PubMed Health⌕ Search

Biomedical subjects

Y Miyake

Publications and source records attributed to Y Miyake.

At least 703 records · Page 39Linked to original sources
PubMed1975

Alpha reduced nicotinamide adenine dinucleotide-dependent reductase reactions of rat liver microsomes.

The kinetics of alpha-NADH-dichlorophenolindophenol (DCPIP) and alpha-NADH-cytochrome c reductase reactions of rat liver microsomes showed that the reactio ns proceeded by a ping-pong mechanism, and that the oxidation of alpha-NADH was the rate-determining reaction. The DCPIP-reducing activity with alpha-NADH in the presence of ADP was about 1% of that with beta-NADH. ADP inhibited the alpha-NADH-DCPIP reductase reaction in a competitive manner with respect to alpha-NADH and a value of 1.2 mM for the inhibition constant was obtained. ADP also inhibited cytochrome b5 reduction with alpha-NADH. More than 90% of cytochrome b5 was reduced under conditions where 90% of the alpha-NADH-DCPIP reductase activity was suppressed with ADP. The reduction of DCPIP with alpha-NADH preceded that of cytochrome b5, but the reductions partly overlapped. From these results, a diversed electron flow from alpha-NADH to cytochrome b5 and electron sharing between cytochrome b5 and DCPIP were indicated. alpha-NAD+ also inhibited the alpha-NADH-DCPIP reductase reaction. Analyses of the inhibition indicated that two types of alpha-NADH-DCPIP reductase reaction existed, one of which was resistant to alpha-NAD+ inhibition. In contrast to the reoxidation of beta-NADH-reduced cytochrome b5, the process was largely monophasic when cytochrome b5 was reduced with alpha-NADH.

2,6-Dichloroindophenol↗
PubMed1975

[Relation of time of administration of drugs to their acute toxicity to experimental animals].

The circadian rhythms of acute toxicity of N-methyl D-aspartic acid, picrotoxin, pentetrazol, strychnine, chlorpromazine and Na-methylhexabital in dd-mice were investigated. The drugs were injected into mice on the hour at 2, 6, 10, 14, 18 or 22 in one day, after which the cumulative mortalities were calculated for 72 hours. Regarding central stimulants, the mortality of mice injected at 22 (o'clock) was lowest, and when injections were given at 2, 10 or 18 (o'clock), the mortality was higher than at any other time. On the other hand, regarding central depressants, the mortality was lowest at 10, and highest at 14 or at 18 o'clock. Thus, the administration time of central stimulants showing the lowest mortality was shifted about 12 hours in comparison with central depressants. As compared to the central depressants, the mortality rate as the result of central stimulants showed a great contrast when injected at 10 o'clock.

Animals↗
PubMed1975

Affinity labeling of D-amino acid oxidase with an acetylenic substrate.

The acetylenic substrate, D-2-amino-4-pentynoic acid (D-propargylglycine), was oxidatively deaminated by hog kidney D-amino acid oxidase[EC 1.4.3.3], with accompanying inactivation of the enzyme. The flavin which was extracted by hot methanol from the inactivated enzyme was identical with authentic FAD by thin-layer chromatography and circular dichroism. The excitation spectrum of emission at 520 nm of the released flavin was very similar to the absorption spectrum of oxidized FAD. The released flavin was reduced by potassium borohydride. The apoenzyme prepared after propargylglycine treatment did not show restored D-amino acid oxidase activity on adding exogenous FAD. The absorption spectrum of this inactivated apoenzyme showed absorption peaks at 279 and 317 nm, and a shoulder at about 290 nm. These results strongly indicate that the inactivation reaction is a dynamic affinity labeling with D-propargylglycine which produces irreversible inactivation of the enzyme by a covalent modification of an amino acid residue at the active site.

Affinity Labels↗