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Biomedical subjects

K Taketa

Publications and source records attributed to K Taketa.

At least 127 records · Page 7Linked to original sources
PubMed1976

Prompt elevation of rat serum alpha-fetoprotein by acute liver injury following a single injection of ethionine.

The mechanism of increased alpha-fetoprotein (AFP) production following a single injection of ethionine was investigated by using rats aged 5 weeks at the time of killing. Marked elevations of serum AFP concentrations occurred within 4 days in both male and female rats after administration of DL-ethionine or L-ethionine, although the increased levels of serum AFP and liver triglyceride in the adults were less marked in the male than in the female. No apparent necrosis of liver cells was observed in ethionine-treated rats. Frequent administrations of adenosine triphosphate after a single dose of ethionine prevented the increases in liver triglyceride and serum AFP levels. The increased concentrations of serum AFP, reaching a maximum level within 4 days, occurred before a slight increase in incorporation of 3H-thymidine into liver DNA. The serum AFP from ethionine-treated rats was immunologically and electrophoretically indistinguishable from that of fetal, carbontetrachloride-treated or hepatoma-bearing rats. These observations suggest that the increased production of AFP in ethionine-treated rats is closely associated with hepatic injury and is not the consequence of liver cell regeneration.

Adenosine Triphosphate↗
PubMed1976

Undifferentiated patterns of key carbohydrate-metabolizing enzymes in injured livers. I. Acute carbon-tetrachloride intoxication of rat.

In acute CCL4 intoxication of rats significantly increased activities of hepatic low-Km hexokinases, glucose-6-phosphate dehydrogenase, phosphofructokinase, aldolase A and pyruvate kinase M2 with concurrently decreased activities of glucokinase, glucose-6-phosphatase, fructose-1,6-diphosphatase, aldolase B and pyruvate kinase L were observed. The resulting enzyme pattern was apparently different from that in dietary induction. Principal component analysis revealed that the degree of enzyme deviation in the injured liver was much greater than that in the regenerating liver after partial hepatectomy and was closer to that in fetal liver or hepatoma tissue.

Adenosine Monophosphate↗
PubMed1976

Differential effects of glucagon on induction of rat liver glucose-6-phosphate dehydrogenase by liver injury and dietary change.

Glucagon effectively prevented the increase in glucose-6-phosphate dehodrogenase activity of rat liver following the administration of a glucose-casein mixture without altering the amount of the diet consumed. However, the increase of the enzyme level in carbon tetrachloride-injured rat liver was virtually insensitive to glucagon. The results obtained gave further evidence for the difference between these two induction mechanisms of glucose-6-phosphate dehydrogenase.

Animals↗
PubMed1976

Undifferentiated patterns of key carbohydrate-metabolizing enzymes in injured livers. II. Human viral hepatitis and cirrhosis of the liver.

Activities of key carbohydrate-metabolizing enzymes were determined on biopsied liver tissues obtained from patients with acute and chronic viral hepatitis and postnecrotic cirrhosis of the liver. The results indicated that the activities of fetal or prototype enzymes, low-Km hexokinases, glucose-6-phosphate dehydrogenase and pyruvate kinase type M2 increased, while those of adult type liver enzymes, glucokinase, glucose-6-phosphatase, fructose-1, 6-diphosphatase and pyruvate kinase type L decreased in livers of these cases. Phosphofructokinase activity tended to increase only acute hepatitis. Principal component analysis revealed that the enzyme patterns of acute hepatitis and liver cirrhosis were most deviated from the control and closely resembled those of hepatocellular carcinomas.

Carcinoma, Hepatocellular↗
PubMed1976

Prevention of dietary induction of rat liver glucose-6-phosphate dehydrogenase by cyclic adenosine 3'.5'-monophosphate and its elimination by glucose prefeeding.

Glucagon, epinephrine and cyclic adenosine 3',5'-monophosphate (cyclic AMP) prevented the induction of liver glucose-6-phosphate dehydrogenase (G6PD) by refeeding a glucose-casein mixture to starved rats. The prevention by these agents occurred without any change in the amount of diet consumed. When the injection of cyclic AMP and the refeeding of glucose-casein diet were initiated simultaneously, there was an inhibiton of G6PD induction depending upon the dose and frequency of cyclic AMP administration during the period of refeeding, while when cyclic AMP was given later than 12 h of the refeeding, the lag period for induction of this enzyme, there was no preventive effect. A glucose prefeeding was also found to counteract the inhibitory effect of cyclic AMP on G6PD induction by the subsequent glucose-casein refeeding. The present data together with the elimination of actinomycin D effect by the glucose prefeeding suggest that the inhibitory effect of cyclic AMP on the induction of G6PD dehydrogenase is exerted at the level of transcription.

Animals↗
PubMed1976

Differential mechanisms of increased alpha 1-fetoprotein production in rats following carbon tetrachloride injury and partial hepatectomy.

Possible differences in the mechanisms of increased alpha1-fetoprotein (AFP) production following carbon tetrachloride (CCl4) intoxication and partial hepatectomy were studied with 5-week-old rats at the time of sacrifice. The maximum level of serum AFP reached in 4 days after a single dose of CCl4 was much higher than that after partial hepatectomy, although the incorporation of [3H]thymidine into liver DNA increased nearly to the same extent by either of these treatments. In the remnant after partial hepatectomy, the DNA synthesis that was further accelerated by treatment with a lower dose of thioacetamide was not associated with any further increases of serum AFP levels. However, CCl4 given to partially hepatectomized rats had an additive effect on increased AFP levels. The increases of serum AFP concentrations in CCl4-injured rats had an additive effect on increased AFP levels. The increases of serum AFP concentrations in CCl4-injured rats were depressed by Mitomycin C given in vivo, whereas the increases in partially hepatectomized rats were not. Treatment with 8-azaguanine inhibited both increase of serum AFP levels, although the inhibition was much less or was insignificant in partially hepatectomized rats. These results suggest that existence of different underlying mechanisms of the increased AFP production for the two experimental conditions.

Animals↗
PubMed1976

Increased alpha1-fetoprotein production in rat liver injuries induced by various hepatotoxins.

Serum alpha1-fetoprotein (AFP) concentration in 5-week-old rats was measured by the radioimmunoassay technique after a single administration of various hepatotoxins. Marked elevation of serum AFP concentrations occurred in rats treated with carbon tetrachloride, thioacetamide, D-galactosamine, allyl alcohol, allyl formate, and ethionine in 4 days of these treatments. The increased production of AFP appeared to be correlated with the induction of liver glucose-6-phosphate dehydrogenase (G-6-PD) among biochemical parameters studied for hepatocellular injuries. However, the difference in time courses of the increase in liver G-6-PD activity and serum AFP level following CC14 treatment suggested that the increased production of serum AFP and the induction of G-6-PD in injured liver were caused by closely related but different mechanisms. Pretreatment of CC14-injured rats with N,N'-diphenyl-p-phenylenediamine or aminoacetonitrile was effective not only in lowering the increased level of serum AFP and liver G-6-PD but also in preventing liver cell necrosis and steatosis induced by CC14. Treatment with a lower dose of thioacetamide resulted in littel elevation of serum AFP and liver G-6-PD with a markedly increased incorporation of 3H-thymidine into liver DNA without any evidence of liver injury. On the other hand, the administration of ethionine, which caused little necrosis of liver cells, produced increase in both serum AFP and liver G-6-PD levels with an only small increase of hepatic DNA synthesis compared to those following thioacetamide as well as CC14. These results suggest that the elevation of serum AFP is not directly related to the stimulation of hepatic DNA synthesis. Some additional mechanisms of specific gene amplification for AFP, which is geared to hepatic injury per se, appear to play a major role in the increased AFP production in injured liver.

Aminoacetonitrile↗
PubMed1975

Microheterogeneity of rat alpha-fetoprotein.

A purified and homogeneous preparation of rat AFP, as judged by both electrophoresis on Cellogel and immunoelectrophoresis, was separated into two components, AFPa and AFPb, by disc electrophoresis on 7% polyacrylamide gel. These two components had a definite difference in electrostatic net charge and gave only a single band on SDS-electrophoresis. Immunological reactivity or electrophoretic separation or mobility of the two components could be altered by treatment with either sulfhydryl inhibitors or reducing agents but not by treatment with protein denaturants. Electrophoresis of neuraminidase-treated AFP on 5% polyacrylamide gel yielded clearly separable, slower moving four to six and finally two components depending on the time of incubation with neuraminidase. The time-dependent conversion of faster into slower migrating components of both AFPa and AFPb upon neuraminidase treatment was confirmed by reelectrophoresis of separated and similarly treated AFPa and AFPb. Two bands of sialized or desialized AFP were also observed on isoelectric focusing. Both AFPa and AFPb treated with and without neuraminidase gave single fused precipitin lines against the antiserum in Ouchterlony double-diffusion analysis. On the basis of the changes in electrophoretic mobilities of the intermediates following neuraminidase treatment, AFPa and AFPb were estimated to have at least 2.5 and 4.5 molecules of sialic acid per molecule, respectively.

Animals↗
PubMed1975

Hexokinase isozyme pattern in CCl(4)-injured rat liver.

Activities of hexokinase isozymes in carbon tetrachloride (CCl(4))-injured rat liver were determined quantitatively by DEAE-cellulose column chromatography and compared with those of regenerating liver, fetal liver and ascites hepatoma cells (AH 130). The CCl(4)-injured liver revealed an isozyme distribution with predominant Types I, II and III (3.2, 8.8 and 6.8 times higher than the control values, respectively) and with undetectable activity of Type IV hexokinase (glucokinase). Although the isozyme pattern generally resembled that of fetal liver or hepatoma cells, the relatively high activity of hexokinase Type III in CCl(4) treatment characterizes the pattern of hexokinase isozyme in acue liver damage.

Animals↗
PubMed1975

Undifferentiated patterns of key glycolytic and gluconeogenic enzymes in epithelial cell lines derived from rat liver.

Established epithelial cell lines derived from livers of 7-day (B, B-R, B-3-4-7, J-C-1, J-C-13, J-5-2-1, E-C-4 and E-C-7) and adult (AL-2, AL-3, AL-4, AL-5 and AL-6) rats were analyzed for hexokinase (HK), pyruvate kinase (PK), glucose 6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glucose 6-phosphatase (G6Pase) and fructose 1,6-diphosphatase (FDPase). None of the cell lines showed appreciable activities of adult type liver enzymes (HK Type IVs (glucokinase), PK Type L, G6Pase and FDPase). On the contrary, the activities of fetal type liver enzymes (HK Types I and II, PK Type M2 and G6PD) increased markedly as compared with dispersed cells or tissues of adult liver. 6PGD gave minimum changes in activity, and the 6PGD/G6PD ratio decreased consistently. HK Type III was found only in J-C-13, AL-5 and AL-6, while HK Type IVf (high Km) was present in all the cell lines examined. Possible explanations for the undifferentiated patterns of carbohydrate-metabolizing enzymes in the established cell lines, which have several evidence of hepatocyte origin, are presented.

Alcohol Oxidoreductases↗
PubMed1975

Microheterogeneity of rat alpha-fetoprotein.

A purified and homogeneous preparation of rat alpha-fetoprotein (AFP) was separated into two components, AFPa and AFPb, by polyacrylamide gel electrophoresis. These two components had a definite difference in electrostatic net charge and gave only a single band on sodium dodecyl sulfate-electrophoresis. Neuraminidase-treated AFP gave clearly separable, slower moving four to six and finally two components depending on the time of incubation with neuraminidase. The time-dependent conversion of each AFPa and AFPb into slower migrating components upon neuraminidase treatment was confirmed by re-electrophoresis of separated and similarly treated AFPa and AFPb.

Animals↗