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At least 235 records · Page 13Linked to original sources
PubMed1986

Sensitizing capacity of 2-methylol phenol, 4-methylol phenol and 2,4,6-trimethylol phenol in the guinea pig.

The sensitizing capacities of 2-methylol phenol (2-MP), 4-methylol phenol (4-MP) and 2,4,6-trimethylol phenol (2,4,6-MP) were investigated with the guinea pig maximization test. These compounds are known sensitizers in phenol-formaldehyde resins. The study was performed in order to assess and compare the degree of the sensitizing capacities of these chemically related substances. The animals were also rechallenged with the sensitizer and 5 chemically related compounds in order to study the cross-reaction patterns. 2-MP was demonstrated to be a strong sensitizer, 4-MP a moderate sensitizer and 2,4,6-MP a weak sensitizer. With 2-MP as the sensitizer, o-cresol and 2,4-dimethyl phenol were possible cross-reacting substances. p-cresol and 2,4,-dimethylol phenol were possible cross-reacting compounds for 4-MP. The chemical investigation by high pressure liquid chromatography indicated that the compounds tested were pure and separable.

Animals↗
PubMed2004

The inhibitory mechanism of YC-1, a benzyl indazole, on smooth muscle cell proliferation: an in vitro and in vivo study.

The pharmacological mechanisms of a synthetic compound 1-benzyl-3-(5'-hydroxymethyl-2'-furyl) indazole (YC-1) in preventing smooth muscle cell proliferation remains to be elucidated. The present study was aimed to explore the effects of YC-1 on certain molecules responsible for cell proliferation, including transforming growth factor (TGF)-beta1, soluble guanylyl cyclase (sGC) and focal adhesion kinase (FAK). The in vivo assay was correlated to the in vitro results of YC-1 on vascular stenosis. YC-1 was applied topically via a pluronic gel onto the balloon-injured rat carotid arteries, which were then harvested two weeks later for histological analysis. Our in vitro results showed that TGF-beta1 was suppressed by YC-1 by 50%. The translational level of sGC was threefold activated by YC-1 while the transcription level of sGC was increased up to 24-fold. FAK, the molecule responsible for cell proliferation and migration, was suppressed by YC-1 on the translational levels for 72%. These in vitro results were in consistent with the in vivo observation that the area ratio of neointima to media was reduced by YC-1. This study provides insights into the pharmacological mechanisms of YC-1 in preventing abnormal smooth muscle cell proliferation and thus supports the use of YC-1 as an adjuvant therapy for balloon injury-induced restenosis.

Administration, Topical↗
PubMed1980

Sterol-content lowering action of o-chlorobenzylchloride in yeast.

o-Chlorobenzylchloride, a simple aromatic halogen compound, was found to inhibit the growth of Saccharomyces cerevisiae and to lower the contents of sterols and fatty acids. The growth inhibition was considerably alleviated by the presence of sterols such as ergosterol and cholesterol and of unsaturated fatty acids such as oleate and linolenate. Inspection of effect of the inhibitor on the electron transport system related to the biosyntheses of these compounds revealed that the cytochrome contents and some enzyme activities in the system of the inhibited cells were much lower than those of the control cells. The features of the inhibition were similar to those of inhibition for other organisms by the hypocholesterolemic compounds such as triparanol and benzmalecene.

Benzyl Compounds↗
PubMed1997

Studies on propafenone-type modulators of multidrug-resistance IV1): synthesis and pharmacological activity of 5-hydroxy and 5-benzyloxy derivatives.

A series of 5-hydroxy and 5-benzyloxy analogs of the antiarrhythmic and multidrug resistance (MDR) modulating drug propafenone was synthesized and the MDR-modulating activity of the compounds was evaluated using a daunomycin efflux assay system. The key step of the synthesis is the selective reduction of the double bond in 1 without cleavage of the benzyl group thus leading to the phenol 3. Alkylation with epichlorohydrine followed by nucleophilic epoxide ring opening gave the benzylated target compounds 5a-d. Subsequent cleavage of the benzyl group gave the 5-hydroxy analogs 6a-d. Structure activity relationship studies showed, that the 5-hydroxy derivates 6a-d fit the log P/log potency correlation line previously established for a series of propafenone analogs. In contrast, all four 5-benzyloxy analogs 5a-d showed almost identical EC50 values, independent of their log P value.

Anti-Arrhythmia Agents↗
PubMed2005

Regioselective debenzylation of C-glycosyl compounds by boron trichloride.

Boron trichloride has been found to promote selective deprotection of 1,2- or 1,3-cis oriented secondary benzyl ethers of per-benzylated C-glycosyl derivatives. The reactivity towards BCl(3) follows the order: C-4>or=C-2>C-6>C-3 for C-glucopyranosyl derivatives and C-3>or=C-4>C-6>C-2 for C-galactopyranosyl derivatives. Preparatively useful selective debenzylation at secondary positions was possible after careful control of reaction conditions.

Benzyl Compounds↗
PubMed2004

Synthesis and antiproliferative activity of 2,6-diamino-9-benzyl-9-deazapurine and related compounds.

Treatment of 6-bromomethyl- or 6-dibromomethyl-5-nitropyrimidine-2,4-diamine with KCN gave the same product--(2,6-diamino-5-nitropyrimidinyl)acetonitrile. Benzylation of the nitrile took place on the alpha-carbon to the cyano group preferentially affording the corresponding mono- and dibenzyl derivative, whose reductive cyclization resulted in 7-benzyl-5H-pyrrolo[3,2-d]pyrimidine-2,4-diamine and 7,7-dibenzyl-7H-pyrrolo[3,2-d]pyrimidine-2,4,6-triamine, respectively. Suitability of the protection of N(2) and N(4) atoms with benzyl, acetyl, or benzoyl groups was also investigated. The in vitro evaluation of cell growth inhibition on CCRF-CEM, HL-60, HeLa S3, and L1210 cell lines showed significant activity in 8 new compounds. The most potent compounds were the above mentioned 6-dibromomethyl derivative (IC(50)=0.54, 1.7, 5.0, and 1.9 molL(-1)) and 7,N(2),N(4)-tribenzyl-5H-pyrrolo[3,2-d]pyrimidine-2,4-diamine (IC(50)=1.9, 2.7, 7.3, and 1.0 molL(-1)).

Aza Compounds↗
PubMed2006

Different effects of two cyclic chalcone analogues on cell cycle of Jurkat T cells.

It has been previously shown that the cyclic chalcone analogues E-2-(4'-methoxybenzylidene)- (2) and E-2-(4'-methylbenzylidene)-1-benzusuberone (3) inhibited proliferation of various murine and human tumor cells. In order to gain new insights into the cytotoxic mechanism of the two compounds detection of apoptosis and necrosis of Jurkat T cells exposed to 2 and 3 were performed by flow cytometry using the Annexin V-FITC and propidium iodide double staining method. Analysis of the DNA histograms at 8, 24 and 48 h exposure times showed that near equitoxic doses of 2 and 3 had different effects on the cell cycle of the exposed cells. The immediate (8h) effect of 2 was a remarkable decrease of cells in the G(0)/G(1) phase and increase in the G(2)/M phase. This effect could also be seen in the histogram of cells at the 24h time point. On the contrary, such an effect of 3 could not be observed. At the 24 and 48 h time points accumulation of sub-G(0) (apoptotic and necrotic) and hyperdiploid cells could be detected after both treatments. Incubation of 2 and 3 with reduced glutathione under cell-free conditions indicated spontaneous conjugation (non-redox) reaction at pH 7.4 and pH 9.0. Analyzing the mechanism of action the total thiol content of the cells exposed to compounds 2 and 3 was determined. Compound 2 showed to reduce the total cellular thiol level both under nutrient-free and nutrient-supplemented conditions. Under the latter conditions an increase of the total thiol level of the cells exposed to 3 for 4h could be observed. The different effect of the two compounds on the cellular thiol status might contribute to the different tumor cytotoxicity of the cyclic chalcone analogues 2 and 3. Investigation of antioxidant capacity of the compounds by monitoring time course of the Fenton-reaction initiated in vitro degradation of 2-deoxyribose indicated that both compounds displayed hydroxyl radical scavenger activity. The experiments provide further details of dual--cytotoxic and cytoprotective (chemopreventive)--effects of the compounds.

Annexins↗
PubMed2001

Synthesis and analgesic activity of some 1-benzyl-2-substituted-4,5-diphenyl-1H-imidazole derivatives.

In this study, derivatives of 1-benzyl-2-substituted-4,5-diphenyl-1H-imidazole were synthesized and their analgesic activity assayed in two tests. 1,2,4,5-Tetrasubstituted imidazole compounds were obtained by the treatment of purified imidazole compounds with benzyl chloride in the presence of sodium hydride. The structure elucidation of the compounds was performed by IR, 1H-NMR and mass spectroscopic data and elemental analysis results. Generally the prepared compound exhibited only moderate analgesic activity in mice at the dose of 100 mg/kg i.p.; however, a few of them exhibited good activity, almost equivalent to that of morphine at 1 mg/kg i.p. was observed. At the above dosage, no toxicity was observed for all compounds.

Analgesics, Non-Narcotic↗
PubMed1986

Glutathione- and cysteine-mediated cytotoxicity of allyl and benzyl isothiocyanate.

Ally isothiocyanate has been reported to be a bladder carcinogen in male rats. On the other hand, benzyl isothiocyanate is an anti-carcinogen. These contradicting properties led us to investigate the cytotoxicity of these compounds in RL-4 rat hepatocytes. Since conjugation with glutathione plays an important role in the metabolism of these isothiocyanates, the glutathione and L-cysteine derivatives were also tested for cytotoxicity (electron microscopy, trypan blue exclusion, cell attachment, and inhibition of cell division). Both types of conjugates caused considerable toxicity: allyl isothiocyanate conjugates gave effects comparable to the parent compound, but benzyl isothiocyanate was more toxic than its conjugates. Addition of excess glutathione (greater than 4mM) to the free isothiocyanates as well as their conjugates abolished cytotoxicity up to the highest concentration tested (250 microM). Addition of excess L-cysteine (5 to 20 mM) lowered the effects but did not abolish them. The reaction of thiols with isothiocyanates was readily reversible: 15 min after dissolving the conjugates in buffer, pH 7.4, an equilibrium was established in which 9 to 15% of the conjugates was converted to free isothiocyanate. Two hours after addition of 1 mM of the L-cysteine conjugates to medium containing 5 mM glutathione, 80% of the total conjugates was present as the glutathione derivatives. The glutathione conjugates were similarly converted to L-cysteine conjugates. Glutathione conjugates are not able to enter the cell, thus their toxicity is presumably due to the release of free isothiocyanate, and in the presence of excess glutathione no toxicity was observed. L-cysteine derivatives are able to cross the cell membrane, thus excess L-cysteine diminishes cytotoxicity, since less free isothiocyanate is present outside the cells, but does not completely protect the cells. Glutathione and cysteine can be regarded as transporting agents for the isothiocyanates through the body. Initial detoxification can be followed by release of the reactive compound at some other site.

Animals↗