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Biomedical subjects

S Fukui

Publications and source records attributed to S Fukui.

At least 253 records · Page 14Linked to original sources
PubMed1981

Sulfohydrolytic degradation of 3'-phosphoadenosine 5'-phosphosulfate (PAPS) and adenosine 5'-phosphosulfate (APS) by enzymes of a nucleotide pyrophosphatase nature.

The sulfohydrolytic activity to degrade active sulfate (3'-phosphoadenosine 5'-phosphosulfate, PAPS) and its precursor, APS (adenosine 5'-phosphosulfate), with a pH optimum at 9.5 was found to be widely distributed in various tissues of rats. In the liver, the activity was located in plasma membranes and endoplasmic reticula. Triton X-100 solubilized rough and smooth endoplasmic reticula gave two peaks of the activity on gel filtration, both of which had nucleotide pyrophosphatase activities, hydrolyzing the pyrophosphate linkages of ATP, NAD, and UDP-Glc, and the phosphodiester linkage of PNTP (p-nitrophenyl-thymidine 5'-monophosphate) besides PAPS and APS.

Adenine Nucleotides↗
PubMed1981

Modification of tryptophanase with tetranitromethane.

Modification of apotryptophanase with tetranitromethane [C(NO2)4] resulted in a loss of enzymatic activity, whereas holotryptophanase was highly resistant against C(NO2)4-inactivation. The essential importance of the active-site-bound pyridoxal 5'-phosphate (pyridoxal-P) for the protection was confirmed by the agreement of K 1/2 (protection) (1.2 microM) for pyridoxal-P with Km (1.5 microM) in enzyme catalysis. Amino acid analyses and inactivation stoichiometry showed that modification of 1--2 tyrosyl residues per monomer caused complete inactivation. The appearance of 430-nm species upon incubation of C(NO2)4-inactivated apoenzyme with pyridoxal-P indicated that the C(NO2)4-inactivated apoenzyme could still bind the coenzyme, although an affinity of the enzyme for pyridoxal-P (Kd = 51 microM) was much lower than that of the native enzyme (Kd = 0.7 microM). A close relationship was observed between the cofactor activity of monovalent cations and their effectiveness in the protection by pyridoxal-P: in the presence of active monovalent cations (K+, NH+4 and Rb+) pyridoxal-P could provide the protection but not in the presence of inactive cations (Li+, Na+ and Cs+) as well as in the absence of inorganic monovalent cations. From the experimental results obtained it was suggested strongly that tryptophanase has essential tyrosyl residues near the active site. The tyrosyl residues were prevented from the attack of C(NO2)4 by the active-site-bound pyridoxal-P only in the catalytically active holoenzyme.

Amino Acids↗
PubMed1981

Mechanism of thiamine-induced respiratory deficiency in Saccharomyces carlsbergensis.

Cells of Saccharomyces carlsbergensis 4228 grown aerobically with added thiamine (1 microgram . ml-1) in a vitamin B6-free medium contained no detectable heme precursors, such as delta-aminolevulinate, coproporphyrin III, or protoporphyrin IX. The deficiency in heme precursors in the thiamine-grown cells was accompanied by previously reported phenomena, i.e., growth depression, vitamin B6 deficiency, and respiratory deficiency due to a marked decrease in the activities of heme-containing enzymes and cytochrome level (I. Nakamura et al., FEBS Lett. 62: 354-358, 1976). It has been reported that all of the effects of thiamine are abolished by adding pyridoxine to the medium. delta-Aminolevulinate was found to have quite similar effects to those of pyridoxine, except that growth was partially improved by delta-aminolevulinate, whereas it was fully restored by pyridoxine. Incubation of the thiamine-grown cells with delta-aminolevulinate resulted in the appearance of the heme precursors and the heme-containing enzymes. Consistent with the lowered amount of vitamin B6, the thiamine-grown cells had a lowered activity of delta-aminolevulinate synthase, a pyridoxal phosphate-dependent enzyme. Not only the holoenzyme activity but also the apoenzyme activity was very low in these cells. These results indicate that the thiamine-induced vitamin B6 deficiency brings about the decrease in delta-aminolevulinate synthase activity, which leads to heme deficiency and therefore to respiratory deficiency.

5-Aminolevulinate Synthetase↗
PubMed1981

Clinical significance of exercise-induced ST changes in patients with prior myocardial infarction: comparison of electrocardiographic and angiographic findings.

In order to investigate the clinical significance of exercise-induced ST changes in patients with prior myocardial infarction, we performed an exercise tolerance test using bicycle ergometer, coronary arteriography and left ventriculography in 77 patients with prior myocardial infarction and compared exercise-induced ST changes with coronary arteriographic and left ventriculographic findings. At end-point time in the exercise test, we observed abnormal ST elevation in 36 patients (46.7%), ST depression in 11 (14.3%) and no significant ST changes in the remaining 30 (39.0%). After exercise, 29 out of 48 patients (60.4%) with prior anterior myocardial infarction had significant ST elevation, 9 (18.8%) had ST depression, and 10 patients (20.8%) had no significant ST changes. Of the 29 patients with exercise-induced ST elevation, 26 (89.6%) had no significant coronary lesion or simply had single vessel disease, and 6 of 9 patients with ST depression (66.7%) had multiple vessel disease. Furthermore, 18 of 29 patients with exercise-induced ST elevation (62.1%) had dyskinesis, 8 (27.6%) had akinesis and only 3 (10.3%) had hypokinesis. ON the other hand, only 2 of 9 patients with exercise-induced ST depression (22.2%) had dyskinesis, 5 had akinesis, and 2 had hypokinesis. Only 7 out of 29 patients (24.1%) with prior inferior myocardial infarction had ST elevation, 2 (6.9%) had ST depression, and no significant ST changes were observed in the remaining 20 (69.0%). No significant correlation was obtained between exercise-induced ST changes and coronary arteriographic and left ventriculographic findings. These findings strongly suggest that exercise-induced ST elevation is commonly observed in patients with anterior myocardial infarction and correlated with the severity of abnormal left ventricular wall movement, and ST depression is related with the extent of coronary artery lesion.

Adult↗
PubMed1980

Subcellular localization of long-chain alcohol dehydrogenase and aldehyde dehydrogenase in n-alkane-grown Candida tropicalis.

Long-chain alcohol dehydrogenase and long-chain aldehyde dehydrogenase were induced in the cells of Candida tropicalis grown on n-alkanes. Subcellular localization of these dehydrogenases, together with that of acyl-CoA synthetase and glycerol-3-phosphate acyltransferase, was studied in terms of the metabolism of fatty acids derived from n-alkane substrates. Both long-chain alcohol and aldehyde dehydrogenases distributed in the fractions of microsomes, mitochondria and peroxisomes obtained from the alkane-grown cells of C. tropicalis. Acyl-CoA synthetase was also located in these three fractions. Glycerol-3-phosphate acyltransferase was found in microsomes and mitochondria, in contrast to fatty acid beta-oxidation system localized exclusively in peroxisomes. Similar results of the enzyme localization were also obtained with C. lipolytica grown on n-alkanes. These results suggest strongly that microsomal and mitochondrial dehydrogenases provide long-chain fatty acids to be utilized for lipid synthesis, whereas those in peroxisomes supply fatty acids to be degraded via beta-oxidation to yield energy and cell constituents.

Acetate-CoA Ligase↗
PubMed1980

In situ reactivation of glycerol-inactivated coenzyme B12-dependent enzymes, glycerol dehydratase and diol dehydratase.

The catalytic properties of coenzyme B12-dependent glycerol dehydratase and diol dehydratase were studied in situ with Klebsiella pneumoniae cells permeabilized by toluene treatment, since the in situ enzymes approximate the in vivo conditions of the enzymes more closely than enzymes in cell-free extracts or cell homogenates. Both dehydratases in situ underwent rapid "suicidal" inactivation by glycerol during catalysis, as they do in vitro. The inactivated dehydratases in situ, however, were rapidly and continually reactivated by adenosine 5'-triphosphate (ATP) and Mn2+ in the presence of free adenosylcobalamin, although in cell-free extracts or in cell homogenates they could not be reactivated at all under the same reaction conditions. ATP was partially replaced by cytidine 5'-triphosphate or guanosine 5'-triphosphate but not by the beta, gamma-methylene analog of ATP in the in situ reactivation. Mn2+ was fully replaced by Mg2+ but only partially by Co2+. Hydroxocoblamin could not replace adenosylcobalamin in reactivation mixtures. The ability to reactivate the glycerol-inactivated dehydratases in situ was only seen in cells grown anaerobically in glycerol-containing media. This suggests that some factor(s) required for in situ reactivation is subject to induction by glycerol. Of the two possible mechanisms of in situ reactivation, i.e., the regeneration of adenosylcobalamin by Co-adenosylation of the bound inactivated coenzyme moiety (B12-adenosylation mechanism) and the displacement of the bound inactivated coenzyme moiety by free adenosyl-cobalamin (B12-exchange mechanism), the former seems very unlikely from the experimental results.

Adenosine Triphosphate↗
PubMed1980

Significance of ribosomal ribonucleic acid synthesis for control of the G1 period in the cell cycle of the heterobasidiomycetous yeast Rhodosporidium toruloides.

A cell cycle mutant strain which is defective in the G1 period, B2-39, was selected from 1,200 temperature-sensitive mutants of the heterobasidiomycetous yeast Rhodosporidium toruloides M-1057. In the mutant cells, ribosomal ribonucleic acid synthesis was initially inhibited upon temperature shift-up from a permissive (25 degrees C) to a restrictive (36 degrees C) temperature. Moreover, the mutant was found to be temperature sensitive in deoxyribonucleic acid-dependent ribonucleic acid polymerase I activity in vitro. In a revertant-mutant strain, B2-39-R-2, both ribosomal ribonucleic acid synthesis in vivo and enzyme activity in vitro were simultaneously recovered. These results indicate that the mutant has a temperature-sensitive, deoxyribonucleic acid-dependent ribonucleic acid polymerase I and suggest that ribosomal ribonucleic acid synthesis acts as one of the control factors for initiation of both deoxyribonucleic acid synthesis and bud emergence.

Basidiomycota↗
PubMed1980

Site and severity of coronary narrowing and infarct size in man.

The relation between the site and severity of coronary artery lesion and infarct size was investigated in 59 patients with acute myocardial infarction. All patients had no prior myocardial infarction and had at least one significant coronary narrowing (greater than or equal to 75%) in one of the major coronary arteries or in the first diagonal branch. Left ventriculography and selective coronary arteriography were performed on average 2.2 months after the onset of infarction to identify the site and severity of coronary narrowing and to assess the extent of the non-contracting segment (akinetic, dyskinetic, or aneurysmal). Thirty-four of 59 patients were studied enzymatically and total CK released was taken as an indication of infarct size. Non-contracting segment and total CK released in group L-I (narrowing proximal to the first diagonal branch) were significantly larger than those in group L-II (a coronary lesion distal to the branch). The data also indicate that the perfusion area of the first diagonal branch is as large as that of the left anterior descending artery below the first diagonal branch. In contrast to left anterior descending artery disease, the involvement of the right ventricular branch did not significantly influence the infarct size. However, infarct size was significantly larger in eight patients with the left ventricular branch of the right coronary artery supplying the predominantly large area of posterior wall of the left ventricle than in nine patients with small left ventricular branches. It was also shown that the severity of coronary narrowing does not correlate with the infarct size in either left anterior descending or right coronary artery disease.

Angiocardiography↗