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Biomedical subjects

T Kishi

Publications and source records attributed to T Kishi.

At least 217 records · Page 12Linked to original sources
PubMed1976

Bioenergetics in clinical medicine. XI. Studies on coenzyme Q and diabetes mellitus.

The activity of the succinate dehydrogenase-coenzyme Q10 reductase from 120 diabetic patients was significantly lower (P less than 0.001) and the per cent deficiency was significantly higher (P less than 0.001) than that of the controls. The diabetes of 37 patients was controlled by diet; the enzyme activity was lower (P less than 0.001) and the deficiency was higher (P less than 0.02) than for controls. In decreasing effectiveness, Dymelor, Glyburide, Phenformin and Tolazamide inhibited the COQ10-enzyme, NADH-oxidase. Tolbutamide, Glypizide, and Chlorpropamide were noninhibitory to succinoxidase and NADH-oxidase. Patients receiving Tolazamide and Phenformin showed a higher incidence (P less than 0.001 to P less than 0.05) of COQ10-deficiency than patients controlled by diet or normal controls. Certain diabetic patients controlled by diet may have a deficiency of COQ10 which may be enhanced by the inhibition by certain commonly used antidiabetic drugs of COQ10-enzymes. A deficiency of COQ10 in the pancreas could impair bioenergetics, the generation of ATP, and the biosynthesis of insulin.

Adult↗
PubMed1976

Models for clinical disease. I. Biochemical cardiotoxicity of a coenzyme Q10-inhibitor in rats.

The pharmacology and toxicity in animals of synthetic analogs of essential metabolites, which show in vitro antagonism of the metabolite, may point out pathology associated with a deficiency of the metabolite. On this basis, 2-hydroxy-3-n-dodecylmercapto-1,4-naphthoquinone, a potent in vitro inhibitor of a mitochondrial coenzyme Q10-enzyme, was administered to rats. The specific activities and the percent deficiencies of the succinate dehydrogenase-coenzyme Q10 reductase in cardiac mitochondria were significantly increased (0.001 less than P less than 0.01). These enzyme activities were unchanged in leucocytes and in the dorsal aorta. This biochemical cardiotoxicity of an antimetabolite of coenzyme Q10 adds to the advancing knowledge on coenzyme Q10 in cardiac metabolism and disease, and could correlate with the cardiotoxicity of the clinical antitumor drug, adriamycin.

Animals↗
PubMed1976

Vitamin B6 deficiency in patients with a clinical syndrome including the carpal tunnel defect. Biochemical and clinical response to therapy with pyridoxine.

Ten individuals having a severe clinical status associated with the carpal tunnel syndrome were selected for treatment with pyridoxine. The status of vitamin B6, as pyridoxal phosphate, was determined by the specific activities of the glutamic oxaloacetic transaminase of the erythrocytes (EGOT). Before treatment, the patients showed a deficiency of vitamin B6 as determined by 1) a comparison of the specific activities of EGOT with those of a control group (P less than 0.001); and 2) a differential assay based upon the principle of unsaturation and saturation of a Coenzyme-Apoenzyme System (CAS), as applied to EGOT. These patients were treated with pyridoxine, and the specific activities of EGOT were determined after 2 and 4 weeks. Not only was there a disappearance of the deficiency of pyridoxal phosphate, but the level of EGOT activity increased 55-68% during 2-4 weeks, respectively. More apoenzyme was apparently biosynthesized, because the specific activities were significantly higher than before therapy (P less than 0.001/4 wks). Clinical evaluation showed a great improvement in their status, and anticipated surgery for some of the patients became unnecessary. It is concluded that patients with a severe syndrome including the carpal tunnel defect have a deficiency of vitamin B6, and that both the syndrome and the deficiency are relived by therapy with pyridoxine.

Adult↗
PubMed1976

Apparent deficiency of vitamin B6 in typical individuals who commonly serve as normal controls.

Individuals who typically serve as normal controls were found by the differential assay of the glutamic oxaloacetic transaminase in their erythrocytes to have a deficiency (P less than 0.001) of enzyme activity as well as a deficiency (P less than 0.001) of pyridoxal phosphate. Contrary to the understanding that the diet provides an adequate intake of vitamin B6, the dietary intake of vitamin B6 of these controls was inadequate.

Adult↗
PubMed1976

Bioenergetics in clinical medicine. IX. Gingival and leucocytic deficiencies of coenzyme Q10 in patients with periodontal disease.

The specific activities of the succinate dehydrogenase-coenzyme Q10 reductase in mitochondria were determined for patients from a normal periodontal practice. The criteria for selection were patients having a bone score of 1.0-4.0 and a pocket depth of 2.5-5.2 mm. All 29 patients showed a deficiency of 20-63% of CoQ10-enzyme activity in gingival biopsies. The mean value was elevated (P less than 0.001) over that of controls. For corresponding blood samples, 24/28 (86%) showed deficiencies of 20-66% and a higher (P less than 0.001) mean value than that of controls. Periodontal patients frequently have significant gingival and leucocytic deficiencies of CoQ10. The leucocytic deficiency indicates a systemic nutritional imbalance and is not likely caused by neglected oral hygiene. A gingival deficiency could predispose this tissue to periodontitis and this disease could even augment the deficiency. These results support previously suggested adjunctive use of CoQ10 with oral hygiene for improved treatment presumably through bioenergetics.

Adult↗
PubMed1975

Studies on lankacidin-group (T-2636) ANTIBIOTICS. IX Preparation of C-labeled lankacidin C 14-propionate.

To investigate the metabolic fate of lankacidin C 14-propionate in experimental animals, the 14-C-labeled antibiotic was prepared by the fermentation of Streptomyces rochei var, volubilis in the presence of various 14-C-labeled organic carboxylic acids, amino acids and carbohydrates. Significant incorporation (20 similar to 40%) was observed with L-methionine-methyl-14-C. Lankacidin C 14-propionate-14-C (specific activity 49.6 muCi/mg) was obtained from lankacidin C-14-C and ethyl propionate by the action of an acylase of the streptomyces.

Acylation↗
PubMed1975

Bioenergetics in clinical medicine. III. Inhibition of coenzyme Q10-enzymes by clinically used anti-hypertensive drugs.

Background data revealed that some American and Japanese patients with essential hypertension, including many who were not being treated with any anti-hypertensive drug, had a deficiency of coenzyme Q10. Eight clinically used anti-hypertensive drugs have now been tested for inhibition of two mitochondrial coenzyme Q10-enzymes of heart tissue, succinoxidase and NADH-oxidase. Diazoxide and propranolol significantly inhibited the CoQ10-succinoxidase and CoQ10-NADH-oxidase, respectively. Metoprolol did not inhibit succinoxidase, and was one-fourth as active as propranolol for inhibition of NADH-oxidase. Hydrochlorothiazide, hydralazine, ans clonidine also inhibited CoQ10-NADH-oxidase. Reserpine did not inhibit either CoQ10-enzyme, and methyldopa was a very eak inhibitor of succinoxidase. The internationally recognized clinical side-effects of propranolol may be due, in part, to inhibition of CoQ10-enzymes which are indispensable in the bioenergetics of cardiac function. A pre-existing deficiency of coenzyme Q10 in the myocardium of hypertensive patients could be augmented by subsequent treatment with propranolol, possibly to the "life-threatening" state described by others.

Animals↗
PubMed1975

Human deficiencies of vitamin B6. I. Studies on parameters of the assay of the glutamic oxaloacetic transaminase by the CAS principle.

Human deficiencies of vitamin B6 may be detected and accurately measured by a dual enzymic assay which is based on the CAS principle, i.e., the unsaturation and saturation of the coenzyme (pyridoxal 5'-phosphate) of a Coenzyme - Apoenzyme System. Glutamic oxaloacetic transaminase (GOT) is excellent for this assay. Two control groups (24 athletes and 25 students) showed deficiencies of GOT activity of 11+/-6% and 12+/-7%, respectively, which are negligible and which may be compared with analogous data from disease states. Contrary to a previous report, GOT activities must be determined within one day of preparation of the enzyme for meaningful assays. Frozen storage of erythrocyte hemolysates up to 21 days showed increasing apparent dissociation of pyridoxal 5'-phosphate from the coenzyme - apoenzyme system corresponding to increasing false deficiency levels. Dilution of the hemolysates and frozen storage augmented the apparent dissociation and false levels. This dual GOT assay is effective to detect and measure human deficiencies of vitamin B6.

Apoenzymes↗
PubMed1975

Coenzyme Q deficiency in mice following infection with Friend leukemia virus.

The specific activities of the succinate dehydrogenase-coenzyme Q reductase were assayed on mitochondrial preparations of this enzyme from spleen, liver, blood and peritoneal macrophages of mice infected with Friend leukemia virus, and of control mice. Significant increases in the deficiency of coenzyme Q-enzyme activity were found in the spleen and blood of infected animals as the infection progressed. No significant deficiency was observed in the liver or the peritoneal macrophages. The development of the deficiency and splenomegaly during infection seemingly correlate with previous data which showed that administration of coenzyme Q resulted in a reversal of splenomegaly and a reduction in mortality. A limiting factor in the resistance of mice to Friend leukemia virus appears to be the availability of coenzyme Q.

Animals↗