Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comparative studies of enzyme activities during the dedifferentiation of hepatic cells and through their development into overt hepatomas are few and contradictory. This study was designed to investigate the histochemical, biochemical and morphologic features of the altered liver cells with particular emphasis on the importance and validity of the histoenzymatic behavior of glucose-6-phosphatase (G6Pase) as a marker for the detection of precancerous hepatic cells. Serum and hepatic levels of G6Pase were analyzed and compared with the histoenzymatic behavior of this enzyme. The use of other enzymes, such as adenosine triphosphatase (ATPase) and gamma glutamyl-transpeptidase (GGT) as histochemical markers for malignancy was also tested. The activities of a variety of enzymes commonly used as diagnostic tools were also evaluated in both the liver homogenates and sera of rats treated with 2 mg diethylnitrosamine (DENA)/kg body weight for 2-28 weeks. Using G6Pase as a histoenzymatic marker, precancerous cells appeared after 4 weeks of exposure to DENA in the form of small islets devoid of G6Pase activity. These G6Pase free cells increased in number forming larger islands and finally appeared as tumor nodules after 28 weeks of treatment. The histoenzymatic behavior of ATPase was identical to that of G6Pase. The precancerous cells, as well as the tumor cells appeared devoid of ATPase activity. The application of GGT as a marker, showed significantly increased activity in the altered liver and tumor cells. Increased serum levels of G6Pase were noted after 10 weeks and were greatly elevated in the late stages of the evolution of the precancerous cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum and hepatic enzyme activity in rats treated with diethylnitrosamine. 610 Feb 19

An enzyme histochemical study was performed to investigate abnormal enzyme activity in human hepatocellular carcinoma (HCC) and, by application of these staining reactions to noncancerous liver disorders, to clarify the true nature of putative percancerous lesions. The enzyme activity of hepatocytes in cirrhotic livers, hepatitis B virus (HBV)-positive cells, and dysplastic liver cells was investigated. Although the tumor cells in HCC gave an intensively positive reaction for gamma-glutamyl transpeptidase activity at the cytoplasm and the whole-cell membrane, they were essentially deficient in glucose-6-phosphatase, alkaline phosphatase, acid phosphatase, and nonspecific esterase activities. Cirrhotic liver showed loss of the orderly zonal difference of enzyme activity that is present in normal liver. However, a pattern of enzyme deviation similar to that of HCC was not recognized anywhere. Neither HBV-positive hepatocytes nor dysplastic liver cells were shown enzymatically to be direct precusors of HCC.
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PMID:Human hepatocellular carcinoma and putative precancerous disorders: their enzyme histochemical study. 611 3

Characteristic alterations of marker enzymes and tumor-associated antigens have been detected in the preneoplastic lesions of experimental hepatocarcinogenesis. An identical pattern of enzyme activity (increased gammaglutamyl transferase, loss of glucose-6-phosphatase, and canalicular adenosine triphosphatase) was demonstrated in a case of nodular "regenerative" hyperplasia of liver. The lack of marker antigens (alphafetoprotein, carcinoembryonic antigen, alpha 1-antitrypsin) in the hyperplastic nodules in this patient may be related to the discontinuation of oral contraceptive steroids four years earlier. The phenotypic changes of enzyme activity suggest that nodular "regenerative" hyperplasia of the liver in man is preneoplastic.
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PMID:Enzyme pattern and marker antigens in nodular "regenerative" hyperplasia of the liver. 611 60

The effects of a chronic 8- to 12-week administration of the hepatic tumor promoter, phenobarbital, on further altering the biochemical enzyme deviation patterns shown by hyperplastic liver nodules was examined in rats previously subjected to the initiation/selection protocol of Solt and Farber. Hyperplastic liver nodules of various size classes from the phenobarbital-treated group exhibited a significant increase in GGT specific activity, as well as 2- to 3-fold higher levels of microsomal cytochrome P-450 than was shown by control nodules. The increase in GGT specific activity was also found in many cases to be higher in those hyperplastic liver nodules from the phenobarbital-treated group with diameters greater than 3.0-3.5 mm than in nodules of a smaller size. In contrast, the GGT specific activity of the control nodules did not correlate with differences in their sizes. Furthermore, while histochemical staining of GGT activity appeared uniform in sections of the various sized hyperplastic nodules from the phenobarbital-treated group, biochemical measurements indicated a consistently higher specific activity for this enzyme in tissue taken from the central portion of the nodule than in tissue from the peripheral portion of the nodule. On the other hand, the specific activities of glucose-6-phosphatase, 5'-nucleotidase, and fructose-1,6-diphosphate aldolase of the hyperplastic liver nodules were not found to be significantly altered over control values by the chronic phenobarbital treatment, suggesting a stability of these other marker enzyme alterations during the early promotional phase of hepatocarcinogenesis.
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PMID:Effect of phenobarbital on the altered biochemical phenotypes expressed by hyperplastic liver nodules during hepatocarcinogenesis in the rat. 614 62

The change in the activity of several hepatic enzymes during hepatocarcinogenesis suggests a pattern of dedifferentiation. This category of enzymes includes glucose-6-phosphatase and gamma-glutamyltranspeptidase (GGT). A detailed kinetic analysis of microsomal glucose-6-phosphatase activity revealed that both the translocase and phosphohydrolase activities were markedly reduced in Morris 7777 hepatoma transplanted in male Buffalo rats. In addition, the activity of the translocase component increased 2.4-fold, while the phosphohydrolase activity decreased 1.6-fold in the liver of tumor-bearing animals. GGT activity in the host liver was not effected by the presence of the tumor. These results suggest differences in the effect of Morris 7777 hepatoma on: the phosphohydrolase and translocase activities of microsomal glucose-6-phosphatase and the sensitivity of glucose-6-phosphatase and GGT activities in the host liver.
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PMID:Effect of Morris 7777 hepatoma on microsomal glucose-6-phosphatase latent activity. 614 32

PLC/PRF/5, a tissue culture cell line derived from a human hepatocellular carcinoma and producing hepatitis B surface antigen (HBsAg), was studied by immune and enzyme histochemical techniques. HBsAg was demonstrated in the cytoplasm and on the surface of tumor cells. The percentage of HBsAg-positive cells in subculture increased with time until almost all cells expressed HBsAg when the monolayer reached confluence. Similar patterns were found for alpha 1-anti-trypsin and carcino-embryonic antigen, whereas alpha-fetoprotein was observed only in small foci of cells. Hepatitis B core antigen and albumin were not detected. gamma-Glutamyl transferase activity was markedly increased in the tumor cells, whereas adenosine triphosphatase and glucose-6-phosphatase activities were not demonstrable. Patterns of antigenic expression and enzyme phenotype of PLC/PRF/5 cells show remarkable resemblance to those observed in vivo in human hepatocellular carcinoma. Therefore, this cell line may be a useful model to study the control and modulation of both oncofetal antigens and HBsAg.
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PMID:Immune and enzyme histochemical studies of a human hepatocellular carcinoma cell line producing hepatitis B surface antigen. 616 57

The histochemical enzyme activity of alkaline phosphatase, nonspecific esterase, 5-nucleotidase, beta-glucuronidase, glucose-6-phosphatase, succinate dehydrogenase, and glucose-6-phosphate dehydrogenase in human bladder cancer was investigated. Tumors of 84 patients, classified into grades I-III according to the WHO classification, were compared with 12 normal and 16 inflamed bladder epithelia. As a rule, loss of alkaline phosphatase activity and a decrease of nonspecific esterase activity was found in most of these tumors. The activity of beta-glucuronidase was decreased and compared with normal tissue, also the activity of 5-nucleotidase. The succinate dehydrogenase activity in tumor tissue was frequently increased, whereas glucose-6-phosphate dehydrogenase did not show any significant reaction.
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PMID:[Histochemical investigations on human bladder cancer (author's transl)]. 626 65

The correlation between the cytochemistry (glycoprotein, glycogen, glucose-6-phosphatase, catalase, alkaline phosphatase) and the growth rate of the fast-growing Morris hepatoma 3924A and the slow-growing Morris hepatoma 9618A was studied by utracytochemical techniques. By the chromic acid-phosphotungstic acid technique, acid glycoprotein is stained in glycocalyx, Golgi saccules and vesicles, and secretory granules of the tumor cells of both hepatomas. However, the hepatoma 3924A cells contain thicker glycocalyx and more numerous glycoprotein-rich granules than hepatoma 9618A cells. Abundant alpha and beta glycogen particles are found in hepatoma 3924A. Moderate glucose-6-phosphatase activity is observed in the cisternae of endoplasmic reticulum and nuclear envelope of hepatoma 9618A, but it is totally absent in hepatoma 3924A. High catalase activity is present in numerous peroxisomes of hepatoma 9618A. Hepatoma 3924A contains only a few catalase-positive microperoxisomes. Weak to moderate alkaline phosphatase is present in the plasma membrane and nuclear envelope of hepatoma 9618A cells, while hepatoma 3924A shows no activity of the enzyme. All the cytochemical parameters except glycoprotein show an inverse relationship with the growth rate of the hepatomas. The higher intracellular glycoprotein content of hepatoma 3924A may be related to differences in cell coat secretion (composition and activity) from the slower-growing hepatoma 9618A
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PMID:Correlation between growth rate and cytochemistry in Morris hepatomas. 627 86

Hepatocellular neoplasms are known to differ in enzyme activity from the surrounding non-neoplastic liver. We have compared histochemically the enzyme activity of spontaneous hepatocellular tumors in mice with tumors induced by diethylnitrosamine and dieldrin. Some neoplasms had increased activity, others had decreased enzyme activity, yet other had the same activity as the surrounding liver. Alkaline phosphatase, glucose-6-phosphatase, succinic dehydrogenase and adenosine triphosphatase, as well as glycogen levels were studied. Carcinomas differed from adenomas in having elevated enzyme activity significantly more often than adenomas. However, the carcinomas showed elevated glycogen levels less frequently than adenomas. Histochemically, pulmonary metastases resembled the primary hepatocellular carcinomas from which they were derived. Tumors of dieldrin animals were notable in having increased activity of all the enzymes which we studied more frequently than tumors of diethylnitrosamine animals or of controls. Differences in enzyme activity between the three mouse strains were slight.
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PMID:Enzyme histochemical characteristics of spontaneous and induced hepatocellular neoplasms in mice. 629 95

The livers from a total of 51 Sprague-Dawley rats treated with different doses of N-nitrosomorpholine (80-120 mg/l in the drinking water) for up to 14 weeks together with the livers of 28 control animals were histochemically investigated at the cessation of carcinogenic insult and at varying periods thereafter for their glycogen content, basophilia and activities of various enzymes of carbohydrate metabolism: glycogen synthetase, glycogen phosphorylase, glucose-6-phosphatase, glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase. The enzymatic patterns of normal tissue, preneoplastic and neoplastic lesions were characterized and compared with reference to the morphologically defined stages of tumor development in the liver. The early appearing glycogen storing areas, localized in the peripheral and intermediate lobular regions, did not show significant changes in the histochemically demonstrable activities of the enzymes tested. After cessation of the carcinogen treatment the more pronounced glycogen storage foci which developed within the aforementioned regions of the liver acinus usually showed a reduction in the activities of phosphorylase and glucose-6-phosphatase while the activity of glucose-6-phosphate dehydrogenase, a key enzyme for the pentose phosphate pathway, was increased. The mixed cell foci, neoplastic nodules and tumors which emerged at later stages were characterized by a progressive shift away from glycogen metabolism towards glycolysis and the pentose phosphate pathway, as indicated by an increase in glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase activities. These changes in enzyme pattern are supportive of a developmental sequence leading from glycogen storage foci through mixed cell foci and neoplastic nodules to hepatocellular carcinomas.
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PMID:Correlative histochemistry of some enzymes of carbohydrate metabolism in preneoplastic and neoplastic lesions in the rat liver. 629 53


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