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Biomedical subjects

M Hollstein

Publications and source records attributed to M Hollstein.

59 records · Page 4Linked to original sources
PubMed1983

A randomized study comparing clinical efficacy and safety of thienamycin formamidine (MK0787)/renal dipeptidase inhibitor (MK0791) and cefazolin.

Twenty-one hospitalized patients with infectious diseases were randomly assigned to receive either thienamycin formamidine/renal dipeptidase inhibitor or cefazolin. Infections treated included septicaemia, pneumonia, osteomyelitis, pyelonephritis, cellulitis and cutaneous abscesses. All eleven patients treated with thienamycin formamidine/renal dipeptidase inhibitor responded well to therapy. One of the ten patients treated with cefazolin developed a superinfection with Pseudomonas aeruginosa. Side effects detected were minor in both groups.

Adolescent↗
PubMed1982

A new Salmonella tester strain (TA102) with A X T base pairs at the site of mutation detects oxidative mutagens.

A new tester strain, TA102, is described as an addition to the set of strains for the Salmonella/microsome mutagenicity test. This strain contains A X T base pairs at the site of the mutation (determined by DNA sequence analysis) in contrast to the other Salmonella tester strains that detect mutagens damaging G X C base pairs. This strain differs from previous tester strains in that the mutation has been introduced into a multicopy plasmid, so that approximately equal to 30 copies of the mutant gene are available for back mutation. The new strain detects a variety of oxidative mutagens, including x-rays, bleomycin, hydrogen peroxide and other hydroperoxides, streptonigrin and other quinones, and phenylhydrazine; a variety of aldehydes, including formaldehyde, glyoxal, kethoxal, glutaraldehyde, and malondialdehyde; a number of psoralens (in the presence of near-UV light), mitomycin C, neocarzinostatin, and UV light. Some of these mutagens have been previously shown to damage thymine in DNA. Several auxiliary tester strains also are described, including TA96, a frameshift tester strain with a hot spot for mutation at a run of five A X T base pairs with a specificity similar to that of TA102. The importance of oxidative mutagens is discussed.

Base Sequence↗
PubMed1978

Quinoline: conversion to a mutagen by human and rodent liver.

Quinoline, a hepatocarcinogen in rats, and 23 quinoline derivatives were tested for mutagenic activity with the Ames Salmonella typhimurium assay. Quinoline, 5-hydroxyquinoline, and 8-hydroxyquinoline were mutagenic in strain TA 100 when Aroclor 1254-induced rat (male outbred Sprague-Dawley) liver homogenate was present in the incubation mixture. Enzyme preparations from rats pretreated with P-448-dependent aryl hydrocarbon hydroxylase inducers [3-methylcholanthrene (MCA) and beta-naphthoflavone] and MCA-treated "responsive" C57BL mice also metabolized quinoline to a mutagen, but phenobarbital and pregnenolone-16alpha-carbonitrile pretreatment did not yield active preparations. The mutagenicity of quinoline was blocked by the in vitro addition of menadione, butylated hydroxytoluene, alpha-naphthoflavone, vitamin A acetate, and glutathione to the test system. Depletion of glutathione by diethyl maleate pretreatment in vivo enhanced the mutagenic potential of the liver enzyme preparation. Mutagenic activity was correlated to the formation of water-soluble quinoline metabolites, and we suggested that the reactive quinoline intermediate is quinoline-2,3-epoxide. Microsomal enzymes isolated from human liver tissue, but not lung tissue, also converted quinoline to a mutagen.

Animals↗