Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preneoplastic and neoplastic liver cell lesions, induced by EHEN (N-ethyl-N-hydroxyethylnitrosamine) in rats, were investigated to establish the numbers of simultaneously expressed altered enzyme phenotypes within the lesion cells. The lesions were divided into 5 classes on the basis of altered expression in one or more of the following 5 enzymes: glutathione S-transferase placental form, glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, adenosine triphosphatase, and gamma-glutamyl transpeptidase. Class 1 lesions contained cells expressing one altered enzyme. Similarly, class 2, 3, 4 and 5 lesions had cells simultaneously expressing 2, 3, 4, and 5 enzyme alterations, respectively. Four histopathological categories of lesions, ACF (altered cell foci) (274 lesions), HN (hyperplastic nodules) (47 lesions), HCC (hepatocellular carcinomas) (99 lesions) and THC (transplanted hepatocellular carcinomas) (5 lesions) were studied. Proliferation potential was assessed in terms of 5-bromo-2'-deoxyuridine (BrdU) incorporation. The distribution profiles of classes 1 to 5 showed a clear reciprocal change from low class (1 to 2 enzymes) predominance in ACF to high class (4 to 5 enzymes) predominance in HN. Increase of BrdU labeling indices was clearly correlated with progression from HN to HCC. Only a small population of class 5 ACF showed a high BrdU labeling index, indicating particular potential for further development. Thus, the stages of EHEN-induced neoplasia were found to be characterized by gradual increase in the number of altered enzyme phenotypes, with acquisition of proliferative potential being associated with further progression towards malignant conversion.
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PMID:Number of simultaneously expressed enzyme alterations correlates with progression of N-ethyl-N-hydroxyethylnitrosamine-induced hepatocarcinogenesis in rats. 790 86

Neuromuscular activity was eliminated in the tibialis anterior muscle of adult cats for 6 months by spinal isolation (SI), i.e., complete spinal cord transections at T-12-13 and at L-7-S-1, plus bilateral dorsal rhizotomy between the two transection sites. One motor unit from each muscle was isolated using ventral root teasing procedures and physiologically tested. The fibers belonging to each motor unit were visualized in PAS-stained sections by the loss of glycogen following prolonged repetitive stimulation. Qualitatively, the normal enzymatic interrelationships among fibers identified by myosin heavy chain composition were unchanged by SI. Generally, each motor unit from SI cats were of a single myosin immunohistochemical type. The same physiological motor unit types that typify control muscles were found in SI cats. In SI compared to control cats, there was approximately a 10% increase in the number of muscle fibers expressing fast myosin. Mean fiber activity levels of ATPase and SDH for a given fiber type (based on MHC antibody reactions) decreased by approximately 10% and 25%, whereas GPD activity increased approximately 35%. It is concluded that differential levels or patterns of activity are not essential to maintain the range of histochemical and physiological motor unit types found in the tibialis anterior of normal adult cats.
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PMID:Level of independence of motor unit properties from neuromuscular activity. 793 55

Cyanophage N-1 multiplication was investigated during the latent period of the virus, when 14CO2 fixation was inhibited whereas respiratory O2 uptake increased approximately 67% at 4 h after infection. A simultaneous decrease (70%) in the glycogen content of infected cells indicated its catabolic involvement. A chloramphenicol-sensitive rise in glucose-6-phosphate dehydrogenase activity as a result of N-1 infection partly explained the increase in aerobic respiration. The total ATP pool declined to 53% of the control while Ca(2+)-dependent ATPase activity also declined (25%). In contrast, Mg(2+)-dependent ATPase activity increased (80%) in comparison with uninfected cells. Results suggest that oxidative phosphorylation was more crucial in the control of cyanophage N-1 development than photophosphorylation under photoautotrophic growth conditions.
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PMID:Energetics of cyanophage N-1 multiplication in the diazotrophic cyanobacterium Nostoc muscorum. 807 15

Injections with different doses (0.1, 0.25, 0.5, 1.0, 2.0, and 4.0 micrograms/g) of estradiol-17 beta (E2), administered three days consecutively, showed a statistically significant increase in mitochondrial Na(+)-K(+)-ATPase, cytosolic malate dehydrogenase, and cytosolic glucose-6-phosphate dehydrogenase activities in a dose-dependent manner in the hepatopancreas of the freshwater prawn (Macrobrachium rosenbergii) on the 4th day of treatment compared to the control values. A lower dose of 0.05 microgram/g was without any effect on these enzyme activities. A uniform increase in the Mg(2+)-ATPase activity was observed after injections with 0.5, 1.0, and 2.0 micrograms/g of E2. Ergosterol, a nonsex steroid did not show any change in the malate dehydrogenase and glucose-6-phosphate dehydrogenase activities on which this compound was tested at a 2.0 micrograms/g dose, compared to the control values. Simultaneous injection of tamoxifen (0.5 microgram/g), an antiestrogenic compound, with E2 (2 micrograms/g) caused inhibition of the E2-induced rise in mitochondrial Na(+)-K(+)-ATPase and cytosolic NADP-linked malate dehydrogenase activities. Conversely, tamoxifen (0.5 and 1.0 microgram/g) behaved as an estrogen agonist to the response (increase) of Mg(2+)-ATPase and cytosolic glucose-6-phosphate dehydrogenase activities. Potentiation of the estrogen effect with tamoxifen (1.0 microgram/g) was observed in these enzyme activities when used simultaneously with E2 (2 micrograms/g). Use of cycloheximide (0.5 mg/liter), a protein synthesis blocker, inhibited the inhibited the E2 (2 micrograms/g)-induced increase in all the enzyme activities studied. The data show specific and prominent subcellular action of estrogen with an indication of its role in energy-dependent ion transport and metabolic activation in hepatopancreas of the freshwater prawn.
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PMID:Subcellular action of estradiol-17 beta in a freshwater prawn Macrobrachium rosenbergii. 822 54

Metastases in rat liver were generated experimentally by intraportal injection of colon cancer cells to investigate the effects of cancerous growth on the metabolism of surrounding liver tissue. Maximum activities (capacity) of glucose-6-phosphate dehydrogenase, phosphogluconate dehydrogenase, lactate dehydrogenase, succinate dehydrogenase, alkaline phosphatase, 5'-nucleotidase, xanthine oxidoreductase, purine nucleoside phosphorylase and adenosine triphosphatase have been determined. Two types of metastases were found, a small type surrounded by stroma and a larger type in direct contact with hepatocytes. Both types affected the adjacent tissue in a similar way suggesting that the interactions were not mediated by stroma. High capacity of the degradation pathway of extracellular purines released from dead cells of either tumours or host tissue was found in stroma and sinusoidal cells. Metastases induced both an increase in the number of Kupffer cells and proliferation of hepatocytes. The distribution pattern in the liver lobulus of most enzymes investigated did not change distinctly. However, activity of alkaline phosphatase, succinate dehydrogenase and phosphogluconate dehydrogenase was increased in hepatocytes directly surrounding metastases. These data imply that the overall metabolic zonation in liver lobuli is not dramatically disturbed by the presence of cancer cells despite the fact that various metabolic processes in liver cells are affected.
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PMID:Experimentally induced colon cancer metastases in rat liver increase the proliferation rate and capacity for purine catabolism in liver cells. 822 8

As demonstrated previously, liver acini draining the blood from intraportally transplanted pancreatic islets in streptozotocin-diabetic rats are altered in various respects. The hepatocytes in these acini store glycogen and/or fat, and they show an increase in proliferation as well as in apoptotic activity. Thus, they are phenotypically similar to carcinogen-induced preneoplastic liver foci (glycogen-storing foci and sometimes also mixed cell foci). By means of catalytic enzyme histochemistry or immunohistochemistry, we investigated the activity of key enzymes of alternative pathways of carbohydrate metabolism and some additional marker enzymes (well known from studies on preneoplastic hepatic foci) in the altered liver acini surrounding the islet isografts. In addition, the expression of glucose transporter proteins 1 and 2 (GLUT-1 and GLUT-2) were investigated immunohistochemically. The activities of hexokinase, pyruvate kinase, glyceraldehyde-3-phosphate dehydrogenase, and glucose-6-phosphate dehydrogenase were increased, whereas the activities of glycogen phosphorylase, adenylate cyclase, glucose-6-phosphatase, and membrane-bound adenosine triphosphatase were decreased in the altered liver acini. The expression of GLUT-2 was also decreased. GLUT-1 and glutathione S-transferase placental form were not expressed, and the activities of glycogen synthase and gamma-glutamyl-transferase remained unchanged. All changes of the enzyme activities were in line with the well known effects of insulin and resembled alterations characteristic of preneoplastic liver foci observed in different models of hepatocarcinogenesis. It remains to be clarified in long-term experiments whether or not these foci represent preneoplastic lesions and may proceed to neoplasia.
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PMID:Altered liver acini induced in diabetic rats by portal vein islet isografts resemble preneoplastic hepatic foci in their enzymic pattern. 864 65

The direct effects of cadmium on the functions and metabolism of renal tubular epithelial cells were observed with radio-immune assay, cytochemical and biochemical methods to study further the mechanism of nephrotoxicity of cadmium. Results revealed uptake of alpha-methyl-D-glucoside (alpha-MG) in renal tubular epithelial cells obviously reduced, outflow of potassium ions increased, c-AMP content reduced and activity of Na+-K+-ATPase was inhibited significantly after exposure to cadmium. Electrochemical gradient of tubular cells maintained by Na+-K+-ATPase played an important role in transference of sodium and glucose, and damage in energy resource system within tubular epithelial cells may be one of the pathogenic mechanisms of kidney injury caused by cadmium. In addition, changes in a group of biological markers and functional enzymes (alkaline phosphatase, AKP; gamma-glutamyltransferase, gamma-GT; lactate dehydrogenase, LDH; glucose-6-phosphate dehydrogenase, G-6-PD; N-acetylglucoside, NAG) were determined in the study, and it was found that they all could reflect better the degree of injury in tubular epithelial cells and their metabolic status and could be used in clinical practice.
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PMID:[Toxicity of cadmium and its mechanism on renal tubular epithelial cells in vitro]. 875 54

By participating in glutathione (GSH) synthesis, gamma-glutamyl transpeptidase (GGT) influences the GSH redox cycle, which is a major contributor in protecting against reactive oxygen metabolites. This study determined the effect of prolonged exposure of neonatal rats to > 98% oxygen on expression of GGT and on GSH metabolism. Lungs of neonatal rats chronically exposed to hyperoxia had increased expression of GGT mRNA, resulting in significantly higher GGT protein levels and enzyme activity than in lungs of animals raised in room air. Hyperoxia also upregulated glucose-6-phosphate dehydrogenase, but Na-K-ATPase activity was not changed. GGT mRNA, protein level, and enzyme activity returned to control levels after recovery in room air for 3 days. Levels of GSH, glutathione disulfide, and protein-bound GSH (S-glutathiolated protein) rose with hyperoxia and fell during recovery. S-glutathiolation is likely a mechanism for protection and a regulatory modification of protein sulfhydryl groups. Hyperoxia-induced upregulation of GGT and the concomitant increase in protein S-glutathiolation appear to be additional components fundamental in protecting the lung against oxidative injury.
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PMID:Hyperoxia enhances expression of gamma-glutamyl transpeptidase and increases protein S-glutathiolation in rat lung. 877 34

In 63 children with severe meningococcal infection (MI) and meningitides of another origin red cell metabolism was studied: levels of ATP, ADP, AMP, ATP/ADP, ATP/AMP, energetic charge, 2,3-DPG, FAD, piruvate, lactate, activity of lactate dehydrogenase, piruvate kinase, glucose-6-phosphate dehydrogenase, glutatione reductase, Mg2+, Na+, K(+)-dependent ATPase. All the disease periods were characterized by combined pathobiochemical shifts of different degree typical for varying metabolic systems and correlating with the infection severity. The discussion covers pathogenetic and clinical significance of red cell metabolism shifts in patients with MI and purulent meningitides.
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PMID:[The dynamics of erythrocyte metabolism in severe forms of meningococcal infection and suppurative meningitis in children]. 904 77

The pregnant rats were treated with formaldehyde (0.5 mg/kg daily per os) during whole period of pregnancy. The activity of cytochrome-c-oxidase, malate dehydrogenase, nucleotidase, glucose-6-phosphatase, beta-glucuronidase, N-acetyl-beta-glucosaminidase, beta-galactosidase, H(+)-ATPase, glutamate dehydrogenase, NAD- and NADP-isocitrate dehydrogenase, fructose-bisphosphate aldolase, glucose-6-phosphate dehydrogenase and content of protein in liver celts of offsprings (newborns, 2 weeks age and 2 months age) were studied. It was shown differences in development enzyme systems of control and experimental animals during ontogenesis.
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PMID:[Experimental study of the effect of formaldehyde during embryogenesis on the activity of rat liver enzyme systems in ontogenesis]. 913 53


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