as acids. In the body, they are actually present as iens. For example, citric acid is present as citrate ions. [Pg.565]

The citrate shuttle transports acetyl CoA groups from the mitochondria to the cytoplasm for fatty acid synthesis. Acetyl CoA combines with oxaloacetate in the mitochondria to form citrate, but rather than continuing in the citric add cycle, citrate is transported into the cytoplasm. Factors that indirectly promote this process indude insuKn and high-energy status. [Pg.208]

Aconitase [citrate(isocitrate) hydro-lyase, EC 4.2.1.3] is the second enzyme of the citric acid cycle, which plays a central role in metabolism for all aerobic organisms. This enzyme catalyzes a dehydration-rehydration reaction interconverting citrate and 2R,3S-isocitrate via the allylic intermediate ds-aconitate. [Pg.343]

A similar aldol reaction is encountered in the Krebs cycle in the reaction of acetyl-CoA and oxaloacetic acid (see Section 15.3). This yields citric acid, and is catalysed by the enzyme citrate synthase. This intermediate provides the alternative terminology for the Krebs cycle, namely the citric acid cycle. The aldol reaction is easily rationalized, with acetyl-CoA providing an enolate anion nucleophile that adds to the carbonyl of oxaloacetic acid. We shall see later that esters and thioesters can also be converted into enolate anions (see Section 10.7). [Pg.363]

The Krebs cycle intermediate that reacts with acetyl-CoA is oxaloacetate, and this reacts via an aldol reaction, giving citryl-CoA. However, the enzyme citrate synthase also carries out hydrolysis of the thioester linkage, so that the product is citrate hence the terminology citric acid cycle . The hydrolysis of the thioester is actually responsible for disturbing the eqnilibrinm and driving the reaction to completion. [Pg.585]

Potent metabolic inhibitors of the citric acid cycle. Fluo-roacetate (F-CH2COO ) must first be converted to flu-oroacetyl-S-CoA (by acetyl-CoA synthetase) and thence to fluorocitrate (by citrate synthase) before it can act as a potent metabohc inhibitor of the aconitase reaction as well as citrate transport. Submicromolar concentrations of ( )-erythro-Q iOTOcitTate can irreversibly inhibit citrate uptake by isolated brain mitochondria. [Pg.291]

Fluoroacetate produces its toxic action by inhibiting the citric acid cycle. The fluorine-substituted acetate is metabolized to fluoroci-trate that inhibits the conversion of citrate to isocitrate. There is an accumulation of large quantities of citrate in the tissue, and the cycle is blocked. The heart and central nervous system are the most critical tissues involved in poisoning by a general inhibition of oxidative energy metabolism. ... [Pg.635]

The toxicity of fluoroacetic acid and of its derivatives has played an historical decisive role at the conceptual level. Indeed, it demonstrates that a fluorinated analogue of a natural substrate could have an activity profile that is far different from that of the nonfluorinated parent compound. The toxicity of fluoroacetic acid is due to its ability to block the citric acid cycle (Krebs cycle), which is an essential process of the respiratory chain. The fluoroacetate is transformed in vivo into 2-fluorocitrate by the citrate synthase. It is generally admitted that aconitase (the enzyme that performs the following step of the Krebs cycle) is inhibited by 2-fluorocitrate the formation of aconitate through elimination of the water molecule is a priori impossible from this substrate analogue (Figure 7.1). [Pg.224]

Phosphorylation of an enzyme can affect catalysis in another way by altering substrate-binding affinity. For example, when isocitrate dehydrogenase (an enzyme of the citric acid cycle Chapter 16) is phospho-rylated, electrostatic repulsion by the phosphoryl group inhibits the binding of citrate (a tricarboxylic acid) at the active site. [Pg.230]

The biosynthetic pathway to glucose described above allows the net synthesis of glucose not only from pyruvate but also from the four-, five-, and six-carbon intermediates of the citric acid cycle (Chapter 16). Citrate,... [Pg.548]

In examining the eight successive reaction steps of the citric acid cycle, we place special emphasis on the chemical transformations taking place as citrate formed from acetyl-CoA and oxaloacetate is oxidized to yield C02 and the energy of this oxidation is conserved in the reduced coenzymes NADH and FADH2. [Pg.608]


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See also in sourсe #XX -- [ Pg.242 ]




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