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Biomedical subjects

E Suzuki

Publications and source records attributed to E Suzuki.

At least 487 records · Page 27Linked to original sources
PubMed1980

Synthesis and mutagenicity of 4-(N-butylnitrosamino)-4-hydroxybutyric acid lactone, a possible activated metabolite of the proximate bladder carcinogen N-butyl-N-(3-carboxypropyl)nitrosamine.

4-(N-Butylnitrosamino)-4-hydroxybutyric acid lactone (BBAL) was synthesized as a possible intermediate produced by metabolic activation of a selective bladder carcinogen, N-butyl-N-(3-carboxypropyl)nitrosamine. BBAL was stable in neutral sodium phosphate buffer (ionic strength, 0.2), having a half-life of more than 30 hr at 25 degrees. The mutagenic effects of BBAL were tested with the use of Salmonella typhimurium TA1535 and Escherichia coli B/rWP2-try-, WP2-try-hcr-, and Sd4. The gene-damaging effects were assayed by repair tests with Bacillus subtilis H17 (rec+) and M45 (rec-). BBAL showed potent effects in the mutation and repair tests on all the strains tested without activation. A possibility is suggested for the metabolic activation of N-butyl-N-(3-carboxypropyl)nitrosamine to BBAL by alpha-hydroxylation at the site of the 3-carboxypropyl chain followed by lactonization in target tissues prior to interaction with macromolecules to lead to carcinogenesis.

Bacillus subtilis↗
PubMed1980

Mutagenic and DNA-damaging effects of N-(omega-acetoxyalkyl and omega-methoxycarbonylalkyl)-N-(alpha-acetoxyalkyl)nitrosamines, models for metabolically activated N,N-dialkylnitrosamines with an omega-functional group.

Mutagenic and DNA-damaging effects of a series of N,N-dialkylnitrosamines having an alpha-acetoxy group together with an alpha-acetoxy or an omega-methoxycarbonyl group were tested in Salmonella typhimurium, Escherichia coli, and Bacillus subtilis without metabolic activation. The compounds comprised each of 3 N-(omega-acetoxyalkyl)-N-(acetoxymethyl)nitrosamines, N-(omega-methoxycarbonylalkyl)-N-(acetoxymethyl)nitrosamines, and N-(omega-methoxycarbonylalkyl)-N-(alpha-acetoxybutyl)nitrosamines. All the compounds gave positive results in these mutagenicity and repair tests. No definite differences were observed in the mutagenic and DNA-damaging effects between the model compounds derived from the carcinogenic compounds and those derived from the non-carcinogenic counterparts. The strongest mutagenic activity was observed so far with N-(2-methoxycarbonylethyl)-N-(l-acetoxybutyl)nitrosamine in all of the four bacterial strains.

Bacillus subtilis↗
PubMed1980

Formation, deoxygenation and mutagenicity of alpha-hydroperoxydialkylnitrosamines.

N-Nitroso-N-alkyl-alpha-hydroperoxyalkylamines were prepared either by treatment of N-nitroso-N-alkyl-alpha-acetoxyalkylamines with hydrogen peroxide in acetic acid or by oxygenation of lithiated N-nitrosodialkylamines with oxygen. They were strongly mutagenic towards S. typhimurium TA1535 and E. coli WP2 strains without metabolic activation. Treatment of the alpha-hydroperoxy compounds with deoxygenating agents, such as sodium bisulfite, gave the alpha-hydroxynitrosamine, which could be isolated in aprotic solvents and characterized. The alpha-hydroperoxy compounds can possibly be formed from N-nitrosodialkylamines by biochemical and environmental routes and can serve as precursors for the alpha-hydroxynitrosamines.

Chemical Phenomena↗
PubMed1980

Metabolic fate of N-butyl-N-(4-hydroxybutyl)nitrosamine in the rat.

The metabolic fate of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was studied in the rat, to investigate the possibility of a relationship between urinary metabolites and organotropic carcinogenicity to the urinary bladder of this N-nitrosamine. The principal urinary metabolite of BBN was identified as N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN). Several minor metabolites characterized were transformation products of BCPN formed by beta-oxidation according to the Knoop mechanism, i.e., N-butyl-N-(2-hydroxy-3-carboxy-propyl)nitrosamine, N-butyl-N-(carboxymethyl)nitrosamine and N-butyl-N-(2-oxopropyl)nitrosamine; glucuronic acid conjugates of BBN and BCPN were also detected. No BBN was detected in the urine. A possible correlation of the urinary excretion of BCPN with selective induction of bladder tumors by BBN in rats is discussed in relation to the carcinogenic action of BCPN.

Animals↗
PubMed1980

Metabolic fate of N,N-dibutylnitrosamine in the rat.

The metabolic fate of N,N-dibutylnitrosamine (DBN) was studied in the rat, to elucidate the possibility of a correlation between its metabolism and its organotropic carcinogenicity to the urinary bladder and other organs. It was extensively metabolized in the rat, no unchanged DBN being found in the urine. DNA underwent metabolic transformation in at least three ways. The major pathways demonstrated on the basis of urinary metabolites were omega- and (omega-1)-oxidations of one butyl chain to give N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN) and N-butyl-N-(3-hydroxybutyl)nitrosamine, respectively. The third minor pathway was (omega-2)-oxidation of the butyl chain to afford N-butyl-N-(2-hydroxybutyl)nitrosamine. Both hydroxylated metabolites were excreted into the urine as such and as their glucuronic acid conjugates. The omega-oxidation of DBN to BCPN is responsible for the induction of bladder tumors in rats, while the products of the (omega-1)- or (omega-2)-oxidation may be involved in tumor induction in the liver.

Animals↗
PubMed1980

Improved method for gas-liquid chromatographic determination of clopidol in chicken tissues.

A sensitive and specific gas-liquid chromatographic (GLC) method has been developed for determining low levels of clopidol in chicken tissues. Clopidol is extracted from the tissues with methanol, and cleaned up on an alumina column and an anion exchange resin column with 0.1% acetic acid--methanol as eluate. Clopidol is methylated with diazomethane, and then determined by GLC. 2,4-Dinitro-1-chlorobenzene is used as an internal standard. The method is applicable to levels as low as 2 ppb in chicken tissues. Recoveries of 2--20 ppb clopidol added to tissues averaged 87% for muscle, 84% for liver, 80% for kidney, and 76% for fat.

Animals↗
PubMed1979

[The effects of sphincteroplasty on manometric profile of common bile duct and the duodenum (author's transl)].

A simultaneous manometric monitoring of the common bile duct (CBD) and the duodenum were performed 2 weeks after choledocholithotomy on 15 patients whose common bile ducts were explored without sphincteroplasty and 30 patients with sphincteroplasty. These manometric studies were carried out by open-tip catheters intubated into the CBD and duodenum through the T-tube at the operation. In patients without sphincteroplasty, no effects of the duodenal pressure on a CBD pressure profile were recognized, while a synchronized pressure profile of the CBD and the duodenum was obtained in patients with sphincteroplasty. By stimulation with morphine (Morphine sulfate; 0.17 mg/Kg iv bolus), waxing and waning of the pressured in the CBD without sphincteroplasty were observed with 20 cmH2O in maximum at about 13 minutes after injection. However, in the CBD with sphincteroplasty, scale-over increase of the pressure curve was seen immediately after duodenal contraction caused by morphine stimulation. A direct infusion of 5 ml of 0.1 N hydrochloride to the duodenum causes hyperperistalsis of the duodenum, which made a synchronized pressure profile in the CBD with sphincteroplasty but made no remarkable change in a pressure profile of the CBD without sphincteroplasty. These findings conclude that the sphincter of Oddi plays an important role as a "pressure barrier" between the CBD and the duodenum, and that with the destruction of this sphincter by sphincteroplasty, a pressure profile of the CBD becomes close to that of the duodenum. This simultaneous manometric study of the CBD and the duodenum might be one of most valuable methods for evaluation of completeness of the sphincteroplasty.

Ampulla of Vater↗
PubMed1979

Mutagenic and DNA-damaging effects of N-alkyl-N-(alpha-acetoxyalkyl)nitrosamines, models for metabolically activated N,N-dialkylnitrosamines.

Mutagenic and DNA-damaging effects of a series of N,N-dialkylnitrosamines monosubstituted at the alpha-carbon with an acetoxyl group were tested in Salmonella typhimurium, Escherichia coli, and Bacilus subtilis in the absence of metabolic activation system. The compounds comprised 8 N-alkyl-N-(acetoxymethyl)nitrosamines (alkyl=methyl, ethyl, propyl, isopropyl, butyl, isobutyl, sec-butyl, or tert-butyl) and N-butyl-N-(1-acetoxybutyl)nitrosamine. All the compounds, except one with a tert-butyl group, gave positive results in these mutagenicity and repair tests. Presumed release of alkyl cations from the corresponding alpha-acetoxy derivatives by hydrolysis and heterolysis caused mutagenic and DNA-damaging effects in the bacteria. Structure-activity correlation of the compounds was noted in these tests and discussed in regard to the mutagenicity with metabolic activation and carcinogenicity of N,N-dialkylnitrosamines. The results support the hypothesis that alpha-carbon hydroxylation is one probable mechanism involved in the metabolic activation of N,N-dialkylnitrosamines.

Bacillus subtilis↗
PubMed1978

Subacute sclerosing panencephalitis with special reference to the ultrastructure of inclusions in the brain and lung.

A 7-year-old boy, who was diagnosed as typical SSPE by clinical data and laboratory findings, was autopsied and observed by immunofluorescent techniques, light and electron microscope. The morphological characteristics in the brain were perivascular cuffings with plasma cells, lymphocytes and mononuclear cells, gliosis and a large number of intranuclear and intracytoplasmic inclusions in the neuroglias and nerve cells. Various kinds of intranuclear inclusions were elucidated by electron microscopy and the fin structures of these inclusions were described in detail. At least five types of intranuclear inclusions were regarded as specific in SSPE. The presence of intranuclear inclusions of mononuclear cells in the lungs resembling the inclusions in the neuroglias suggested that the disease was not localized in the brain but could be disseminated throughout the body.

Brain↗