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Biomedical subjects

E Suzuki

Publications and source records attributed to E Suzuki.

At least 469 records · Page 26Linked to original sources
PubMed1982

Chemistry and mutagenicity of alpha-hydroxy nitrosamines.

N-Nitroso-N-(hydroxymethyl)alkylamines, which are key intermediates in the metabolic activation of nitrosamines having a methyl group, were synthesized and their chemical and mutagenic properties were examined. Six N-nitroso-N-(hydroxymethyl)alkylamines (alkyl = methyl, ethyl, n-propyl, n-butyl, sec-butyl, tert-butyl) were prepared by the deoxygenation of N-nitroso-N-(hydroperoxymethyl)alkylamines. Their stability in aqueous solution was highly dependent on pH, being stable in acidic media, but unstable in neutral or alkaline media. The structure also exerted a profound effect on the stability. Thus a branched alkyl group accelerated the decomposition, although compounds with a normal alkyl group showed a similar response to the change of pH. The alkylating activity of the compounds toward deoxyguanosine and thymidine was demonstrated, and was dependent on the reaction solvent used. The overall alkylating activity was found to be highest with the compound ultimately yielding a methylating agent, while a more selective alkylation towards the oxygen, compared to the nitrogen, was observed with the ethylating, propylating and butylating species. Reactions with cysteine and histidine were also observed. A potent mutagenic effect of the N-nitroso-N-(hydroxymethyl)alkylamines was demonstrated in Salmonella typhimurium TA1535 and Escherichia coli WP2 and WP2 hcr-, in the absence of the S9 mix. A good correlation of the activities of the N-nitroso-N-dialkylamines and the N-nitroso-N-(hydroxymethyl)alkylamines with the same alkyl group was demonstrated.

Alkylation↗
PubMed1981

[The effects of zinc on cadmium-induced ultrastructural changes in rat livers (author's transl)].

The superimposed effects of oral zinc administration on cadmium-induced ultrastructural changes in rat livers were studied. Twenty female rats were divided into 4 groups. To the diet for group I was added 200 ppm Cd for daily about 10 g diet, to that for group II 200 ppm of Zn and that for group III 200 ppm of Cd and Zn each. The group IV was the control. All of the four groups was sacrificed after 9 months of administration. In addition to examine the liver by an electron-microscope, Cd concentration in the liver was analyzed by atomic absorption spectrophotometry. The Cd contents in the livers of group III were significantly reduced compared with those of group I. Apparent ultrastructural changes; i.e., deterioration of rough endoplasmic reticula, losses of glycogen particles, and proliferation of smooth endoplasmic reticula, were observed in the livers of group I. Meanwhile, these changes were significantly mild in those of group III. From these results, it is suggested that Cd inhibits protein synthesis and glycogen metabolism in the liver and that Zn partly protects the liver from Cd-induced ultrastructural changes.

Animals↗
PubMed1981

Separative determination of ascorbic acid and erythorbic acid in animal tissues by high-performance liquid chromatography.

A method for the separation and determination of ascorbic acid (AsA) and erythorbic acid (ErA) in animal tissues is described. It employs high-performance liquid chromatography on a LiChrosorb-NH2 column in conjunction with a mixture of acetonitrile, acetic acid and water as an eluant. Application of the method, which is sensitive, rapid and simple, to the analyses of AsA and ErA in animal tissues such as liver, adrenals, spleen, kidneys and heart gave satisfactory results. Dehydro-AsA and dehydro-ErA in rat liver could be determined after reduction with H2S. The method was shown to be useful for the routine analyses.

Adrenal Glands↗
PubMed1981

Metabolic fate of N-butyl-N-(4-hydroxybutyl)nitrosamine homologs in the rat, in relation to their organotropic carcinogenicity to the urinary bladder.

The metabolic fate of alkyl homologs (alkyl=methyl, ethyl, propyl, pentyl, and tert-butyl) of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), a potent bladder carcinogen, was investigated in the rat, in order to elucidate any possible correlation of structure and metabolism with organospecific carcinogenicity to the urinary bladder of these N-nitrosamines. They were extensively metabolized in the rat, no unchanged compounds being found in the urine. The metabolic pattern of these alkyl homologs of BBN was essentially similar to that of BBN. Their principal urinary metabolite was the corresponding N-alkyl-N-(3-carboxypropyl)nitrosamine except in the case of the pentyl homolog. Minor metabolites characterized were subsequent transformation products of the principal metabolite by beta-oxidation according to the Knoop mechanism (i.e., N-alkyl-N-(2-hydroxy-3-carboxypropyl)nitrosamine, N-alkyl-N-(carboxymethyl)nitrosamine and N-alkyl-N-(2-oxopropyl)nitrosamine) and the glucuronic acid conjugate excretion of the N-alkyl-N-(c-carboxypropyl)nitrosamine with selective induction of bladder cancer by the N-alkyl-N-(4-hydroxybutyl)nitrosamine in rats is discussed.

Animals↗
PubMed1981

Metabolic fate of N-alkyl-N-(3-hydroxypropyl and 2-hydroxy-ethyl)nitrosamines in the rat in relation to the induction of bladder cancer by N-butyl-N-(4-hydroxybutyl)nitrosamine and its homologs.

The metabolic fate of N-alkyl-N-(3-hydroxypropyl)nitrosamines and N-alkyl-N-(2-hydroxyethyl)nitrosamines (alkyl=butyl, ethyl) [analogs of N-alkyl-N-(4-hydroxybutyl)nitrosamines, which are potent bladder carcinogens] was investigated in the rat in order to elucidate a possible relationship between chemical structure, in vivo metabolism, and organotropic carcinogenicity to the urinary bladder of N-alkyl-N-(4-hydroxybutyl)nitrosamines. The principal urinary metabolites of N-alkyl-N-(3-hydroxypropyl)nitrosamines and N-alkyl-N-(2-hydroxyethyl)nitrosamines, which are not carcinogenic to the urinary bladder but are hepato-carcinogenic in rats, were the corresponding 2-carboxyethyl and carboxymethyl compounds. Urinary metabolites with a 2-carboxyethyl or carboxymethyl group are not important, as far as the induction of bladder cancer is concerned, and the urinary excretion of metabolites having a 3-carboxypropyl chain is essential for the induction of bladder cancer.

Animals↗
PubMed1981

Metabolic fate and carcinogenicity of N-(omega-hydroxyalkyl) N-(4-hydroxybutyl) nitrosamines analogs of N-butyl-N-(4-hydroxy-butyl) nitrosamine, in the rat.

The metabolic fate and carcinogenicity fo three omega-hydroxy derivatives of N-alkyl-N-(4-hydroxybutyl) nitrosamines, potent bladder carcinogens, were investigated in the rat. They were N-(2-hydroxyethyl)-N-(4-hydroxybutyl)-nitrosamine (HEHBN), N-(3-hydroxypropyl)-N-(4-hydroxybutyl) nitrosamine (HPHBN), and N-N-bis(4-hydroxybutyl) nitrosamine (BHBN). The principal urinary metabolite of HEHBN as well as HPHBN was identified as the corresponding 3-carboxypropyl compound, while the main metabolite of BHBN was N,N-bis (3-carboxypropyl) nitrosamine, indicating the preferential metabolic oxidation of the 4-hydroxybutyl chain to the 3-carboxypropyl group in the N-(omega-hydroxyalkyl)-N-(4-hydroxybutyl) nitrosamines. All three N-nitrosamines having the 4-hydroxybutyl chain induced neither bladder tumor nor any tumor in other organs under conditions similar to those used for N-alkyl-N-(4-hydroxy-butyl) nitrosamines. The essential structural and metabolic requirements in N-nitrosamines for the induction of bladder cancer in the rat are discussed.

Animals↗
PubMed1981

Metabolic fate of N-butyl-N-(4-hydroxybutyl) nitrosamine and N, N-dibutylnitrosamine in the guinea pig, with reference to their carcinogenic effects on the urinary bladder.

The metabolic fate of two urinary bladder carcinogens, N-butyl-N-(4-hydroxy-butyl) nitrosamine (BBN) and N-N-dibutylnitrosamine (DBN), was studied in the guinea pig, in order to elucidate species differences of response to these N-nitrosamines in this animal species and the rat. Based on the urinary metabolites characterized after oral administration of these compounds, the metabolic pathways of BBN and DBN in the guinea pig were shown to be essentially similar to those in the rat. The principal urinary metabolite of BBN and DBN in the guinea pig, however, was not N-butyl-N-(3-carboxypropyl) nitrosamine (BCPN), as was the case in the rat, but the glucuronic acid conjugate of BBN and that of N-butyl-N-(3-hydroxybutyl) nitrosamine, respectively. The species variation in response to BBN and DBN as bladder carcinogens in these animals is discussed on the basis of the urinary excretion of BCPN.

Animals↗
PubMed1981

Metabolic fate of N, N-dipropylnitrosamine and N, N-diamylnitrosamine in the rat, in relation to their lack of carcinogenic effect on the urinary bladder.

The metabolic fate of N, N-dipropylnitrosamine (DPN) and N, N-dipentyl-(=diamyl) nitrosamine (DAN), which induced tumors principally in the liver and esophagus but not in the urinary bladder, was studied in the rat, in order to elucidate the reason for this lack of carcinogenicity to the urinary bladder in contrast with the butyl homolog, N, N-dibutylnitrosamine (DBN), a potent bladder carcinogen. The principal urinary metabolite of DPN was identified as the omega-oxidation product N-propyl-N-(2-carboxyethyl) nitrosamine. The (omega-1)-oxidation product N-propyl-N-(2-hydroxypropyl) nitrosamine and its glucuronic acid conjugate were also characterized as metabolites. The principal urinary metabolite of DAN was N-amyl-N-(2-carboxyethyl) nitrosamine, which was formed by metabolic shortening of the amyl chain by omega- and beta-oxidations according to the Knoop mechanism. Besides this, seven compounds oxidized at omega-, (omega-1)-, (omega-2)-, and (omega-3)- positions of one or both amyl chains were isolated and characterized, some of which were shown to be also present as the corresponding glucuronide. The metabolic pattern of DPN and DAN was compared with that of DBN, and the lack of carcinogenicity of the former N-nitrosamines to the urinary bladder of rats is discussed on the basis of their urinary metabolites.

Animals↗
PubMed1981

Metabolic fate of n-methyl-N-dodecylnitrosamine in the rat, in relation to its carcinogenicity to the urinary bladder.

The metabolic fate of N-methyl-N-dodecylnitrosamine (MDN) was investigated in the rat, in order to elucidate a possible correlation between urinary metabolites and organotropic carcinogenicity to the urinary bladder of this N-nitrosamine. MDN was extensively metabolized in the rat, no unchanged MDN being found in the urine. The urinary metabolites identified were N-methyl-N-(3-carboxypropyl) nitrosamine (MCPN), N-methyl-N-(2-hydroxy-3-carboxy-propyl) nitrosamine, N-methyl-N-(carboxymethyl) nitrosamine, and N-methyl-N-(2-oxopropyl) nitrosamine. Thus the metabolic pattern of MDN was essentially similar to that of N-methyl-N-(4-hydroxybutyl) nitrosamine, a potent bladder carcinogen, in the rat. A possible important role of MCPN in the induction of bladder tumors by MDN is discussed.

Animals↗
PubMed1981

Metabolic fate of asymmetric N,N-dialkylnitrosamines having butyl group in the rat.

The metabolic fate of N-alkyl-N-butylnitrosamines (alkyl=ethyl, propyl, and pentyl), which induce tumors in the liver and esophagus but do not induce bladder tumors, was investigated in the rat, in order to elucidate any possible correlation between metabolism and the noncarcinogenicity to the urinary bladder of these N-nitrosamines. They were extensively metabolized in the rat, no unchanged compounds being found in the urine. The metabolic pattern of these N-nitrosamines having a butyl chain was essentially similar to that of N,N-dibutyl-nitrosamine, which induces tumors in the bladder as well as in the liver and esophagus. They were mainly metabolized via omega-oxidation followed by beta-oxidation and/or (omega-1)-oxidation of either of the two alkyl chains. Thus the N-alkyl-N-(3-carboxypropyl)nitrosamine and/or the N-alkyl-N-(2-carboxyethyl)nitrosamine were identified as the principal urinary metabolites. Possible important factors concerned with the induction of bladder tumors by N,N-dialkylnitrosamines are discussed from the metabolic point of view.

Animals↗
PubMed1980

The structure of cucurbitin: subunit symmetry and organization in situ.

The low-resolution (2 nm) subunit symmetry of cucurbitin, the crystalline seed storage globulin of cucurbits, has been determined by X-ray diffraction. The wet crystals belong to the cubic space group F23 and there are 4 molecules per unit cell. The molecules therefore possess point-group symmetry 23 and contain 12 structural units which at this resolution are indistinguishable. On drying, the crystal lattice dimension shrinks from 13.6 nm to 12.4 nm with no apparent change in symmetry. Diffraction patterns of small crystals spun into a pellet, and sections of dry and wet native seed indicate that in situ the protein is organised in microcrystals of the same unit cell and symmetry. Edestin, the crystalline storage globulin from cannabis, and a crystalline globulin from tobacco seed both have the same crystal lattice as cucurbitin and, very likely, the same subunit symmetry.

Crystallization↗
PubMed1980

An attempt for eradication of Sendai virus from a mouse breeding colony.

Eradication of Sendai virus from an infected mouse breeding colony was successfully made by sacrificing all offspring younger than 5 weeks of age at a time and then newborns as well as severely affected breeder mice for successive 2 weeks. By this method, number of breeders decreased of two third of those in the original colony but recovered again about 2 months later.

Animals↗