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Biomedical subjects

M Okada

Publications and source records attributed to M Okada.

At least 1,747 records · Page 97Linked to original sources
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

Differences in cell-bound C8 sites on chicken erythrocytes measured by their reactivity with guinea pig and human C9.

Methods for preparing chicken erythrocytes (CE) with C7 bound to their surface were devised by using either the classical pathway (CEA1-7) or an activated 56hu reagent (CE567) derived from inulin-treated human serum. These intermediates were used to study the lysis of CE by functionally purified C8 and C9 isolated from guinea pig and human serum. The results indicated that GPC9 was less efficient in lysing CEA1-8 or CE5678 than HuC9. This finding was observed irrespective of the species of C8 used. Experiments designed to analyze this difference indicated that there were two functionally distinct forms of C5b-8 that were randomly distributed among the cells but differed in their ability to generate a C lesion depending on the species of C9 used to complete the reaction. The implications of these results on the mechanism of generation of C lesions are briefly discussed.

Animals↗
PubMed1979

Reversibility of Parinaud syndrome in thalamic hemorrhage.

Parinaud syndrome, associated with a left thalamic hemorrhage, disappeared completely in a 57-year-old woman after ventriculoperitoneal shunt. The syndrome may be attributed to increased intracranial pressure owing to mass effect on the pretectal region and tectum, or to tightness in the incisura causing hydrocephalus secondary to aqueduct compression. The lesions responsible for the syndrome may not be irreversible.

Cerebral Hemorrhage↗
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↗
PubMed1979

The differentiation of cytotoxic T cells in vitro. I. Amplifying factor(s) in the primary response is Lyt 1 + cell dependent.

Within 15 hr of establishment of a murine mixed lymphocyte culture, a soluble mediator was produced that was capable of augmenting primary cytotoxic responses to alloantigen. The factor did not induce responsiveness in the absence of antigen, since the amplified response seen in its presence was specific for the stimulating alloantigen. The factor did not therefore appear to function by polyclonal activation of cytotoxic precursor cells. Production of the amplifying factor(s) was induced by unfractionated spleen cells, but not by cells subjected to UV irradiation or to sonication, making it likely that this deficiency is the basis of the well-documented failure of these stimulator cells to induce primary cytotoxic responses. The amplifying effects of the factor were distinctive from, but synergistic with, those of 2-mercaptoethanol. Production of the amplifying mediator did not require cell division but was dependent upon the presence of Lyt 1 + cells. On the other hand, Lyt 2 + cells were not needed for mediator production, but served as target cell population on which the factor exerted its action. These findings are compatible with the hypothesis that direct T-T cell collaboration can amplify the differentiation of cytotoxic cells.

Animals↗