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Biomedical subjects

S Nagayama

Publications and source records attributed to S Nagayama.

At least 55 records · Page 3Linked to original sources
PubMed1991

Occurrence of autoimmune antibodies to liver microsomal proteins in association with fulminant hepatitis in the LEC strain of rats.

The Long Evans Cinnamon (LEC) rat, which has been established as a strain showing hereditary hepatitis and hepatic carcinoma, was found to possess autoimmune antibodies to liver microsomal proteins, particularly to a protein with the molecular weight of 56kD. The antibodies also recognized a protein(s) in liver microsomes from Long Evans Agouti and Sprague-Dawley rats. About 42 and 15 percent of respective female and male LEC rats died within a week after acute hepatitis; sera from all of the animals contained the antibodies. About 43 and 0 percent of the surviving female and male LEC rats possessed the antibodies, respectively. These results suggest that the autoantibodies occur in association with acute lethal hepatitis in the LEC rats.

Animals↗
PubMed1990

Influence of vitamin B2 deficiency on polychlorinated biphenyls-induced liver lipid peroxides formation in rats.

The present study is carried out to explore whether the liver microsomal drug-metabolizing enzymes induced by PCB are associated with the PCB-induced liver lipid peroxide formation in rats. For this purpose, variations of the drug-metabolizing enzyme activities mediated by vitamin B2 deficiency were utilized. The administration of PCB to rats induced the liver microsomal cytochrome P-450 and vitamin B2 deficiency promoted the induction. The cytochrome b5 was also induced by PCB but no further induction by vitamin B2 deficiency was observed. The flavoenzyme, NADPH-cytochrome c reductase, was induced by PCB when the vitamin B2-supplemented PCB diet was fed to rats, but the activity of the enzyme was decreased by vitamin B2 deficiency and PCB further decreased the activity. The liver lipid peroxide levels increased in PCB groups with and without vitamin B2 compared with each PCB-free group, but the lipid peroxide level in vitamin B2-deficient PCB group was significantly lower than in vitamin B2-supplemented PCB group. From these results, the PCB-induced liver lipid peroxide formation was not necessarily related to the variations of the liver microsomal drug-metabolizing enzymes.

Animals↗
PubMed1989

A sensitive enzyme-linked immunosorbent assay of ochratoxin A based on monoclonal antibodies.

We prepared seven monoclonal antibodies (mAbs, OTA.1, 2, 3, 4, 5, 6 and 7) which were reacted with ochratoxin A (OTA), and have developed a specific and highly sensitive enzyme-linked immunosorbent assay (ELISA) for detection of OTA. The mAbs, OTA.1, 3, 4, 5 and 7, specifically reacted with OTA but much less with its analogs, ochratoxin B (OTB, about 1% of OTA) and ochratoxin alpha (OT alpha, less than 0.1% of OTA). One of the mAbs, OTA.2, equally reacted with OTA and OTB but hardly at all with (4R)-4-hydroxyochratoxin A or OT alpha (less than 0.1% of OTA). All of the mAbs reacted with ochratoxin C. None of the mAbs reacted with coumarin, 4-hydroxycoumarin or L-beta-phenylalanine. In the competitive ELISA with OTA.1 and OTA.7, the lowest detectable amount of standard OTA in solution was 50 pg/ml (2.5 pg per assay). This assay was applied for the quantitation of OTA added to chicken meat, wheat flour, porcine plasma and bovine serum. With minimal sample preparation, reliable and reproducible determinations were possible when concentrations of OTA were higher than 0.1-1 ng/g.

Animals↗
PubMed1988

Application of an enzyme-linked immunosorbent assay for screening of T-2 toxin-producing Fusarium spp.

Culture filtrates of Fusarium species were subjected without clean-up procedures to an indirect competitive enzyme-linked immunosorbent assay with anti-T-2 toxin monoclonal antibody. Fusarium sporotrichioides, F. poae, F. tricinctum, and F. culmorum strains were positive for T-2 toxin, with a minimum detection limit of 5 pg per assay (100 pg/ml of culture filtrate), and the assay data correlated well with the gas-liquid chromatographic data.

Antibodies, Monoclonal↗
PubMed1984

Effect of indigestible polysaccharides on pancreatic exocrine secretion and biliary output.

The present study was designed to determine the effect of purified viscous polysaccharides on pancreatic exocrine secretion and biliary output. Male Sprague-Dawley rats aged 5 weeks were fed either on the control diet which contained no fiber or on the experimental diets that contained 5% indigestible polysaccharides (agar, kappa-carrageenan, Na-alginate and konjac mannan). After pretreatment with each diet for 2 weeks, the diet was discontinued overnight, and the animals were then allowed to eat 4 g of the test diet in 1 h. Immediately after this, a polyethylene tube was placed in the common bile duct, under anesthesia. Combined, free drained pancreatic-bile juice was collected for the following 1 h. Long-term (2 weeks) administration of Na-alginate and konjac mannan gave rise to increases in the volume of secreted juice and in the output of total bile acids, amylase and protease, whereas that of agar and kappa-carrageenan had no affect. Since a single dose of Na-alginate and konjac mannan was ineffective as regards pancreatic-bile secretion, the elevated secretion observed over prolonged periods may result from processes of adaptation against highly viscous polysaccharides.

Alginates↗
PubMed1982

Activities of various enzymes of pyrimidine nucleotide and DNA syntheses in normal and neoplastic human tissues.

The activities of the key enzymes of pyrimidine nucleotide and DNA syntheses in 43 human tumors and 28 normal human tissues were investigated. The activities of cytidine triphosphate synthetase, deoxycytidine monophosphate deaminase, uridine kinase, thymidine kinase, thymidine monophosphate kinase and DNA polymerase were markedly increased in tumor tissues, compared with those in the corresponding normal tissues, while the activities of deoxycytidine kinase, cytidine deaminase and deoxycytidine deaminase were only slightly increased. The use of thymidine and deoxyuridine as substrates of human pyrimidine nucleoside phosphorylase gave 1 to 2 orders of magnitude higher activity than that of uridine.

Carbon-Nitrogen Ligases↗
PubMed1981

Metabolism of 5-fluorouracil in various human normal and tumor tissues.

The metabolism of 5-fluorouracil (5-FU) in tumors and normal tissues of humans was investigated in vitro. Phosphorylation of 5-FU was faster in tumor tissues than in normal tissues. Phosphorylating activity with 2-deoxy-alpha-D-ribose 1-phosphate (dRiblP) and ATP as cofactors was more active than that with alpha D-ribose 1-phosphate (RiblP) and ATP, or 5-phospho-alpha-D-ribosyldiphosphate (PPRibP) as cofactors. Phosphorylating activity in squamous cell carcinoma of the lung was similar to that in adenocarcinomas. Degradation of 5-FU was much faster in the liver than in other tissues including tumor tissues.

Adenocarcinoma↗
PubMed1980

Studies on the metabolism of 1-(2-tetrahydrofuryl)-5-fluorouracil and uracil co-administered orally to tumor-bearing rats.

The metabolism of 1-(2-tetrahydrofuryl)-5-fluorouracil (FT) plus uracil (1:4, UFT) was compared with that of FT alone and that of uracil alone in tumor-bearing rats by using 3H-tracer. After oral administration of UFT, both FT and uracil were rapidly absorbed and no interaction of their absorptions was observed. The levels of 5-fluorouracil (5-FU) in the blood and tissues and the excretion of 5-FU in the urine of rats given UFT were temporarily higher, and the levels of alpha-fluoro-beta-ureidopropionic acid (a catabolic metabolite of 5-FU) in almost all tissues were lower than in rats given FT. The levels of 5-FU, 5-fluorouridine, and fluoronucleotides increased more in the tumors than in normal tissues of rats given UFT, but not in those given FT. The metabolism of uracil administered exogenously as UFT was not influenced by 5-FU or its metabolites derived from FT.

Administration, Oral↗
PubMed1976

Further studies on the reduction of vitamin A content in the livers of rats given polychlorinated biphenyls.

Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed.

Animals↗