Sulfonamides and Folic Acid Antagonists

Jukes, Thomas H.; Broquist, Harry P.

doi:10.1016/b978-0-12-395622-4.50018-5

Cited by 30 publications

(5 citation statements)

References 140 publications

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“…Numerous experimental systems, including several microbial species, have been selected and examined (reviewed by Hutchison, 1963) in attempts to explain the metabolic alterations that contribute to, or are responsible for, the resistance phenomena. The metabolic roles of folic acid (FA) and the mode of action of antifolates were detailed in recent reviews by Huennekens (1963) and Jukes and Broquist (1963).…”

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confidence: 99%

FOLIC ACID METABOLISM IN ANTIFOLIC-RESISTANT MUTANTS OF STREPTOCOCCUS FAECALIS

Johnson

Hutchison

1964

J Bacteriol

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JOHNSON, ALVA H. (Sloan-Kettering Institute for Cancer Research, Rye, N.Y.), AND DORRIS J. HUTCHISON. Folic acid metabolism in antifolicresistant mutants of Streptococcus faecalis. J. Bacteriol. 87:786-791. 1964.-Streptococcus faecalis ATCC 8043 and three of its mutants resistant to amethopterin were compared for their quantitative requirements for serine, purines, and thymine; for their quantitative requirements of folic acid (FA) for the synthesis de novo of serine, purines, and thymine; for the susceptibility to amethopterin of each pathway; and for the relative capacity of resting cells of each culture to synthesize N5-formyltetrahydrofolate (5-CHOFAH4) from FA and serine or FA and formate. The mutants were found to be both qualitatively and quantitatively different from one another and from the wild strain. The growth conditions, specifically the composition of the medium in which each mutant strain was selected, had a marked effect on the metabolic capacities of the mutants. The ability to synthesize serine, purines, and thymine, as observed from the FA requirements, directly reflected the level of resistance of each pathway to amethopterin. The resistant mutants were more efficient than the wild strain in the formation of 5-CHOFAH4 from FA and formate and, furthermore, this formate activation paralleled their capacities in the synthesis de novo of serine. Alterations in purine and thymine biosyntheses were also observed.

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confidence: 99%

FOLIC ACID METABOLISM IN ANTIFOLIC-RESISTANT MUTANTS OF STREPTOCOCCUS FAECALIS

Johnson

Hutchison

1964

J Bacteriol

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“…lase; LDH, lactic dehydrogenase; MDH, malic dehydro¬ genase; ICDH, isocitric dehydrogenase; ALD, aldolase; GA3PHD, glyceraldehyde-3-phosphate dehydrogenase; PFK, phosphofructokinase; PK, pyruvic kinase; GDH, glycerol dehydrogenase; ME, malic enzyme; and Fl, 6 diP, fructose-1, 6-diphosphatase. of 50 mg of methotrexate, they had fallen even further to approximately 68% of their original values.…”

Section: Resultsmentioning

confidence: 99%

Methotrexate

Halprin¹

1967

Arch Dermatol

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“…Antimetabolites, amethopterin among them, inhibit cell growth by interfering with specific enzymatic activities at crucial physiological sites, including the synthesis of nucleic acids and certain amino acids. Resistance to these agents has often been shown to be a result of genetically induced alteration in enzyme structure or enzyme level, either of the inhibited enzyme itself, or in a compensating way, some enzyme at a related metabolic step (see reviews by JUKES and BROQUIST 1963;HUTCHISON 1963). The magnitude of resistance, therefore, would not only depend upon the number of mutational events which have occurred, but also on the nature of the enzymatic alteration evoked, i.e., the specific loci involved.…”

Section: Discussionmentioning

confidence: 99%