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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 97 (1980), S. 137-144 
    ISSN: 1432-1335
    Keywords: α-Ketoglutarat ; Citrat ; Succinat ; Malat Glutamat ; Yoshida Sarcom ; Tumorträger ; Leber ; Skelettmuskel ; Gastrocnemius ; Blut ; Wirt ; α-Ketoglutarate ; Citrate ; Succinate ; Malate ; Glutamate ; Yoshida sarcoma ; Tumor bearer ; Liver ; Skeletal muscle ; Gastrocnemius ; Blood ; Host
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary To elucidate the origin of increased concentrations of α-ketoglutarate (KG) in tumor bearers the tissue distribution of KG together with the related metabolites citrate, succinate, malate, and glutamate was determined in tumor, liver, gastrocnemius muscle, and blood of rats bearing the solid Yoshida sarcoma and of tumor-free rats. The sum of these metabolites was significantly increased in host liver and blood, respectively, compared with the corresponding tissues of normal rats. Among single metabolites glutamate and malate were significantly increased in host liver. The absolute concentrations were highest in host liver with the exception of KG, which was highest in the tumor. This was taken as indicative for the tumor as the prime source of increased KG in blood of tumor-bearers. No significant metabolic deviations were found in gastrocnemius muscle. The concentration of KG in this muscle of both normal and host animals correlated significantly with that of glutamate. In the tumor the concentration of KG correlated significantly with that of citrate plus succinate plus malate. This type of correlation was absent in liver and muscle of both normal and host animals. Moreover, no correlation existed between KG and glutamate either in liver or in tumor. It was suggested that the metabolic flux through the citric acid cycle determines the concentration of KG in the tumor.
    Notes: Zusammenfassung Zur Untersuchung der Ursache der erhöhten α-Ketoglutarat (KG) Konzentration in Tumorträgern wurde die Konzentration des KG sowie der Metaboliten Citrat, Succinat, Malat und Glutamat in Tumor, Leber, Gastrocnemius-Muskel und Blut von tumorfreien und Ratten, die das solide Yoshida Sarcom trugen, untersucht. Die Summe dieser Metaboliten war in der Leber und im Blut von Tumorträgern signifikant erhöht gegenüber den entsprechenden Geweben gesunder Ratten Unter den einzelnen Metaboliten waren Glutamat und Malat in der Wirtsleber signifikant erhöht. Die absoluten Konzentrationen waren jeweils in der Wirtsleber am höchsten, mit Ausnahme des KG, dessen Konzentration im Tumor am höchsten war. Es wurde geschlossen, daß die Erhöhung der KG Konzentration im Blut von Tumorträgern hauptsächlich auf den Tumor selbst zurückzuführen ist. Im Gastrocnemius-Muskel wurden keine signifikanten Stoffwechselveränderungen beobachtet. Die Konzentration des KG in diesem Muskel sowohl von gesunden als auch von Wirtstieren korrelierte signifikant mit jener des Glutamats. Im Tumor korrelierte die KG Konzentration signifikant mit der Summe der Konzentrationen von Citrat, Succinat und Malat. Diese Art der Korrelation war in der Leber und im Muskel gesunder und tumortragender Tiere nicht gegeben. Weiteres wurde weder in der Leber noch im Tumor eine Korrelation zwischen KG und Glutamat beobachtet. Diese Ergebnisse sprechen dafür, daß der metabolische Fluß durch den Citrat-Zyklus bestimmend ist für die Konzentration des KG im Tumor.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 93 (1979), S. 293-300 
    ISSN: 1432-1335
    Keywords: α-ketoglutarate ; Blood ; Urine ; Serum albumin ; Walker carcinoma 256 ; Yoshida sarcoma ; Rhabdomyosarcoma ; Tumor bearer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Referring to the increased α-ketoglutarate (I) concentration in blood of cancer-bearing humans, the concentration of (I) in blood and of albumin (II) in serum were measured in 85 tumor-bearing and control rats by fluorimetry and cellulose acetate electrophoresis, respectively. (I) was elevated on the average by a factor of 1.82 and (II) was decreased by a factor of 0.73 in rats bearing the solid Rhabdomyosarcoma BA 1112 and the ascitic or solid forms of Walker-carcinoma 256 and Yoshida-sarcoma compared with tumor-free animals. All deviations were found to be statistically significant for the different tumor types, with the exception of the increase of (I) in Walker-ascites tumor-bearing rats. For rats bearing the ascitic and solid Yoshida-sarcoma and the ascitic Walker-carcinoma 256 and for tumor-free rats a negative correlation could be observed between increase of (I) and decrease of (II). The increase of (I) in blood was paralleled by an increased excretion rate of (I) into urine. In rats bearing the solid Yoshida-sarcoma the daily excreted amount of (I) was significantly increased by a factor of 1.86 compared with tumor-free animals. The excretion of (I) was already increased in the first week after tranplantation, remained constant for two more weeks and decreased sharply below normal values prior to death. The results suggest that rats bearing the inquested tumors are suitable models for metabolic studies on causes of pathological concentrations of (I) in blood of cancer patients.
    Type of Medium: Electronic Resource
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