Biomedical subjects

U Hollstein

Publications and source records attributed to U Hollstein.

16 recordsLinked to original sources

PubMed1988

Synthesis of some substituted quinazolinediones as potential inhibitors of smooth muscle contraction.

3-Substituted 2,4(1H,3H)-quinazolinediones were prepared from the corresponding N-substituted 2-aminobenzamides by treatment with ethyl chloroformate and KOH in ethanol. Also, a series of 3-substituted and 1-methyl-3-substituted 2,4(1H,3H)-quinazolinediones were synthesized by the reaction of 1-methyl-1,4-dihydro- and 1,4-dihydro-2,4-dioxo-3(2H)-quinazolineacetic acid with the corresponding N-substituted piperazines. The 13C NMR spectra and mass spectra of the compounds were measured and signals were assigned. Some of the compounds showed inhibitory action on contractile function of smooth muscle.

Animals↗

PubMed1987

An integrated concept of amebicidal action: electron transfer and oxy radicals.

Cyclic voltammetry data were obtained for most of the main categories of antiamebic agents, specifically, quinones, heterocyclic nitro compounds, metal derivatives and chelators, and iminium-type ions. The reductions (our data and literature values) were for the most part reversible, with potentials usually in the favorable range of +0.10 to -0.56 V. The drug effect is believed to result generally from the catalytic production of oxidative stress usually arising from the formation of superoxide via electron transfer. In addition, relevant literature data are provided.

Amebicides↗

PubMed1986

Cyclic voltammetry of phenazines and quinoxalines including mono- and di-N-oxides. Relation to structure and antimicrobial activity.

Cyclic voltammetry data were obtained for eight phenazines and phenazine-N-oxides, and eleven quinoxalines and quinoxaline-N-oxides: 1,6-phenazine-diol-5,10-dioxide (iodinin), iodinin copper complex, 6-methoxy-1-phenazinol-5,10-dioxide 1,6-dimethoxyphenazine-5-oxide, 1,6-phenazinediol, 1,6-dimethoxyphenazine, quinoxaline-1,4-dioxide, 2-methylquinoxaline-1,4-dioxide, 2,3-diphenylquinoxaline-1,4-dioxide, 2-carboxyquinoxaline-1,4-dioxide, 5-hydroxyquinoxaline-1,4-dioxide, 5-hydroxy-8-methoxyquinoxaline-1,4-dioxide, 2-methylquinoxaline, 2,3-diphenylquinoxaline, 5-hydroxyquinoxaline, 5-hydroxy-8-methoxyquinoxaline and 2-(2-quinoxalinylmethylene)hydrazine carboxylic acid methyl ester-1,4-dioxide (Carbadox). The di-N-oxides exhibit the most positive E1/2 values within each class. Reversible first wave reductions were observed for iodinin, iodinin copper complex, 1,6-dimethoxyphenazine-5-oxide, 1,6-dimethoxyphenazine, quinoxaline-1,4-dioxide, 2-methylquinoxaline-1,4-oxide and 2,3-diphenylquinoxaline-1,4-dioxide. The results are correlated with structure. Some relationships exist between reduction potential and reported antimicrobial activity. A possible mechanism of drug action is addressed.

Anti-Bacterial Agents↗

PubMed1985

Effect of purified lithospermic acid and its oxidation product on luteinizing hormone release in vitro.

Crude aqueous extracts of the plant Lithospermum ruderale have been shown to have antigonadotropic activity that resides in its polyphenolic fractions. This study examined the ability of one such polyphenol, lithospermic acid (LA), and its oxidation product(s) (oxyLA) to inhibit luteinizing hormone (LH) secretion in vitro. Primary pituitary cultures were exposed for 4.5 or 6 h to either LA or oxyLA. In the presence of gonadotropin-releasing hormone (GnRH), oxyLA was at least 10 times more potent than LH in inhibiting LH release. In the absence of GnRH, oxyLA but not LA caused an increase in LH release. After washing to remove the oxyLA and LA, cultures were challenged with GnRH. Only cultures pretreated with oxyLA showed a decrease in GnRH-stimulated LH release. These results indicate that oxyLA may contain the primary antigonadotropic agents in L. ruderale. The different responses observed in the presence and absence of GnRH, and the morphologic features of the oxyLA-treated cultures, suggest that the mechanism of action may involve the cell membrane of the gonadotrope.

Animals↗

PubMed1978

Degradation of nucleic acid in aqueous solution by ionizing radiation. III. The correlation of radiation damage with change in melting transition--model experiments.

The melting behavior of polydeoxynucleotide double helices of known structure is analyzed in terms of the thermodynamics of helix stability, taking into account separately those contributions to the transition free energy that are proportional to the numbers of polymer molecules and those that are proportional to the numbers of base pairs formed. From the analysis of the melting transitions of helices having an alternating (d-)A.T, G.C base-pair sequence and containing either single-strand nicks or both nicks and damaged thymine bases, the effects of these structural lesions are assessed; it is concluded that, in a moderately long helix of this sequence (400 base pairs), the initial introduction of one mid-chain double-strand break or single-strand break produces respectively some 3.5 or 4 times as much depression in the transition temperature (Tm) as does the destruction of a single internal A.T base pair.

DNA, Single-Stranded↗

PubMed1977

First-neighbor specificities of actinomycin-DNA bindings by circular dichroism.

The circular dichroism spectra of eleven double-stranded DNAs, five natural with known nearest neighbor frequencies and six synthetic polydimers and polytrimers, were measured from 210 to 310 nm in the absence and presence of increasing amounts of actinomycin up to saturation. Based on the fact that the circular dichroism of nucleic acids is a nearest-neighbor frequency-dependent property, matrix analysis of the problem revealed which neighbor sets were perturbed by actinomycin, presumably by intercalation of the planar moiety of the molecule. The intercalation sites can be separated into three families. The first-neighbor units GpC and CpG are very favorable binding sites for actinomycin. ApG, CpC, ApC, TpC, and TpG appear to be less attractive sites, while ApT, TpA, and ApA are unfavorable sites.

Binding Sites↗

PubMed1976