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Biomedical subjects

M Tada

Publications and source records attributed to M Tada.

At least 577 records · Page 32Linked to original sources
PubMed1982

Mutagenicity of the optical isomers of the diastereomeric bay-region chrysene 1,3-diol-3,4-epoxides in bacterial and mammalian cells.

The mutagenic activities of the four optically pure (+)- and (-)-enantiomers of the two diastereomeric bay-region chrysene 1,2-diol-3,4-epoxides were evaluated in histidine-dependent strains of Salmonella typhimurium and in cultured Chinese hamster V79 cells. In strain TA98 of S. typhimurium, (-)-1 alpha, 2 beta-dihydroxy-3 beta, 4 beta-epoxy-1,2,3,4-tetrahydrochrysene was 5 to 10 times more active than the other three optical isomers. However, in strain TA100 of S. typhimurium and in Chinese hamster V79 cells, (+)-1 beta, 2 alpha-dihydroxy-3 alpha, 4 alpha-epoxy-1,2,3,4-tetrahydrochrysene was the most mutagenic diol-epoxide and was from 5 to 40 times more active than the other three optical isomers. The bay-region (+)- and (-)-3,4-epoxy-1,2,3,4-tetrahydrochrysene isomers has identical mutagenic activities in all three systems. These studies indicate that the presence and orientation of the hydroxyl groups play an important role in modulating the mutagenic activity of bay-region epoxides of chrysene in both bacterial and mammalian cells.

Animals↗
PubMed1981

[Antibody production in rats vaccinated with inactivated Sendai virus (author's transl)].

Adult male and female rats were inoculated with tween 80-ethylether-formalin-ultraviolet inactivated Sendai virus (Sv-V) and examined for the production of hemagglutination inhibition (HI) antibody. There were no significant differences in the antibody titers between males and females, and among the various routes of inoculation except for the intranasal which was not effective. The antibody became detectable 7 days after a single inoculation with 10(5) HAU of Sv-V. The antibody titer, which had its peak 21 days after the inoculation, persisted for 200 days and declined gradually thereafter. The HI antibody titers were correlated with inoculated Sv-V doses and a predominant booster reaction with the vaccine was observed. Maternal antibodies were detected in sucklings born to dams hyperimmunized with the vaccine. The titers were similar to those of the dams until 3 weeks after birth but declined rapidly after weaning at 4-week-old. The titers of fetuses and neonates before suckling were significantly lower than those of the sucklings.

Animals↗
PubMed1981

Amino acid conjugation of N-hydroxy-4-aminoazobenzene dyes: a possible activation process of carcinogenic 4-aminoazobenzene dyes to the ultimate mutagenic or carcinogenic metabolites.

The activation process of N-hydroxy-4-aminoazobenzene (N-OH-AAB) dyes, proximate mutagenic or carcinogenic metabolites of AAB dyes, to the ultimate mutagenic or carcinogenic metabolites was studied by the use of an amino acid conjugation (aminoacylation) system catalyzed by yeast seryl-tRNA synthetase and [3H]ATP. A potent mutagen, N-hydroxy-3-methoxy-AAB (N-OH-3-MeO-AAB), as well as a non-mutagen, N-OH-2-MeO-AAB, were equally susceptible to N-O-serine conjugation. A weak mutagen, N-OH-AAB, and a moderate mutagen, N-OH-2,5-diMeO-AAB, were also susceptible to the aminoacylation, but to a lesser extent than the 2- or 3-methoxyl homologs. In contrast, N-hydroxy-N-methyl-4-aminoazobenzene and a moderate mutagen, N-OH-4'-MeO-AAB, were not susceptible to the aminoacylation. The ability of these N-OH-AAB dyes to bind with nucleic acid after serine conjugation was proportional to the susceptibility of the dyes to serine conjugation. Serine conjugates of N-OH-AAB dyes reacted with poly G, but not with poly A, poly C or poly U, suggesting that the azo dyes selectively bind with guanine base of nucleic acids. The susceptibility of N-OH-AAB dyes to aminoacylation was compared with the carcinogenic, mutagenic and unscheduled DNA synthesis-inducing activities of these and the mother AAB dyes.

Animals↗
PubMed1980

Binding of quinoline to nucleic acid in a subcellular microsomal system.

Quinoline, a hepatocarcinogen in rats and mutagen in Salmonella typhimurium, binds to RNA, DNA and certain polyribonucleotides in the presence of NADPH and rat liver microsomes. The binding was pronounced with the help of liver microsome preparations made from the rats pretreated with some inducers of the microsomal monooxygenase system. The binding reaction required NADPH and was inhibited by carbon monoxide or aniline, and also by 7,8-benzoflavone, methyrapone or SKF 525A. These results suggested that the cytochrome P-450-linked monooxygenase system is involved in this binding process. Quinoline bound preferably to poly(A), poly(C), poly(G) and poly(X), but negligibly to poly(U) and poly(I). Most of the quinoline residues of the adducts, regardless of the kind of polynucleotides used, were released by acid or alkali at 100 degrees C in the form of 3-hydroxyquinoline. This suggests that 2,3- or 3,4-epoxy derivative of quinoline is the reactive intermediate for nucleic acid modification.

Animals↗
PubMed1980

Significance of thromboxane A2 in myocardial ischemia in patients with coronary artery disease.

To examine plasma levels of vasoconstrictive prostanoid (thromboxane A2) in patients with coronary artery disease, amounts of its product, thromboxane B2, in acidic lipid extracts from plasma were determined by a radioimmunoassay. Peripheral venous samples were obtained in 14 normal subjects and 12 patients with coronary artery disease, and simultaneous aortic and coronary sinus blood samples were obtained at rest, during pacing, and after pacing in eight cases who were subjected to atrial pacing stress test. Mean thromboxane B2 levels in peripheral venous blood in 14 normal subjects were found to be 243 +/- 96 pg/ml. Of nine cases with angina pectoris on effort (angiographically documented severe coronary artery stenosis), five exhibited increased thromboxane B2 levels in peripheral plasma. Three cases of a variant form of angina pectoris exhibited pronounced increases in peripheral thromboxane B2 levels. Of eight cases subjected to atrial pacing stress test, three exhibited marked increases in thromboxane B2 levels in coronary sinus effluent at peak pacing, two of which were accompanied by typical anginal pain during the test. These findings suggest that increased thromboxane A2 production may be associated with altered thromboxane metabolism. This may occur because of altered interactions between functions of vascular wall and blood platelets within coronary circulation in patients with coronary artery disease.

Angina Pectoris↗