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Folic acid from PABA

A wide range of compounds also inhibit a number of the enzyme systems that are involved in the biosynthesis of purines and pyrimidines in bacteria. For example, sulphonamide bacteriostatics inhibit dihydropteroate synthetase, which prevents the formation of folic acid in both humans and bacteria. However, although both mammals and bacteria synthesize their folic acid from PABA (Figure 7.12), mammals can also obtain it from their diet. In contrast, trimethoprim specifically inhibits bacterial DHF, which prevents the conversion... [Pg.150]

Para-amino benzoic acid (PABA) is considered to be in the B-complex vitamin family. The human body can make it from folic acid, since PABA forms the middle part of that vitamin ... [Pg.5]

Sulfa drugs have a close structural resemblance to PABA. When taken by a person suffering from a bacterial infection, a sulfa drug is transformed by the body to the compound sulfanilamide, which attaches to the bacterial receptor sites designed for PABA, as shown in Figure 14.7, thereby preventing the synthesis of folic acid. Without folic acid, the bacteria soon die. The patient, however, because he or she receives folic acid from the diet, lives on. [Pg.485]

A-2) Sulfonamides. Bacteria need PABA in order to form folic acid. Humans do not need PABA, as they get folic acid from the diet. Sulfonamides are competitive antagonists of PABA and thus can affect bacteria while not harming human cells (fig. 10.4). [Pg.67]

However, because malonic acid has only one methylene group, it is obvious that no oxidation-reduction can take place. Only association of the enzyme and inhibitor, and dissociation of the I complex, can occur. Another classical example of a competitive inhibitor is the sulfa drug sulfanilamide, which interferes with the biosynthesis of folic acid from the precursor -aminobenzoic acid (PABA). [Pg.247]

Sulfamethoxazole like other sulfonamides is bacteriostatic. It acts by inhibiting formation of tetrahydrofolic acid from PABA, thus preventing bacterial cell synthesis of folic acid (see Figure 90). [Pg.659]

We have already seen the importance of folic acid and its derivative, tetrahydrofolate, in several reactions. This importance has been exploited in human medicine. Bacteria synthesize folic acid from p-aminobutyric acid (PABA). A type of antibiotic called a sulfonamide (Figure a) works by competing with PABA in the synthesis of folic acid. Because folic acid is critical to the formation of purines,... [Pg.691]

A competitive inhibitor resembles the substrate in its chemical structure and is able to combine with the enzyme to form an enzyme-inhibitor complex. In so doing it competes with the substrate for the active sites of the enzyme, and formation of the enzyme-substrate complex is inhibited. This type of inhibition may be reversed by the addition of excess substrate, which displaces the inhibitor, forming normal enzyme-substrate complexes. One of the best-known examples is provided by the sulphonamide drugs. The synthesis of folic acid from p-aminobenzoic acid (PABA) is a vital metabolic process in the bacteria controlled by these drugs. The similarity between PABA and sulphanUamide, released by the sulphonamides, is obvious ... [Pg.151]

The answer is c. (Hardman, pp 1058-1059. Katzung, pp 793-795.) Trimethoprim inhibits dihydro folic acid reductase. Sulfamethoxazole inhibits p-aminobenzoic acid (PABA) from being incorporated into folic acid by competitive inhibition of dihydropteroate synthase. Either action inhibits the synthesis of tetrahydrofolic acid. [Pg.80]

Theory Folic acid (I) undergoes cleavage by reduction with Zn-Hg in acidic medium to yield p-aminobenzoylglutamic acid (II). The primary aromatic amino group present in the latter is subsequently diazotized in the usual manner and coupled in acidic solution with N-(l-naphthyl)-ethylenediamine hydrochloride in the absence of light (caution). The colour thus produced has a maximum absorption at 550 nm and the extinction (E) is consequently compared with a calibration curve obtained from / -aminobcnzoic acid (PABA) that has been duly diazotized and coupled exactly in the same fashion as the/ -aminobcnzoylglutamic acid. [Pg.308]

The structure of sulfa drug molecules, however, is very similar to that of the PABA molecule. Compare the structure of sulfanilamide, in part 2 of the diagram, with that of PABA. Notice how easily the sulfanilamide molecule can substitute for the PABA molecule in the synthesis of the bacterium s folic acid. The problem for the bacterium, however, is that folic acid produced from a sulfa drug molecule is... [Pg.8]

Both the sulfonamides and trimethoprim interfere with bacterial folate metabolism. For purine synthesis tetrahydrofolate is required. It is also a cofactor for the methylation of various amino acids. The formation of dihydrofolate from para-aminobenzoic acid (PABA) is catalyzed by dihydropteroate synthetase. Dihydrofolate is further reduced to tetrahydrofolate by dihydrofolate reductase. Micro organisms require extracellular PABA to form folic acid. Sulfonamides are analogues of PABA. They can enter into the synthesis of folic acid and take the place of PABA. They then competitively inhibit dihydrofolate synthetase resulting in an accumulation of PABA and deficient tetrahydrofolate formation. On the other hand trimethoprim inhibits dihydrofolate... [Pg.413]

The only antimalarial drugs whose mechanisms of action are reasonably well understood are the drugs that inhibit the parasite s ability to synthesize folic acid. Parasites cannot use preformed folic acid and therefore must synthesize this compound from the following precursors obtained from their host p-aminobenzoic acid (PABA), pteridine, and glutamic acid. The dihydrofolic acid formed from these precursors must then be hydrogenated to form tetrahydrofoUc acid. The latter compound is the coenzyme that acts as an acceptor of a variety of one-carbon units. The transfer of one-carbon units is important in the synthesis of the pyrimidines and purines, which are essential in nucleic acid synthesis. [Pg.614]

Sulfonamides are used for controlling urinary tract infections, acute and chronic lung infections (norcadiosis), protozoan infections of the nervous system (i.e., toxoplasmosis), and a variety of infections in humans and livestock. Their mode of activity is by inhibiting the multiplication of bacteria by competitively inhibiting para-aminobenzioc acid (PABA) in the folic acid metabolism cycle (O Neil et al., 2001). More specifically, they block the synthesis of folic acid in bacteria as the drugs are structurally similar to PABA. Folic acid is essential to the synthesis of amino acids and nucleic acids. In bacteria, folic acid is synthesized from PABA... [Pg.54]

The compound sulfanilamide exhibits a structural similarity to para-amino benzoic acid (PABA). Woods and Fields proposed the theory that sulfonamides, being structurally similar to PABA, inhibit bacterial folate synthetase so that folic acid is not formed which is needed for a number of metabolic reactions. Folic acid derived from PABA is essential for bacterial metabolism. Sulfonamides inhibit the enzyme folic acid synthetase which is... [Pg.305]

Mammalian cells (and some bacteria) lack the enzymes required for folate synthesis from PABA and depend on exogenous sources of folate therefore, they are not susceptible to sulfonamides. Sulfonamide resistance may occur as a result of mutations that (1) cause overproduction of PABA, (2) cause production of a folic acid-synthesizing enzyme that has low affinity for sulfonamides, or (3) impair permeability to the sulfonamide. Dihydropteroate synthase with low sulfonamide affinity is often encoded on a plasmid that is transmissible and can disseminate rapidly and widely. Sulfonamide-resistant dihydropteroate synthase mutants also can emerge under selective pressure. [Pg.1032]

Being impermeable to folic acid, many bacteria must rely on their ability to synthesize folate from PABA, pteridine, and glutamate. In contrast, human beings cannot synthesize folic acid and must obtain preformed folate as a vitamin in their diet. Because of their structural similarity to PABA, the sulfonamides compete with this substrate for the enzyme dihydropteroate synthetase, thus preventing the synthe-... [Pg.300]

The synergistic antimicrobial activity of co-trimoxazole results from its inhibition of two sequential steps in the synthesis of tetrahydro-folic acid sulfamethoxazole inhibits the incorporation of PABA into folic acid, and trimethoprim prevents reduction of dihydrofolate to tetrahydrofolate (see Figure 29.5). Co-trimoxazole exhibits more potent antimicrobial activity than sulfamethoxazole or trimethoprim alone (seed Figure 29.6). [Pg.305]

Humans cannot synthesise folic acid. Many bacteria, however, synthesise it from PABA this bacteria-specific pathway provides a target for synthetic antimicrobial agents like the sulphonamides and trimethoprim (Figure 20.4). Sulphonamides inhibit dihydropteroate syn-... [Pg.312]

The enzyme dihydrofolic acid (DHF) S5mthase (see below) converts p-aminobenzoic acid (PABA) to DHF which is subsequently converted to tetrahydric folic acid (THF), purines and DNA. The sulphonamides are structurally similar to PABA, successfully compete with it for DHF s)mthase and thus ultimately impair DNA formation. Most bacteria do not use preformed folate, but humans derive DHF from dietary folate which protects their cells from the metabolic effect of sulphonamides. Trimethoprim acts at the subsequent step by inhibiting DHF reductase, which converts DHF to THF. The drug is relatively safe because bacterial DHF reductase is much more sensitive to trimethoprim than is the human form of the enzyme. Both sulphonamides and trimethoprim are bacteriostatic. [Pg.231]

Folic acid is obtained primarily from yeasts and leafy vegetables as well as animal liver. Animal cannot synthesize PABA nor attach glutamate residues to pteroic acid, thus, requiring folate intake in the diet. [Pg.251]

At the branching point of chorismic acid, either anthranilic acid, the precursor of tryptophan, or prephenic acid, the precursor of phenylalanine, itself the precursor of tyrosine and dopa (3,4-dihydroxy-phenylalanine), is formed (Fig. 10). Phosphorylation at the 3-position, condensation with phosphoenolpyru-vate, and elimination of phosphoric acid yields choris-mate from shikimate. Chorismate is also the precursor of a number of simple, and very important, aromatic compounds, including salicylic acid, 4-amino-benzoic acid (PABA), a constituent of folic acid, and 2,3-dihydroxybenzoic acid, a key acylating group of enterobactin. [Pg.233]

Sulfonamides act as inhibitors by mimicking p-aminobenzoic acid (PABA) (Fig. 10.14)—one of the normal constituents of folic acid. The sulfonamide molecule is similar enough in structure to PABA that the enzyme is fooled into accepting it into its active site (Fig. 10.15). Once it is bound, the sulfonamide prevents PABA from binding. As a result, folic acid is no longer synthesized. Since folic acid is essential to cell growth, the cell will stop dividing. [Pg.163]


See other pages where Folic acid from PABA is mentioned: [Pg.608]    [Pg.715]    [Pg.608]    [Pg.715]    [Pg.485]    [Pg.901]    [Pg.227]    [Pg.119]    [Pg.1572]    [Pg.158]    [Pg.485]    [Pg.716]    [Pg.9]    [Pg.413]    [Pg.481]    [Pg.163]    [Pg.124]    [Pg.163]    [Pg.36]    [Pg.292]    [Pg.79]    [Pg.93]    [Pg.40]    [Pg.259]    [Pg.941]   
See also in sourсe #XX -- [ Pg.608 ]




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