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)

Subcutaneous injection of iron dextran resulted in a hepatic siderosis within 2 weeks in rats, as previously reported for mice. Hepatic carcinomas as well as neoplastic nodules in rats were entirely or mainly free of stainable iron and, thus, could be readily identified histologically. In addition, early carcinogen-induced altered foci were resistant to iron accumulation. In rats fed 0.02% N-2-fluorenylacetamide (FAA) for 13 weeks, the number of iron-resistant foci identified following iron injection was the same as that observed with dietary iron overload. Histochemical investigation of enzymatic markers that have been used to identify foci in rats revealed that foci characterized by enzymatic reactions of positive gamma-glutamyl transpeptidase and decreased adenosine triphosphatase and glucose-6-phosphatase corresponded to those characterized by resistance to iron accumulation. However, in quantitative analysis of the early carcinogen-induced foci in rats given iron dextran following a diet containing 0.02% 2-FAA for 13 weeks, more lesions were detected by resistance to iron accumulation than by any of these other properties. There was considerable phenotypic heterogeneity among foci for the enzyme markers. It is concluded that resistance to iron accumulation is a more sensitive and reliable marker for early carcinogen-induced altered hepatocellular foci than is any other histochemical property.
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PMID:The sensitivity and heterogeneity of histochemical markers for altered foci involved in liver carcinogenesis. 22 50

We determined whether alterations in hepatic microsomal function occur in association with iron-induced lipid peroxidation in vivo in rats with chronic dietary iron overload. In rats fed a 2.0% carbonyl iron diet for a period of 20 wk, there was no significant microsomal conjugated diene formation (evidence of microsomal lipid peroxidation) or difference in cytochrome P450 concentration found at mean (+/- SEM) hepatic iron concentrations of 1210 +/- 92 micrograms/g liver (wet wt) or 2730 +/- 100 micrograms/g. At a hepatic iron concentration of 4090 +/- 245 micrograms/g, however, there was significant conjugated diene formation (p less than 0.001) and a 56% decrease in the cytochrome P450 concentration (p less than 0.001). In rats fed a 2.5% carbonyl iron diet for 10 wk, achieving a liver iron concentration of 4820 +/- 420 micrograms/g, there was significant microsomal conjugated diene formation (p less than 0.001), a 35% reduction in cytochrome P450 (p less than 0.005), and a 16% reduction in aminopyrine demethylase activity (p less than 0.025), but only an 8% reduction in glucose-6-phosphatase activity (p = not significant). Finally, in rats fed a 3.0% iron-supplemented diet for 7 wk, achieving a liver iron concentration of 2730 +/- 205 micrograms/g, there was a 23% reduction in cytochrome P450 (p less than 0.025), a 28% reduction in cytochrome b5 (p less than 0.001), and a 47% increase in heme oxygenase activity (p less than 0.025) (heme oxygenase activity measured in this group only). We conclude that oral iron loading can produce microsomal lipid peroxidation in vivo that is associated with selective decreases in microsomal hemoprotein concentrations and cytochrome P450-dependent enzymes.
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PMID:Hepatic microsomal function in rats with chronic dietary iron overload. 300 59

Sequential alterations in enzyme histochemical profiles and reaction of hepatocytes to rapid iron overload were examined in male BALB/c mice during chronic, safrole exposure. At 24 weeks after initiation of safrole treatment, foci of enzyme-altered hepatocytes were noted. These foci were composed of cells showing a decrease in reactivity for glucose-6-phosphatase (Glc-6-Pase) and succinate dehydrogenase (SDH) and an increase for gamma-glutamyl transpeptidase (gamma-Glu-T). In control, iron-loaded mice, the livers were intensely siderotic. In safrole-exposed, iron-loaded mice, foci of iron-negative hepatocytes, varying from a few cells to a lobule in diameter, were initially noted at 24 weeks. Both enzyme-altered and iron-negative foci occurred in the livers of exposed mice at all time periods after 24 weeks. After 36, 52, and 75 weeks of safrole treatment, hepatocellular adenomas were noted with altered enzyme histochemical profiles. Hepatocytes from adenomas were characterized by a decreased staining for Glc-6-pase and SDH and increased staining for gamma-Glu-T and glucose-6-phosphate dehydrogenase (Glc-6-PD). In addition, a few nodules showed a decrease in staining for 5'nucleotidase. In iron-loaded mice, hepatocytes of adenomas showed a decreased to negative reaction for iron when the surrounding parenchyma was siderotic. Hepatocellular carcinomas (HPC) occurred in livers of mice exposed to safrole for 52-75 weeks. The cells of HPC displayed similar enzyme histochemical reactions as cells of adenomas. They were decreased for Glc-6-Pase and SDH activity and increased for gamma-Glu-T and Glc-6-PD. In iron-loaded mice, the HPC cells were negative for stainable iron. Foci, adenomas, and HPC displayed some variability in enzyme histochemical reactions. Variability existed between lesions as well as between cells of the same lesion.
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PMID:Biology of hepatocellular neoplasia in the mouse. II. Sequential enzyme histochemical analysis of BALB/c mouse liver during safrole-induced carcinogenesis. 694 76