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At least 577 records · Page 32Linked to original sources
PubMed1979

Growth inhibition of Candida albicans by folate pathway inhibitors. Their potential in the selection of auxotrophs.

Growth studies were conducted on C. albicans in a glucose - salts - biotin (GSB) medium in the presence of folate inhibitors. Sulfanilamide inhibited growth which was restored by PABA or tetrahydrofolate (THF). Aminopterin inhibited growth to about the same level as did sulfanilamide, but this inhibition was not reversed with PABA nor THF, singly or in combination. Inhibition by combined sulfanilamide and aminopterin was synergistic, reducing growth by more than 90% for 48 h. The sulfanilamide component of the combined inhibition was reversed by PABA or THF to the level of that of aminopterin alone. Cytochrome synthesis was not affected by the inhibitors, but marked increases occurred in alpha-ketoglutarate, malate, isocitrate, and pyruvate dehydrogenases, especially in the presence of both inhibitors. The pyrimidines in combination with sulfanilamide were as inhibitory as was the combination of aminopterin and sulfanilamide, but they had no effect when added alone or in combination with aminopterin. Unlike the pyrimidines, the purines stimulated about a 50% recovery from inhibition by either of the inhibitors. Growth inhibition by combined sulfanilamide and aminopterin was overcome by about 50% by the addition of the THF-mediated end-produits: deoxythymidylate, adenine, histidine and methionine. The use of GSB medium containing adenine, histidine, methionine and the folate inhibitors but without deoxythymidylate resulted in thymineless death of prototrophic cells providing a method for the selection of auxotrophic mutants.

4-Aminobenzoic Acid↗
PubMed1982

Interaction between drug acetylation and ethanol, acetate, pyruvate, citrate, and L(-) carnitine in isolated rat liver parenchymal cells.

The acetylation of sulfanilamide and procainamide in suspensions of isolated rat parenchymal cells was studied in absence and presence of ethanol (33mM), citrate (4 mM), pyruvate (4 mM), and L(-)carnitine (2 mM). Ethanol treatment enhanced the sulfanilamide acetylation whereas the acetylation of procainamide was considered to be unchanged. Acetate (1-5 mM), citrate, and pyruvate treatment enhanced the acetylation of both sulfanilamide and procainamide. Acetate (4 mM) increased both Km and Vmax of both sulfanilamide and procainamide acetylation. Combined treatment with L(-)carnitine and either acetate, pyruvate, or citrate enhanced the acetylation rate of sulfanilamide more than acetate, pyruvate, or citrate, respectively alone. In cell suspensions treated with L(-) carnitine and acetate or pyruvate, the acetylation kinetics of sulfanilamide changed from zero-to apparent first-order. With procainamide as test drug, a further increase of the acetylation rate was found when L(-) carnitine was added to citrate pyruvate. Acetyl-CoA increased the rate of sulfanilamide acetylation in rat liver homogenates in a dose dependent manner.

Acetates↗
PubMed1995

Elixirs, diluents, and the passage of the 1938 Federal Food, Drug and Cosmetic Act.

The Elixir Sulfanilamide disaster of 1937 was one of the most consequential mass poisonings of the 20th century. This tragedy occurred shortly after the introduction of sulfanilamide, the first sulfa antimicrobial drug, when diethylene glycol was used as the diluent in the formulation of a liquid preparation of sulfanilamide known as Elixir Sulfanilamide. One hundred five patients died from its therapeutic use. Under the existing drug regulations, premarketing toxicity testing was not required. In reaction to this calamity, the U.S. Congress passed the 1938 Federal Food, Drug and Cosmetic Act, which required proof of safety before the release of a new drug. The 1938 law changed the drug focus of the Food and Drug Administration from that of a policing agency primarily concerned with the confiscation of adulterated drugs to a regulatory agency increasingly involved with overseeing the evaluation of new drugs. The Elixir Sulfanilamide tragedy, its effect on drug regulations, and the history of other diethylene glycol and diluent mass poisonings are discussed.

Drug Approval↗
PubMed1981

Sulfonamide acetylation in isolated rat liver cells.

Primary suspension of isolated liver cells, prepared from rat livers perfused with Ca++ free buffer and 0.05% collagenase, were used for studies of sulfadimidine uptake and metabolism at various temperatures (29 degrees -41 degrees) and pH (6.4 - 7.8). The intracellular: extracellular ratio for sulfanilamide was found to be insensitive to both temperature and pH variations, while the corresponding ratio for sulfadimidine was pH dependent but insensitive to temperature variation. Decreasing pH increased the cell content of sulfadimidine. Sulfanilamide was metabolized by acetylation only, while sulfadimidine gave rise to several metabolites. The rate of sulfanilamide acetylation in primary cell suspensions was of the same order of magnitude as the acetylation rate of sulfanilamide published previously for the intact organ. Sulfanilamide was acetylated at the highest rate in the pH-region from 7.0 to 7.5, while sulfadimidine was metabolized most rapidly between pH 6.7 and 7.3. At pH 7.5 sulfadimidine was metabolized at a rate only 35% of the rate at pH 7.3. The acetylation rate of both drugs increased with increasing temperature, approximately 5% per degree celcius, and exhibited a Q10 of 1.5.

Acetylation↗
PubMed1977

Fluorescent probe study of sulfonamide binding to povidone.

The possibility of using a fluorescent probe technique for the study of drug-providone (I) interactions was investigated. 1-Anilino-8-naphthalenesulfonate (II) was used as the probe. Sulfanilamide, sulfacetamide, and sulfabenzamide were used as the binding competitors. Both sulfacetamide and sulfabenzamide decreased the fluorescence intensity of the I-II complex, while sulfanilamide increased the intensity. The fluorescence depression was greater with sulfabenzamide than with sulfacetamide, indicating that the former is more strongly bound to povidone. Since sulfabenzamide has a greater hydrophobic group (phenyl) than sulfacetamide (methyl), the binding of these sulfonamides to povidone is probably at least partially hydrophobic in nature. The enhanced fluorescence intensity of the I-II complex in the presence of sulfanilamide is believed to involve hydrogen bonding in which the sulfanilamide acts as an intermediary between I and II. Double reciprocal plots for the I-II and sulfonamide-I interactions were employed to obtain a binding constant of 3.2 X 10(4) M-1 for the I-II interaction. The association constants for sulfacetamide and sulfabenzamide were calculated by means of the Klotz equation to be 13.4 and 56.8 M-1, respectively. The povidone molecules appear to have 1.28 binding sites for these compounds under the experimental conditions.

Anilino Naphthalenesulfonates↗
PubMed1985

Experimental photoallergy to systemic drugs.

We have induced photoallergy in mice to systemically administered drugs, specifically sulfanilamide and chlorpromazine. Mice were photosensitized to systemic sulfanilamide or chlorpromazine by i.p. administration of drug followed by UVB and UVA irradiation of shaved flank skin, on two consecutive days. Control mice received i.p. drug with no irradiation. In some experiments cyclophosphamide pretreatment, or intradermal Corynebacterium parvum (Propionibacterium acnes), was administered as an immunoadjuvant. All animals were photochallenged on day 5 with i.p. drug followed by UVA irradiation of one ear. Mice that had been previously immunized with drug and UV radiation developed ear swelling and erythema, evident 24 h after photochallenge, but not at 4 h. Control animals showed no reactions. In a typical experiment of photosensitization to systemic sulfanilamide, the experimental group had a mean increase in ear thickness of 6.0 X 10(-2) mm 24 h after photochallenge, while unsensitized control animals showed a mean change of -0.8 X 10(-2) mm. The histopathology of the positive challenge reaction was characteristic of a delayed type hypersensitivity. Adoptive transfer of photoallergy to systemic sulfanilamide to naive recipients was accomplished by i.v. injection of lymph node cells (5 X 10(7) harvested from actively photosensitized donors. Clinical reports have suggested that exposure to systemic medications followed by sunlight can induce an eruption having a photoallergic basis. We now report the first experimental proof of that hypothesis. The murine model should facilitate exploration of photoallergic mechanisms and, in addition, it provides the basis for a prospective test of systemic drugs for their photoallergenicity.

Animals↗
PubMed1983

Ethanol interaction with drug acetylation in vivo and in vitro.

The acute effect of ethanol on sulfadimidine or procainamide pharmacokinetics was studied in healthy drug-free volunteers. Ethanol treatment increased the elimination rate, as well as the amount of acetylated drug measured in blood and urine. No changes of apparent volume of distribution or renal drug clearance were found. In three out of seven slow acetylators tested, the rate of acetylation increased so noticeably after ethanol that they would otherwise have been classified as rapid acetylators. Using suspensions of isolated rat liver parenchymal cells, the effect of ethanol, acetate, citrate, pyruvate, and L(-)carnitine on acetylation of sulfanilamide and procainamide was studied. Ethanol treatment enhanced sulfanilamide acetylation, whereas the acetylation of procainamide was unchanged. Acetate, citrate, and pyruvate treatment enhanced the acetylation of both drugs. Acetate treatment increased both Km and Vmax of both sulfanilamide and procainamide acetylation. In rat liver homogenates, acetyl-CoA increased the rate of sulfanilamide acetylation in a dose-dependent manner.

Acetyl Coenzyme A↗