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)

The efficacy of silymarin treatment in preventing biochemical and histological alterations in CCL4-induced liver cirrhosis in rats was studied. Four groups of rats were treated with: (1) CCL4; (2) mineral oil; (3) CCL4 + silymarin; and (4) silymarin. All animals were sacrificed 72 h after the end of treatments. The activities of alkaline phosphatase (alk. phosp.), gamma-glutamyl transpeptidase (GGTP), glutamic pyruvic transaminase (GPT) and glucose-6-phosphatase (G6Pase), and bilirubin content were determined in serum. Na+, K+-ATPase and Ca++-ATPase activities were measured in isolated plasma membranes. Lipoperoxidation, triglycerides (TG), and glycogen contents were also measured in liver homogenates. Liver cirrhosis was evidenced by significant increases in liver collagen, lipoperoxidation, serum activities of alk. phosp., GGTP, GPT, G6Pase, bilirubin content, and liver TG. Activities of ATPases determined in plasma membranes were significantly reduced, as was liver glycogen content. Silymarin cotreatment (50 mg/kg b.wt) completely prevented all the changes observed in CCL4-cirrhotic rats, except for liver collagen content which was reduced only 30% as compared to CCL4-cirrhotic rats. Silymarin protection can be attributed to the agent's antioxidant and membrane-stabilizing actions.
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PMID:Prevention of CCL4-induced liver cirrhosis by silymarin. 254 40

Three fish species were exposed to a sublethal dose (0.35 mg/l) of DDT continuously for a period of 50 days and the effect of hepatic and renal acid and alkaline phosphatases, glucose-6-phosphatase and fructose-1,6-diphosphatase activities was observed at 15, 30 and 45 days. Exposure to DDT at 15 days led to the fall and increase thereafter (at 30 and 45 days) in the activities of acid phosphatase, glucose-6-phosphatase and fructose-1,6-diphosphatase in hepatic tissue, where as alkaline phosphatase in liver registered an increase at 15, 30 and 45 days DDT exposure. In renal tissue the trend of 4 phosphatases was same as that of alkaline phosphatase in the liver. The changes in these 4 phosphatases were more pronounced in C. punctatus than in G. batrachus and L. rohita.
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PMID:DDT toxicity: variations in tissue non-specific phosphomonoesterases and gluconeogenic enzymes in three teleosts. 255 82

Pretreatment of rats with colchiceine (10 micrograms/day/rat) for seven days protected against CCl4-induced liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of alanine amino transferase (ALT), alkaline phosphatase (Alk. Phosph.) gamma glutamyl transpeptidase (GGTP), bilirubins and decreased activity of glucose-6-phosphatase (G-6Pase). Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane GGTP and Alk. Phosph. activities were found. Colchiceine increased 1.5-fold the LD50 of CCl4 and prevented the release of intracellular enzymes as well as the decrease in GGTP and Alk. Phosph. activities in plasma membranes. It also completely prevented the lipid peroxidation induced by CCl4 and limited the extent of the histological changes.
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PMID:Protective effect of colchiceine against acute liver damage. 257 11

In order to determine the specific action of cadmium on bone metabolism, the effect of cadmium on alkaline phosphatase activity, a marker enzyme of osteoblasts, was compared with that of other divalent heavy metal ions, i.e., zinc, manganese, lead, copper, nickel and mercury (10 microM each), using cloned osteoblast-like cells, MC3T3-E1. Cadmium had the strongest inhibitory effect on alkaline phosphatase activity of the cells among the metals tested. At the same dose, however, cadmium failed to inhibit cellular glucose-6-phosphatase and lactate dehydrogenase activities, suggesting that the inhibitory effect of cadmium on alkaline phosphatase was specific and was not dependent on cell injury. Cadmium treatment caused a significant decrease in cellular zinc level, but mercury treatment had no such effect at the dose inhibiting alkaline phosphatase activity. There was a good correlation between decrease of cellular zinc level and inhibition of alkaline phosphatase activity in cadmium-treated cells. Concomitant treatment of the cells with zinc prevented the cadmium-induced inhibition of alkaline phosphatase activity. However, this was not the case in the mercury-induced inhibition. Cadmium also inhibited the mineralization of osteoblasts. When 10 or 20 microM zinc was concomitantly added to the cultures, the inhibition of mineralization was prevented. These data suggest that the inhibitory effect of cadmium in osteoblasts may be closely related to its influence on the cellular zinc metabolism.
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PMID:Preventive effects of zinc on cadmium-induced inhibition of alkaline phosphatase activity and mineralization activity in osteoblast-like cells, MC3T3-E1. 274 54

Growth of cells of the potentially zoopathogenic fungus Basidiobolus haptosporus on a nutritionally defined medium with xanthine or urate as the nitrogen source results in greatly increased populations of microbodies. Modified Gomori procedures at the electron microscopic level suggested the single limiting membrane (and in some cases the granular matrix) of immature microbodies to be the exclusive subcellular locale(s) of alkaline phosphatase, 5'-nucleotidase and nucleoside diphosphatase activities. When grown in the presence of low inorganic phosphate, additional alkaline phosphatase activity was further identified cytochemically at and along profiles of endoplasmic reticulum and on inclusions previously described as "double-membraned vesicles". Cytochemical localization of acid phosphatase at microbody membranes was minimal if not ambiguous; Mg++-dependent adenosine triphosphatase and glucose-6-phosphatase were not identified at these locales. Quantitative biochemical estimates of alkaline phosphatase activity levels in particulate fractions initially increased with age of cells, perhaps as a function of the cultural induction and marked increase in immature microbody populations. We suggest that this enzyme may participate in some manner with protein translocation mechanisms associated with microbody biogenesis, ontogeny, and/or physiological function.
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PMID:Electron cytochemical demonstration of phosphatase activity with microbody membranes of Basidiobolus haptosporus. 282 62

New light microscopic visualization methods were developed for the histochemical detection of non-specific alkaline and acid phosphatase, Mg-, Ca- and Na, K-dependent adenosine triphosphatase, myosin adenosine triphosphatase, glucose-6-phosphatase, 5'-nucleotidase and thiamine pyrophosphatase with cerium ions as trapping agents in cryostat and plastic sections. The techniques are based on the conversion of cerium phosphate into cerium perhydroxide by H2O2 which decomposes at 55 degrees-60 degrees C into cerium hydroxide and oxygen radicals. These radicals are able to oxidize diaminobenzidine (DAB) to DAB brown. Addition of nickel ions to the DAB-H2O2 mixture generates bluish-black stained nickel-DAB complexes. Compared with the classical metal precipitation, azo, azoindoxyl and tetrazolium procedures the H2O2-DAB and especially the H2O2-DAB-nickel methods provided identical or superior results in catalytic phosphatase histochemistry and immunohistochemistry when using non-specific alkaline phosphatase as the enzyme label.
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PMID:The cerium perhydroxide-diaminobenzidine (Ce-H2O2-DAB) procedure. New methods for light microscopic phosphatase histochemistry and immunohistochemistry. 285 63

This paper deals with the conversion of the hepatotoxicity of 1,2-dichlorobenzene (DCB), the nephrotoxicity of hexachloro-1,3-butadiene (HCBD) and the respiratory effects of these two toxicants into quantal data. It aims to provide some useful information on the best strategy used for safety evaluation. A reflex bradypnea indicative of irritation of the nasal cavities of mice occurred during a 15-min oronasal exposure to each chemical. A reduction in the development of staining for liver glucose-6-phosphatase (G6-phosphatase) and an increase in the number of damaged tubules in cryostat kidney sections stained for alkaline phosphatase were the measure of toxicity in mice subjected to a whole-body 4-h exposure to DCB and HCBD vapours, respectively. The immediate irritant responses, as well as the delayed liver and kidney responses, were measured at the peak of the chemical's action. These maximum responses were then used to establish the relationships of exposure level effects and also the median active levels of exposure (MALs). The DCB and HCBD MALs responsible for a 50% decrease in the respiratory rate of mice (RD50) were 181 and 211 ppm, respectively. The MAL required for eliciting a 50% decrease in G6-phosphatase staining intensity in DCB-exposed mice was 598 ppm and that associated with 50% of damaged tubules in HCBD-exposed mice was 7.2 ppm. On the basis of these quantitative data, potency ratios indicated that irritation and kidney injury are the primary manifestations of toxicity associated with short-term exposure to DCB and HCBD, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of the relative hazard involved with airborne irritants with additional hepatotoxic or nephrotoxic properties in mice. 285 85

The activities of acid phosphatase, alkaline phosphatase, glucose-6-phosphatase, uridine diphosphatase, inosine diphosphatase, thiamine pyrophosphatase and 5'-nucleotidase have been investigated cytochemically in hepatocytes of the offspring of alcohol-fed rats, using cerium ions as a capturing agent and qualitative and quantitative electron microscopy. All these enzyme activities were decreased in the experimental animals compared with controls not exposed to ethanol. The pattern of deposition of the product of glucose-6-phosphatase activity in the cisternae of the endoplasmic reticulum was also different in the two groups. The phosphatases analyzed are functional markers of different cell components, and the results suggest that prenatal exposure of rats to ethanol causes functional alterations in the endoplasmic reticulum, Golgi apparatus, lysosomes and plasma membrane of hepatocytes.
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PMID:Alterations in the cytochemical activity of several phosphatases in hepatocytes from rats exposed prenatally to ethanol. 286 48

Enzyme histochemical techniques were utilized to examine the progression and extent of proximal tubular injury during the development of cis-diamminedichloroplatinum (II) (CDDP)-induced acute renal failure. Acute renal failure was induced in male rats by the intraperitoneal administration of 10 mg CDDP/kg body weight. At 6, 24, 48, 72, and 96 hr following treatment, renal function was assessed and tissue was collected for renal morphologic and enzyme histochemical studies. The enzymes examined were gamma-glutamyl transpeptidase, alkaline phosphatase, sodium-potassium ATPase (nitrophenyl phosphatase), acid phosphatase, glucose-6-phosphatase, succinic dehydrogenase, alpha-glycerophosphate dehydrogenase, and lactic dehydrogenase. By 24 hr, the activity of acid phosphatase was reduced throughout the proximal tubule, with the greatest decrease occurring in the P3 segment of the proximal tubule located in the outer stripe of the outer medulla. Changes in the histochemical staining of the remaining enzymes were not consistently observed until 48 or, in some cases, 72 hr. These alterations involved all portions of the proximal tubule with the most severe changes involving P3. The results of the enzyme histochemical studies along with the morphologic findings indicating that the initiation of CDDP-induced acute renal failure, first apparent at 48 hr in this model, is associated with cell injury throughout the proximal tubule. The majority of the histochemical changes did not become apparent until late in the course of tubular injury. This suggests that most of the changes in enzyme activity represent nonspecific effects of CDDP-induced tubular injury, as opposed to direct enzyme inhibition by the drug.
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PMID:Cis-diamminedichloroplatinum (II)-induced acute renal failure in the rat: enzyme histochemical studies. 287 24

Renal tubular lesions induced in male rats by two different carcinogens, N-nitrosomorpholine (NNM) and N-ethyl-N-hydroxyethylnitrosamine (EHEN), using a limited exposure "stop" protocol were investigated histochemically to demonstrate phenotypic cellular changes. The parameters measured included basophilia, glycogen content and the activity of the enzymes glucose-6-phosphatase (G6PASE), glycogen synthetase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphate dehydrogenase (G6PDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), succinate dehydrogenase (SDH), alkaline phosphatase (ALP), acid phosphatase (ACP) and gamma-glutamyl transpeptidase (gamma-GT). The lesions observed were predominantly of either basophilic or oncocytic types. In each case, tubular lesions (altered tubules) appeared to give rise to epithelial tumors (epitheliomas) with the same cellular phenotype. Basophilic tubules and epitheliomas proved to be strongly positive for GAPDH and G6PDH while demonstrating a reduction or loss of G6PASE, ALP, ACP, gamma-GT, and SDH compared with controls and the surrounding proximal or distal tubules. In addition, large basophilic epitheliomas demonstrated an increase in both SYN and PHO activities. In contrast, most oncocytic tubules and oncocytomas characterized by abundant densely granular cytoplasm showed a reduction in the activity of G6PDH, but were intensely positive for SDH. However, a few oncocytic lesions demonstrated a decrease in both SDH and G6PDH activity. Rarely, decreased SDH and elevated G6PDH activities were observed in altered tubules resembling oncocytic tubules. It remains to be clarified whether these tubules represent a variation of the oncocytic lesions or, perhaps, another type of tubular lesion. The results indicate that basophilic and oncocytic epithelial tumors differ in their cytochemical pattern and histogenesis. In line with earlier suggestions, the basophilic tumors apparently originate from the proximal renal tubules, while the oncocytomas develop from the distal parts of the nephron. The basophilic tumors are characterized by an increased pentose phosphate pathway and glycolysis, with a corresponding reduction in mitochondrial respiration. However, the majority of the oncocytomas show an increased activity of the mitochondrial enzyme SDH, and a marked decrease in the activity of the key enzyme of the pentose phosphate pathway.
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PMID:Correlative histochemical studies on preneoplastic and neoplastic lesions in the kidney of rats treated with nitrosamines. 287 45


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