Expression of multiple proteins structurally related to gamma-glutamyl transpeptidase in non-neoplastic adult rat hepatocytes in vivo and in culture

1991 ◽  
Vol 146 (2) ◽  
pp. 234-241 ◽  
Author(s):  
Georg A. Mathis ◽  
Peter A. Wyss ◽  
Erin G. Schuetz ◽  
Rebecca P. Hughey ◽  
Alphonse E. Sirica
Keyword(s):  
Rat Hepatocytes ◽  
Gamma Glutamyl Transpeptidase ◽  
Gamma Glutamyl ◽  
Adult Rat ◽  
Adult Rat Hepatocytes ◽  
Glutamyl Transpeptidase

Acetazolamide and renal ammoniagenesis

1978 ◽  
Vol 234 (3) ◽  
pp. F235-F237 ◽  
Author(s):  
S. K. Chapman ◽  
M. S. Hoover
Keyword(s):  
Ammonium Excretion ◽  
Gamma Glutamyl Transpeptidase ◽  
Gamma Glutamyl ◽  
Enzyme Systems ◽  
Glutamyl Transpeptidase

The effect of acetazolamide on ammonia-producing enzyme systems was determined in vitro at concentrations comparable to those which have been shown to abolish ammonium excretion in vivo. No change in the activity of glutaminase or gamma-glutamyl transpeptidase could be observed at concentrations up to 0.2 mM acetazolamide, and concentrations up to 1 mM were without effect on D-glutamyltransferase activity. Therefore, the effect of acetazolamide to abolish ammonium excretion cannot be explained by an action of the drug to inhibit ammoniagenesis.

Expression of gamma-glutamyl transpeptidase in adult rat liver cells after transformation with SV40 virus

1984 ◽  
Vol 22 (1) ◽  
pp. 31-39 ◽  
Author(s):  
C. Lafarge-Frayssinet ◽  
S. Estrade ◽  
B. Rosa-Loridon ◽  
C. Frayssinet ◽  
R. Cassingena
Keyword(s):  
Rat Liver ◽  
Liver Cells ◽  
Gamma Glutamyl Transpeptidase ◽  
Sv40 Virus ◽  
Gamma Glutamyl ◽  
Adult Rat ◽  
Rat Liver Cells ◽  
Glutamyl Transpeptidase

Hormonal induction of malic enzyme in rat hepatocytes cultured on laminin-rich gels

1992 ◽  
Vol 8 (3) ◽  
pp. 235-242 ◽  
Author(s):  
D. J. Mann ◽  
A. J. Strain ◽  
E. Bailey
Keyword(s):  
Malic Enzyme ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Isolated Hepatocytes ◽  
Specific Expression ◽  
Adult Rat ◽  
Adult Rat Hepatocytes ◽  
Species Being ◽  
Rat Tail

ABSTRACT The levels of malic-enzyme mRNA and activity were determined in primary cultures of adult rat hepatocytes maintained on either rat-tail collagen or a laminin-rich substratum. Cells plated on laminin-rich gels exhibited substantially improved patterns of albumin and malic-enzyme expression when compared with cells maintained on rat-tail collagen. Moreover, hepatocytes plated on the laminin-rich matrix displayed marked malic-enzyme inducibility in response to tri-iodothyronine and dichloroacetate, especially in the presence of insulin. However, Northern blot analysis revealed that the ratio of the amounts of the two major malic-enzyme mRNA species (2.0 and 3.1 kb) was reversed when compared with that found in the liver in vivo, the altered levels of these two species being closer to those found in non-hepatic tissues. These findings indicate that, although the hormonal responsiveness of isolated hepatocytes maintained on laminin-rich gels is markedly improved, and approaches the degree of induction demonstrated in the liver in vivo, the mechanisms of control differ, indicating a loss of liver-specific expression.

The Origin and Significance of Hyperplastic Hepatocellular Islands and Nodules in Hepatic Carcinogenesis

1982 ◽  
Vol 1 (1) ◽  
pp. 119-144 ◽  
Author(s):  
Stanley Goldfarb ◽  
Thomas D. Pugh
Keyword(s):  
Gamma Glutamyl Transpeptidase ◽  
Short Term ◽  
Gamma Glutamyl ◽  
Hepatocellular Carcinomas ◽  
Hepatic Carcinogenesis ◽  
Distinctive Type ◽  
Activity Loss ◽  
Glutamyl Transpeptidase ◽  
Complete Carcinogens

Results of many studies, summarized in this review, support the hypothesis that carcinogen-induced hepatocellular carcinomas develop from phenotypically-altered hyperplastic hepatocellular nodules; these in turn apparently arise from smaller focal collections of hyperplastic cells referred to as hepatocellular islands. The very recent recognition that phenobarbital, when administered after carcinogens, fosters the outgrowth of hepatocellular islands and carcinomas, now provides the means for studying stages of initiation and promotion in hep-atocarcinogenesis. In addition, the recognition that enzymatic alterations, particularly the acquisition of canalicular gamma glutamyl transpeptidase activity, loss of ATP'ase activity, and loss of glucose-6-phosphatase activity that characterize many islands, have been particularly useful for measuring and evaluating the growth kinetics and heterogeneity of the islands. Evidence is presented that periportal gamma glutamyl transpeptidase positive hepatocytes are considerably more abundant after four weeks of feeding .02% 2-acetyl-aminofluorene to young rats than in control animals, and that the outgrowth of these cells is fostered by a distinctive type of periportal reparative hyperplasia. The cells appear to arise from a pool of cells that are normally abundant in periportal location in young growing rats. The studies suggest that it may now be possible to develop short term in vivo bioassays for initiators, promoters, and complete carcinogens in the rodent liver.

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