scholarly journals Pathways of glycogen synthesis in Novikoff ascites-hepatoma cells

1969 ◽  
Vol 115 (2) ◽  
pp. 315-322 ◽  
Author(s):  
V. N. Nigam
Keyword(s):  
Intact Cell ◽  
Glycogen Synthesis ◽  
Hepatoma Cells ◽  
Tumour Cells ◽  
The Other ◽  
Ascites Hepatoma ◽  
Saturation Concentration ◽  
Glucan Phosphorylase ◽  
Glycogen Formation

Affinity of glucose, fructose and mannose for tumour hexokinase and their rates of phosphorylation at saturation concentration have been correlated with rates of glycogen synthesis by intact tumour cells at different concentrations of the three substrates. Competition experiments with one sugar labelled and the other sugar unlabelled indicate inhibition of glycogen synthesis by the sugar with a low Km for hexokinase. Glycogen synthesis from glucose 1-phosphate in aged cells and from nucleoside in freshly prepared cells is stimulated by fructose and inhibited by glucose. The decrease in glycogen formation from glucose 1-phosphate by oligomycin is partially overcome by increased fructose concentrations. These results are explained by an activation of α-glucan phosphorylase by fructose and an inhibition of this enzyme by glucose. It is suggested that differences in localization of glucose 6-phosphate, available to the intact cell in various ways, determine its transformation into glycogen by either the UDP-glucose–α-glucan glucosyltransferase reaction or by the α-glucan phosphorylase reaction.

scholarly journals A study of the Crabtree effect in Novikoff ascites-hepatoma cells

1966 ◽  
Vol 99 (2) ◽  
pp. 413-418 ◽  
Author(s):  
V N Nigam
Keyword(s):  
Glucose Uptake ◽  
Adenine Nucleotides ◽  
Glycogen Synthesis ◽  
Hepatoma Cells ◽  
Significant Loss ◽  
Crabtree Effect ◽  
Ascites Hepatoma ◽  
Short Term ◽  
Mitochondrial Structure ◽  
Glucose Metabolites

Novikoff ascites-hepatoma cells show no Crabtree effect on the addition of glucose to tumour-cell suspensions, and convert a significant part of the added glucose into glycogen. Treatment of the cells with 2-deoxyglucose or glucose in the presence of iodoacetate inhibits respiration and decreases glycogen synthesis from glucose. Short-term experiments indicate a slight inhibition of glucose uptake for a brief period, due either to ATP accumulation in the mitochondria or to glucose 6-phosphate-mediated inhibition of hexokinase. Utilization of glucose metabolites and ATP for glycogen synthesis appears to remove inhibition of glucose uptake, and perhaps accounts for the absence of respiratory inhibition, by relieving a deficiency of ADP for the mitochondria. Decreased respiration in the presence of 2-deoxyglucose or glucose in the presence of iodoacetate could be due to the change in mitochondrial structure or permeability, caused by the significant loss of adenine nucleotides.

EFFECT OF EPINEPHRINE ON GLUCOSE METABOLISM IN NOVIKOFF ASCITES HEPATOMA CELLS

1969 ◽  
Vol 61 (2) ◽  
pp. 209-218
Author(s):  
V. N. Nigam
Keyword(s):  
Lactic Acid ◽  
Glucose Metabolism ◽  
Acid Production ◽  
Lactic Acid Production ◽  
Glycogen Synthesis ◽  
Neoplastic Transformation ◽  
Tumour Cells ◽  
Small Extent ◽  
Ascites Hepatoma ◽  
Stimulation Of

ABSTRACT No major effects of epinephrine on glycogen synthesis and glycolysis by intact Novikoff ascites-hepatoma were noted. However, at 2 × 10−5 m epinephrine concentration glycogen synthesis from glucose was slightly enhanced and lactic acid production was slightly decreased. These effects were attributed to a stimulation of UDPglucose-α-glucan glucosyltransferase and an inhibition of phosphofructokinase. Breakdown of glycogen deposited by the tumour cells was also inhibited to a small extent by epinephrine. The pattern of epinephrine action on glucose metabolism of tumour cells suggests that loss as well as modification of the receptor (of epinephrine) occurs during neoplastic transformation of liver.

EXPRESSION OF SOME IMMUNOLOGIC MARKERS FOR THE DIAGNOSIS OF SUSPECTED LYMPHOID LESIONS OF LYMPHOMA

2018 ◽  
Vol 8 (4) ◽  
pp. 28-33
Author(s):  
Mao Nguyen Van ◽  
Thao Le Thi Thu
Keyword(s):  
Correct Diagnosis ◽  
Tumour Cells ◽  
The Body ◽  
The Other ◽  
Cervical Region ◽  
Cross Sectional ◽  
Immunologic Markers ◽  
Microscopic Features ◽  
Poor Differentiation ◽  
Benign Tumours

Background: In practice it was difficult or impossible to have a correct diagnosis for the lymphoid proliferation lesions based on only H.E standard histopathology. In addition to histopathology, the application of immunohistochemistry was indispensable for the definitive diagnosis of the malignant or benign tumours and the origin of the tumour cells as well. Objectives: 1. To describe the gross and microscopic features of the suspected lesions of lymphoma; 2. To asses the expression of some immunologic markers for the diagnosis and classification of the suspected lesions of lymphoma. Materials and Method: Cross-sectional research on 81 patients diagnosed by histopathology as lymphomas or suspected lesions of lymphoma, following with immunohistopathology staining of 6 main markers including LCA, CD3, CD20, Bcl2, CD30 and AE1/3. Results: The most site was lymph node 58.1% which appeared at cervical region 72.3%, then the stomach 14.9% and small intestine 12.4%. The other sites in the body were met with lower frequency. Histopathologically, the most type of the lesions was atypical hyperplasia of the lymphoid tissue suspecting the lymphomas 49.4%, lymphomas 34.5%, the other diagnoses were lower including inflammation, poor differentiation carcinoam not excluding the lymphomas, lymphomas differentiating with poor differentiation carcinomas. Immunohistochemistry showed that, LCA, CD3, CD20, Bcl2, CD30 and AE1/3 were all positive depending on such type of tumours. The real lymphomas were 48/81 cases (59.3%), benign ones 35.8% and poor differentiated carcinomas 4.9%. Conclusion: Immunohistochemistry with 6 markers could help to diagnose correctly as benign or malignant lesions, classify and determine the origin of the tumour cells as lymphocytes or epithelial cells diagnosed by histopathology as lymphomas or suspected lesions of lymphomas. Key words: histopathology, immunohistochemistry, lymphomas, poor differentiated carcinomas, hyperplasia, atypicality

scholarly journals Studies on glycogen synthesis in pigeon liver homogenates. Glycogen synthesis from glucose monophosphates and uridine diphosphate glucose

1967 ◽  
Vol 105 (2) ◽  
pp. 515-519 ◽  
Author(s):  
V. N. Nigam
Keyword(s):  
Time Course ◽  
Initial Rate ◽  
Glycogen Synthesis ◽  
Uridine Diphosphate ◽  
Cytoplasmic Fraction ◽  
Uridine Diphosphate Glucose ◽  
Diphosphate Glucose ◽  
Liver Homogenates ◽  
Pigeon Liver ◽  
Glycogen Formation

Comparative time-course studies of glycogen synthesis from glucose 6-phosphate, glucose 1-phosphate and UDP-glucose show that glucose 1-phosphate forms glycogen at an initial rate faster than that obtained with glucose 6-phosphate and UDP-glucose. After 5min. the rates from glucose monophosphates are considerably slower. 2,4-Dinitrophenol decreases glycogen synthesis from both glucose monophosphates, whereas arsenate and EDTA increase glycogen synthesis from glucose 1-phosphate and inhibit the reaction from glucose 6-phosphate, galactose and galactose 1-phosphate. Mitochondria-free pigeon liver cytoplasmic fraction forms less glycogen from glucose monophosphates than does the whole homogenate. 2-Deoxyglucose 6-phosphate inhibits glycogen synthesis from glucose monophosphates. Glycogen formation from UDP-glucose is relatively unaffected by dinitrophenol, by arsenate, by EDTA, by 2-deoxyglucose 6-phosphate and by the removal of mitochondria from the whole homogenate.

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