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Biomedical subjects

E Suzuki

Publications and source records attributed to E Suzuki.

At least 505 records · Page 28Linked to original sources

Three glucose 6-phosphate dehydrogenase variants found in Japan.

Three Japanese glucose 6-phosphate dehydrogenase (G6PD) variants were investigated. G6PD 'Mediterranean-like' had markedly decreased activity, normal electrophoretic mobility, low Km G6P, low Km NADP, increased utilization of all three substrate analogues (2-deoxy-G6P, Gal-6P, and deamino-NADP) and slightly decreased heat stability and slightly biphasic pH curve. G6PD 'Ogori' had markedly decreased activity, but otherwise normal characteristics. G6PD 'Hofu' had moderately decreased activity, normal electrophoretic mobility, slightly reduced Km G6P, normal Km NADP, normal utilization of 2-deoxy-G6P and Gal-6P, but increased utilization of deamino-NADP and normal heat stability as well as normal pH curve.

Adolescent↗

Mutagenicity of N-butyl-N-(4-hydroxybutyl)nitrosamine, a bladder carcinogen, and related compounds.

N-Butyl-N-(4-hydroxybutyl)nitrosamine (BBN), which specifically induces bladder tumors, was shown to be mutagenic to Salmonella typhimurium strains TA 1535 and TA100 in the presence of an S-9 mix prepared from the liver of rats treated with polychlorinated biphenyl. Reduced nicotinamide adenine dinucleotide was a more effective cofactor than reduced nicotinamide adenine dinucleotide phosphate in the activation of BBN by the rat liver S-9 fraction, N-Butyl-N-(3-carboxypropyl)nitrosamine, reported to be the main urinary metabolite of BBN as well as of N,N-dibutylnitrosamine and to induce urinary bladder tumors specifically, was found to be mutagenic without metabolic activation by the S-9 mix. The mutagenicities of 31 compounds related structurally or metabolically to BBN and N,N-dibutylnitrosamine were tested. Of these compounds, 13 have previously been demonstrated to be carcinogenic, and nine have been shown to be noncarcinogenic. All the carcinogenic compounds were found to be mutagenic to strain TA1535 with or without the S-9 mix. Four of the nine noncarcinogenic compounds were also mutagenic. These "false-positive" compounds were predicted, in fact, to be carcinogenic.

Animals↗

Carcinogenicity of N-nitrosamines related to N-butyl-N-(4-hydroxybutyl)nitrosamine and N,N,-dibutylnitrosamine in ACI/N rats.

Carcinogenic effect of 14 N-nitrosamines related to N-butyl-N-(4-hydroxybutyl(nitrosamine (BBN) and N,N-dibutylnitrosamine (DBN) was studied in ACI/N male rats by administration in the drinking water. BBN homologs having methyl, ethyl, or pentyl group selectively induced urinary bladder tumors, but a homolog with tert-butyl group did not have any carcinogenic effect. N-Ethyl-N-(3-carboxypropyl)nitrosamine, the principal urinary metabolite of the ethyl homolog of BBN, did also induce bladder tumors selectively, thus providing an additional evidence that N-alkyl-N-(3-carboxypropyl)nitrosamines are responsible for the selective induction of bladder tumors by BBN homologs. N-Butyl-N-(carboxymethyl)nitrosamine and BBN analogs having 3-hydroxypropyl chain together with ethyl or butyl group were found to be noncarcinogenic. N-Propyl-N-butylnitrosamine and DBN induced hepatomas, but simultaneous development of esophageal tumors were observed only with the former. N-Butyl-N-(3-hydroxybutyl)nitrosamine, one of the principal metabolities of DNB, did not induce any tumors, but its further transformation product, N-butyl-N-(3-oxobutyl)nitrosamine as well as N-butyl-N-(2-oxobutyl)nitrosamine, another metabolic intermediate of DBN, induced hepatomas. Possible correlation of structure and metabolism with organotropic carcinogenesis by N-N-dialkylnitrosamines is discussed, with special reference to selective induction of urinary bladder tumors.

Alanine Transaminase↗