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Biomedical subjects

A Yoshida

Publications and source records attributed to A Yoshida.

At least 955 records · Page 53Linked to original sources
PubMed1986

Effect of dietary ascorbic acid and vitamin E on metabolic changes in rats and guinea pigs exposed to PCB.

The effect of the addition of dietary ascorbic acid and/or vitamin E (all-rac-alpha-tocopheryl acetate) in rats and guinea pigs exposed to PCB (polychlorinated biphenyls) was studied. Rats were fed diets containing one of three levels of vitamin E (30, 500 or 1000 mg/kg diet) with or without PCB (200 mg/kg diet). Guinea pigs were fed diets containing PCB (40 mg/kg diet) with 200 or 1000 mg ascorbic acid/kg diet and/or 70 or 2000 mg vitamin E/kg diet. For rats fed PCB, ascorbic acid in urine was 40-fold higher and in liver, 2-fold higher than for rats fed no PCB, and thiobarbituric acid-reactive substances (TBA-RS, indicators of lipid peroxidation) in liver was 1.5-fold higher. In rats fed PCB, high dietary vitamin E significantly lowered the urinary ascorbic acid and TBA-RS. Liver ascorbic acid was lowered by high dietary vitamin E only in control rats. In guinea pigs, feeding PCB caused severe growth retardation and the liver TBA-RS was 1.8-fold higher than in guinea pigs not fed PCB. Feeding high levels of both ascorbic acid and vitamin E was more effective in reversing the growth depression and in lowering TBA-RS level (due to PCB) than feeding the vitamins separately. Ascorbic acid metabolism in rats was affected by high dietary vitamin E. The possibility of a higher requirement for ascorbic acid and vitamin E in guinea pigs exposed to PCB was indicated. Interaction of ascorbic acid and vitamin E in animals exposed to PCB was suggested.

Animals↗
PubMed1986

Ascorbic acid requirement for the induction of microsomal drug-metabolizing enzymes in a rat mutant unable to synthesize ascorbic acid.

We investigated the requirement of ascorbic acid for the induction by polychlorinated biphenyls (PCB) of hepatic drug-metabolizing enzymes in ODS-od/od rat (OD rat) which is a rat mutant unable to synthesize ascorbic acid. ODS- +/+ rats (+/+ rat), which can synthesize ascorbic acid, were used as controls. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and prevent any signs of scurvy is about 300 mg of ascorbic acid per kilogram diet. In this study, dietary levels of ascorbic acid tested were 0, 50, 300, 1000 and 3000 mg ascorbic acid per kilogram diet with or without 200 mg of PCB per kilogram diet. Feeding PCB did not affect growth in rats of either genotype. When statistical analysis was done within groups fed diets without PCB, ascorbic acid deficiency caused significant decreases in body weight gain, hepatic activities of drug-metabolizing enzymes and level of hepatic cytochrome P-450. When OD rats were fed a diet without PCB, the supplementation of about 300 mg ascorbic per kilogram diet was sufficient to maintain normal activities of hepatic aminopyrine N-demethylase, aniline hydroxylase, cytochrome c reductase and reduction of cytochrome P-450 and a normal level of hepatic cytochrome P-450. However, when OD rats were fed a diet supplemented with 200 mg PCB per kilogram of diet, significantly higher activities of hepatic aminopyrine N-demethylase and aniline hydroxylase and significantly higher level of hepatic cytochrome P-450 were observed in OD rats fed a diet supplemented with 1000 mg or 3000 mg ascorbic acid per kilogram of diet than in rats fed a diet supplemented with 300 mg of ascorbic acid. It is concluded that the dietary requirement of ascorbic acid is increased severalfold by the administration of xenobiotics, such as PCB, for the maximum induction of hepatic drug metabolism.

Aminopyrine N-Demethylase↗
PubMed1986

Time-dependent changes in aggregation of hepatic ribosomes after meal feeding of rats.

The effects of consumption of a meal on changes in aggregation of hepatic ribosomes were studied. Hepatic ribosomes were aggregated very rapidly, within 10-20 min, after meal feeding a 25% casein diet. This response of hepatic ribosomes is faster than the half-life of mRNAs of some liver proteins. Therefore, when rats are fed, the translational changes in protein synthesis (polysome pattern) might be quickly affected by the dietary protein, and the observed aggregation of ribosomes could indicate the state of protein synthesis in liver in vivo.

Animals↗
PubMed1986

Effects of excess dietary tyrosine or certain xenobiotics on the cholesterogenesis in rats.

Comparison of the effects of excess dietary tyrosine, DDT, chlorobutanol (Chloretone) or butylated hydroxyanisole (BHA) on serum cholesterol, hepatic activities of the rate-limiting enzyme of cholesterol synthesis,3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.34) and in vivo rates of the hepatic cholesterol synthesis measured by 3H2O incorporation were investigated in rats. Serum cholesterol concentration was significantly higher in rats fed the DDT, chlorobutanol, BHA or excess tyrosine diets than in rats fed the control diet for 7 days. Serum cholesterol concentration remained higher compared to control rats when excess tyrosine was fed for 21 d. When rats were fed a basal diet after feeding a tyrosine excess diet for 2 wk, liver weight and serum cholesterol level returned to normal within 7 d. The incorporation of 3H2O into liver cholesterol and the activity of liver 3-hydroxy-3-methylglutaryl coenzyme A reductase were greater in rats fed excess tyrosine or certain xenobiotics than in control rats. Present results suggested that the increase in serum cholesterol concentration due to excess dietary tyrosine or certain xenobiotics is mainly attributable to the stimulation of liver cholesterol synthesis.

Administration, Oral↗
PubMed1986

Effects of dietary methionine, cystine and potassium sulfate on serum cholesterol and urinary ascorbic acid in rats fed PCB.

Liver weight, liver and urinary ascorbic acid levels and serum cholesterol concentration were higher in rats fed polychlorinated biphenyls (PCB) than in controls. The influences of methionine, cystine and potassium sulfate on these metabolic responses were studied. Methionine or equivalent moles of cystine or potassium sulfate were added to a basal diet containing 10% soy protein isolate. The basal diet contained 0.3% of total sulfur-containing amino acids (S-AAs). When methionine was added to the basal diet, maximum gain in body weight was obtained with 0.5% of dietary S-AAs, while the highest values in serum cholesterol and urinary ascorbic acid were obtained with 0.8% of dietary S-AAs in rats fed PCB. Dietary addition of cystine had little effect on body weight gain. Nevertheless, in rat fed PCB, urinary ascorbic acid and serum cholesterol were significantly higher in rats fed the cystine-supplemented diet than in those fed the unsupplemented diet. Addition of potassium sulfate had no effect on body weight gain, urinary ascorbic acid or serum cholesterol. These results suggest that more S-AAs are required for the highest metabolic response to PCB than for maximum growth, and the higher requirement for S-AAs cannot be replaced by inorganic sulfate.

Animals↗
PubMed1986

Purification and properties of NADH-specific dihydropteridine reductase from human erythrocytes.

NADH-specific dihydropteridine reductase (EC 1.6.99.7) has been purified from human erythrocytes in essentially homogeneous form. The molecular weight of the enzyme was estimated to be 46,000 by Sephadex G-100 gel filtration. The enzyme reacted with antiserum against NADH-specific dihydropteridine reductase from bovine liver and formed a single immunoprecipitin line in the Ouchterlony double-diffusion system. This precipitin line completely fused with that formed between the human liver enzyme and the antiserum. With use of 5,6,7,8-tetrahydro-6-methylpterin, Km values of the erythrocyte enzyme for NADH and NADPH were determined to be 0.94 and 47 mumol/l, respectively. Vmax values were 58.7 mumol/min/mg with NADH and 6.41 mumol/min/mg with NADPH. The average activity of NADH-specific dihydropteridine reductase of 9 human blood samples from healthy males (20-25 years old) was calculated to be approximately 600 mU/g of hemoglobin, 1.8 mU per 20 microliters of blood, or 1.9 mU per 10(8) erythrocytes.

Adult↗
PubMed1986

Receptor dynamics and tyrosine aminotransferase induction during the course of chronic treatment of rats with glucocorticoid.

The changes in the cytosol glucocorticoid receptor (GR) content during a long-term administration of a glucocorticoid were studied to examine the mechanism of the development of steroid hormone resistance. Dexamethasone (Dex) (0.2 microgram/ml and 2.0 micrograms/ml) was given to adrenalectomized rats, and the GR content was determined using the exchange assay 1, 10, 20 and 50 days after the start of administration. The activity of tyrosine aminotransferase (TAT) in the cytosol was also assayed as a measure of the biological responsiveness of these animals to the administered glucocorticoid. The dissociation constant (Kd) was elevated and the Bmaxs of the GR in the cytosol were decreased by the lower concentration of Dex. The Bmaxs decreased to 30% of the untreated controls within 24 h and this lower level was maintained as long as the hormone treatment continued. On the other hand, the cytosol obtained from animals treated with 2.0 micrograms/ml of Dex for 20-24 days did not show any measurable amount of binding to 3H-Dex. The activity of TAT was elevated 24 h after the administration of Dex but decreased gradually and steadily with time during the experimental period. To examine the biological potency of remaining GR in the liver cytosol, 2.0 micrograms/ml Dex was again administered after a long-term treatment. This treatment eliminated the remaining GR completely and induced TAT at almost the same rate as observed in the untreated control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1986

Evidence for decreased activity of guanine nucleotide binding protein in adenylate cyclase of cell membranes in human ACTH-unresponsive adrenocortical carcinoma.

The present investigation was performed in order to study the properties of abnormal membrane function related to ACTH receptor-adenylate cyclase system interaction in human ACTH-unresponsive adrenocortical cancer. Two tissues of adrenocortical cancer obtained from a patient with Cushing's syndrome (CS) and a case presenting no abnormal endocrinological findings (NF) were used for in vitro studies, comparing with three normal adrenal tissues. The addition of ACTH alone and ACTH plus 10(-6) M GppNHp did not enhance the adenylate cyclase (AC) activity in the CS and NF tissues. Relative insensitivity of AC to GTP, GppNHp, and cholera toxin was observed for the NF tissue, while the rate of response to GppNHp for the CS tissue which also showed relative insensitivity to GTP and cholera toxin was similar to that for the normal tissues. Forskolin which is reported to directly activate the catalytic unit of the AC complex increased the AC activity of both CS and NF tissues as well as that of the normal tissues. Therefore, the function of the catalytic unit itself may be rather well preserved in these tumor tissues. These results suggest that the lack of ACTH receptor at the cell membrane surface might be responsible for ACTH-unresponsiveness in the CS tissue, although an accelerated degradation of GTP could contribute to decreased activity of GTP-binding protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

Modified inverse square sensitometry for the determination of the characteristic curve of radiographic screen/film systems.

To determine the characteristic curve of the radiographic screen/film systems in a short focal spot-film distance, the inverse square sensitometric method was modified by changing the radiation intensity with two kinds of filters. The characteristic curves obtained in the two exposure series with these two kinds of filters were overlapped to obtain a complete one. The characteristic curve thus obtained was almost the same as the one obtained by the original inverse square sensitometric method. The accuracy of the characteristic curves obtained by the modified method was well-reflected in the clinical radiographs.

Humans↗
PubMed1986

Effect of ingested winged bean lectin on gastrointestinal function in the rat.

The present study was undertaken to provide further evidence for mechanisms proposed for the toxicity of ingested winged bean lectin in animals: to determine its effect on activities of some hydrolases localized in the brush border membrane of the small intestine. An adaptive increase in sucrase activity of rats given a high-sucrose diet (HSD) was restrained by the addition to HSD of a lectin fraction (WBLF) isolated from raw winged beans but not by that of heated WBLF or soybean trypsin inhibitor. Restraining effects of WBLF added to HSD on time-course changes in activities of sucrase, alkaline phosphatase and leucine aminopeptidase of rats after giving HSD were similar to those of concanavalin A, which had been observed in the previous study. These results substantiate that the mechanism of the toxicity of ingested winged bean lectin involves its binding to the luminal surface of the small intestine and in turn disturbing the functional formation of the brush border membrane.

Alkaline Phosphatase↗
PubMed1986

Human case of dracunculiasis in Japan.

Dracunculus medinensis was recovered from a 42-year-old man residing in Shizuoka, Japan. Part of an adult female worm was removed from an abscess in the subcutaneous tissue on his right gastrocnemial muscle. The worm's morphology and that of the embryos found in its uterus revealed that the parasite was Dracunculus medinensis. This is the first human case of dracunculiasis acquired in Japan.

Adult↗