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Biomedical subjects

H Katsuki

Publications and source records attributed to H Katsuki.

At least 163 records · Page 9Linked to original sources
PubMed1977

A novel pathway for L-citramalate synthesis in Rhodospirillum rubrum.

When [14C]propionate was incubated with a cell-free extract of Rhodospirillum rubrum in the presence of glyoxylate, ATP, CoA, Mg2+, and Mn2+, radioactivity was incorporated into mesaconate (MSA) as well as into beta-methylmalate (MMA) and citramalate (CMA). MSA was suggested to be an intermediate of the conversion of MMA to CMA based on the following observations. (i) When non-labeled MSA was added to the CMA-forming reaction system, radioactivity was trapped in MSA. (ii) When MSA was incubated with the cell-free extract, CMA was formed. (iii) The alpha-carboxyl group of CMA was shown to be derived from the beta-carboxyl group of MMA, implying that CMA was formed from MMA via MSA through successive dehydration and hydration. From the results of Sephadex G-10 column chromatography of the reaction products, beta-methylmalyl-CoA and mesaconyl-CoA were presumed to be involved in the reaction. A new CMA-forming metabolic pathway is proposed as follows: erythro-beta-methylamalyl-CoA leads to mesaconyl-CoA leads to MSA leads to L-CMA.

Glyoxylates↗
PubMed1977

A neuromuscular transmission block produced by a cancer tissue extract derived from a patient with the myasthenic syndrome.

The myasthenic syndrome occasionally is associated with bronchogenic carcinoma. The neuromuscular transmission defect in this syndrome is characterized by a reduction of acetylcholine release from motor nerve endings. This paper reports that an acetone extract of cancer tissue from a patient with the syndrome reduces the acetylcholine release from motor nerve endings and produces a neuromuscular transmission defect in the frog nerve-muscle preparation. This suggests that the pathogenic substance(s) contained in the extract may be produced by certain types of bronchogenic carcinoma and may cause the myasthenic syndrome.

Acetylcholine↗
PubMed1976

Metabolism of threo-beta-methylmalate by a soil bacterium.

Studies on threo-beta-methylmalate metabolism in a soil bacterium of the genus Bacillus which can utilize threo-beta-methylmalate as a sole carbon source were carried out. When DL-threo-beta-methylmalate was incubated with a cell-free extract of the bacterium, citramalate was found to be formed. Similarly, formation of threo-beta-methylmalate from DL-citramalate was confirmed. These dicarbosylic acids were identified by gas chromatography-mass spectrometry. Examination of inducibility, substrate specificity, and cofactor requirement of the enzymes involved in the reactions showed the existence of two interconversion reactions between the threo-beta-methylmalate and citramalate. One was an interconversion reaction between L-threo-beta-methylmalate and L-citramalate via mesaconate and the other was an interconversion reaction between D-threo-beta-methylmalate and D-citramalate via citraconate. These reactions were both reversible and were catalyzed by distinct and inducible enzymes. It is suggested that the two reactions participate in the catabolism of threo-beta-methylmalate.

Bacillus↗
PubMed1975

Effect of temperature on ergosterol biosynthesis in yeast.

Anaerobically grown Saccharomyces cerevisiae was aerated for 7 hr at 20 degrees, 30 degrees, or 40 degrees, in a phosphate buffer containing 2% glucose. At elevated temperature (40 degrees), de novo synthesis of squalene and sterois in the aerated yeast was only 32-35% of that at lower temperature (20 degrees or 30 degrees), and this decrease was attributed to the repression of the enzymes involved in the synthesis of mevalonate from acetyl-COA. In addition, at elevated temperature, the metabolic flux from squalene to ergosterol was blocked at squalene epoxidation, lanosterol demethylation, and ergosta-5, 7, 22, 24(28)-tetraene-3beta-ol reduction.

Acetyl Coenzyme A↗
PubMed1975

Formation of beta-methylmalate and its conversion to citramalate in Rhodospirillum rubrum.

Using a cell-free extract of Rhodospirillum rubrum, studies were made of the condensation reaction between propionyl-CoA and glyoxylate. When [14C]propionate was incubated with the extract in the presence of glyoxylate, ATP, CoA, Mg2+, and Mn2+, radioactivity was incorporated into several compounds. Two of the main products were characterized as citramalate (CMA) and erythro-beta-methylmalate (erythro-MMA) on the basis of their behavior compared with authentic samples of CMA and erythro-MMA in the following three analyses: (i) paper chromatography using two solvent systems, (ii) radio-gas chromatography on their methyl esters, and (iii) chemical conversion to readily crystallizable derivatives, that is, citramalyl chloralide for CMA, and thymine for MMA. The CMA was thought to be of L(+)-form based on the results of optical resolution with brucine and also its susceptibility to L(+)-citramalate lyase of Clostridium tetanomorphum. When the reaction was carried out with lower concentrations of the enzyme, only MMA was accumulated. However, when the reaction was allowed to proceed further after addition of higher concentrations of the enzyme and of excess semicarbazide to prevent further condensation, the amount of accumulated MMA was decreased and CMA was formed instead. Furthermore, the time course of MMA and CMA formation exhibited a pattern typical of a precursor-product relationship. From these results, it was concluded that MMA was formed by alpha-condensation between propionyl-CoA and glyoxylate, and that CMA was derived from MMA, possibly from its CoA derivative.

Adenosine Triphosphate↗
PubMed1975

D-alpha-Hydroxyglutarate dehydrogenase of Rhodospirillum rubrum.

D-alpha-Hydroxyglutarate dehydrogenase of R. rubrum grown anaerobically in the light was partially purified and some properties were investigated. 1. The enzyme catalyze stoichiometrically the dehydrogenation reaction of D-alpha-hydroxyglutarate into alpha-oxoglutarate, coupled with the reduction of 2, 6-dichlorophenolindophenol. 2. Cytochrome c2, cytochrome c, and ferricyanide are effective as electron acceptors with the crude enzyme but not with the purified one, whereas NAD+ and NADP+ are completely ineffective. The enzyme is thought to play a role in the electron transport system of the organism. 3. D-alpha-Hydroxyglutarate is virtually the sole substrate for the enzyme. The apparent activity against L-alpha-hydroxyglutarate is presumed to be due to contamination of the L-isomer sample with the D-isomer. The enzyme shows barely detectable activity against both isomers of malate and virtually no activity against DL-lactate and glycolate. 4. Both isomers of malate and oxalate, which are presumably substrate analogues, inhibit the enzyme activity. 5. The enzyme is not an inducible enzyme but rather is a constitutive one for R. rubrum, unlike from the enzyme of Pseudomonas putida which is an inducible enzyme for the catabolism of lysine.

Alcohol Oxidoreductases↗
PubMed1975

Long-term intermittent adjuvant chemotherapy for primary, resected lung cancer.

Adjuvant chemotherapy for lung cancer has previously been unsuccessful in improving the results of pulmonary resections. During a 12 year period, we tested long-term intermittent chemotherapy (LTIC) with mitomycin C and chromomycin A3 adjuvant to resections. LTIC was begun before the operations and the first course was completed postoperatively. Additional courses of 4 weeks each were scheduled at 3 month intervals during the first postoperative year and at 6 month intervals during the next 2 years. LTIC was defined as three or more full courses, and short-term chemotherapy (STC) was defined as a single course of adjuvant treatment. Resections for cancer in 425 patients over a 22 year period included 117 operations during a 10 year control period in which LTIC was not used and 308 during the LTIC test period. Results from adjuvant LTIC in 85 patients were compared with lesser adjuvant chemotherapy in 155 synchronously treated patients who included 77 STC recipients. Further comparison was made between LTIC and asynchronously treated, comparable control subjects. Although there were side effects and occasional deaths from chemotherapy, they did not alter the operative mortality rate. The over-all 5 year survival rate of the adjuvant LTIC patients was 50.9 per cent, as compared to 22.6 per cent in the asynchronous control subjects (p less than 0.01). For patients who were given LTIC adjuvant to palliative resections the 5 year survival rate was 35.6 per cent, as compared to 4.3 per cent for STC patients or 5.2 per cent for asychronous control subjects (p less than 0.01). Strikingly promising results were obtained from adjuvant LTIC in 10 of 33 patients with undifferentiated cancers. We conclude that LTIC prolonged life among lung cancer patients who were not cured by resection alone. Dual-agent LTIC is safe, apparently beneficial, and worthy of further clinical trials in a research setting.

Adenocarcinoma↗