Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After UV irradiation of human skin there is an increase in epidermal and stratum corneum thickness and an increase in the thymidine autoradiographic labeling index. Previously we have demonstrated that persistent exposure to ultraviolet radiation (UVR) alters the distribution and activities of glucose-6-phosphate dehydrogenase (G-6-PDH) and succinic dehydrogenase (SDH) within the epidermis; G-6-PDH activity is increased over the whole epidermis and SDH activity is diminished in the granular cell area but increased in the basal layer. When skin is protected by an efficient sunscreen and irradiated with UVB, there is almost complete inhibition of the erythema normally seen following UVR exposure. In this study we have investigated the cytochemical, cell kinetic, and histometric changes that take place in the epidermis after UVB irradiation, with and without two different types of sunscreen. Some of the histometric and metabolic changes associated with UVB exposure were still evident despite sunscreen protection and the successful blocking of the erythema response. The implications of these findings are discussed together with the use of sunscreens to prevent development of solar damage.
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PMID:Response of human skin to ultraviolet radiation: dissociation of erythema and metabolic changes following sunscreen protection. 682 29

Weanling Wistar rats were fed a high-fat diet (HFD) or a low-fat diet (LFD) over 3 and 5-6 weeks. In both comparable groups the absorption of energy was almost the same. In the HFD animals glucose-6-phosphate dehydrogenase (G-6-PDH, E.C. 1.1.1.49) showed its well-known restrictive behaviour in the liver and also in the fatty tissues. After 3 weeks on the respective diet, the body fat content of the LFD animals was lower than that of the HFD animals. After 6 weeks on the respective diet, the body fat contents were nearly the same in the animals of both groups. The energy turnover was greater after 3 weeks on the diet than after 6 weeks, the significantly highest values being found in animals fed over 3 weeks. After 5 weeks on the respective diet, all the energy turnover values were at a lower level, but this was the same in both animal groups. It may be concluded that the fatty-acid synthesis de novo indicated by the G-6-PDH activity does not depend upon the experimental time, and is determined only by the amount of dietary fat. In contrast to this, the establishment of the energy turnover during the experimental time is subject to relatively great changes which might be correlated with the regulation of total fat retention in the body.
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PMID:[Behavior of various parameters of lipid and energy metabolism. 6. Energy turnover in various lengths of time in rats fed a low- and high-fat diet]. 688 7

In 14 beagle dogs, paraquat was infused in fractional doses to produce pulmonary fibrosis while avoiding fatal liver and kidney lesions. Activity of the three enzymes of the pentose pathway: glucose-6-phosphate dehydrogenase (G-6-PDH), glutathione reductase (GR) and glutathione peroxidase (GSH Px), which supply reduced equivalents against oxidant agents, were measured in the mediastinal lobe of the lung. After a single low dose (2-3 mg/kg body weight), GR and GSH Px activities were reduced. After repeated paraquat doses, pentose pathway enzyme activities were higher than after a single low dose; however, they did not significantly exceed the normal values as determined in control dogs. The activities of G-6-PDH, GR and GSH Px correlated with the total paraquat dose and with the extent of pulmonary fibrosis measured with an electronic image analyzer. The activity of pulmonary lactate dehydrogenase, which was also reduced after a single low dose of paraquat, did not show the same correlations.
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PMID:Pentose pathway in pulmonary fibrosis due to chronic paraquat poisoning. 744 87

Activities of glucose-6-phosphate dehydrogenase (G-6-PDH) and malate dehydrogenase were measured in the blood of 38 patients with acute nonepidemic parotitis and the status of glutathione antioxidant system assessed. The predominance of free-radical processes in the mechanisms of impairment of the parotid gland was confirmed. Increased level of lipid peroxidation products and decompensation of glutathione antioxidant system were found to be due to incompetence of the malate shuttle and low activity of G-6-PDH. A conclusion is made about the necessity of revising current approaches to prevention and therapy of acute nonepidemic parotitis.
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PMID:[The activity of the glutathione antioxidative system in the blood of patients with acute nonepidemic parotitis]. 757 Jun 96

In order to clarify the preventive action of Dai-Saiko-to (Da-Chai-Hu-Tang) extract (TJ-8) on the progression of acute liver injury in rats intoxicated with carbon tetrachloride (CCl4), we examined the effect of post-oral TJ-8 administration on hepatic active oxygen metabolism following the progression of this liver damage. When TJ-8 (1.0 g/kg body weight) was administered orally to male Wistar rats aged five weeks 2 hrs after i.p. injection of CCl4 (1.0 ml/kg body weight), an apparent liver injury occurred. Significant prevention against the progression of liver injury was found at 24 hrs after injection, judging from the activities of serum transaminases, indexes of liver cell damage. Liver cytosolic superoxide dismutase (SOD) activity decreased 2 and 24 hrs after CCl4 injection, while liver cytosolic catalase and glutathione reductase (GSSG-R) activities decreased 24 hrs after the injection. At 2 and 24 hrs after CCl4 treatment, liver cytosolic Se-containing glutathione peroxidase (GSH-px) activity did not change and liver cytosolic glucose-6-phosphate dehydrogenase (G-6-PDH) activity increased. Post-oral TJ-8 administration significantly ameliorated decreases in liver SOD, catalase, and GSSG-R activities at 24 hrs after CCl4 injection, but did not affect liver Se-GSH-px and increased liver G-6-PDH activities at 24 hrs after the injection. Although increased liver lipid peroxide level and decreased liver reduced glutathione and ascorbic acid levels were observed 2 and 24 hrs after CCl4 injection, post-oral TJ-8 administration significantly prevented these changes found at 24 hrs after injection. These results indicate that post-oral TJ-8 administration can prevent the progression of acute liver injury in CCl4-injected rats by inhibiting enhanced lipid peroxidation and by improving disrupted active oxygen metabolism in the injured liver.
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PMID:Preventive effect of dai-saiko-to (da-chai-hu-tang) extract on disrupted hepatic active oxygen metabolism in rats with carbon tetrachloride-induced liver injury. 759 92

Previous cell culture evaluations have shown that nickel-chromium dental alloys did not affect cellular viability or morphology. However, nickel-based alloys released corrosion products which decreased cellular proliferation. It was hypothesized that this decrease was due to an interference of cellular energy metabolism by released metal ions. To test this hypothesis, we evaluated the effects on cellular energy metabolism, adenosine triphosphate (ATP) levels, and cellular ultrastructure by four nickel-based alloys, including high and low chromium alloys with and without beryllium additions, in human gingival fibroblast cell cultures. Energy metabolism was evaluated by measuring glucose-6-phosphate dehydrogenase (G-6-PDH) activity. ATP levels were measured with the luciferin-luciferase method. Cellular membranes and ultrastructural organization were evaluated by scanning and transmission electron microscopy. The results of this study showed that metal ions released from all alloys completely inhibited G-6-PDH activity and reduced cellular ATP levels as compared to controls. The reduction in intracellular ATP was greater for the beryllium containing alloys than the non-beryllium-containing alloys. However, no morphologic changes in cellular membranes or organelles were observed. These results support the hypothesis that metal ions released from nickel-based dental casting alloys interfere with cellular energy metabolism.
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PMID:Effect of nickel-based dental casting alloys on fibroblast metabolism and ultrastructural organization. 762 46

Mitochondrial manganese-containing SOD (MnSOD) is located at the primary site of O2 metabolism, and its expression may be regulated by changes in O2 level. We hypothesized that lung MnSOD expression and promoter activity would decrease in response to hypoxia. We tested effects of hypoxia (10% O2 at sea level for 7 days) on chloramphenicol acetyltransferase (CAT) reporter and MnSOD gene expression in transgenic mice. The transgene consisted of a 3.3-kb portion of the rat MnSOD gene 5' flanking region coupled to a CAT reporter gene. Lung MnSOD activity in male (but not female) mice decreased significantly after hypoxia exposure. The decrease in MnSOD enzymatic activity in male mice was specific. Neither total SOD nor glucose-6-phosphate dehydrogenase (G-6-PDH) activity decreased significantly in hypoxia. CAT protein expression decreased in transgenic males exposed to hypoxia, while CAT protein expression in hypoxic transgenic females remained comparable with controls. The mRNA for both the native MnSOD and the MnSOD-CAT reporter genes remained constant after hypoxia, as did CuZnSOD and G-6-PDH mRNAs.
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PMID:Effects of hypoxia on MnSOD expression in mouse lung. 765 84

In the course of a long-term L-DOPA administration (14 days) and 2 weeks after its cessation the activities of some protein enzymes (aminopeptidase, acid phosphatase), neuromediator (MAO, ACE) and oxidative (glutamate dehydrogenase, glucose-6-phosphate dehydrogenase) metabolism were studied by quantitative cytochemical methods in brain motor structures (sensorimotor cortex, caudate nucleus) and in structures not directly related to motor functions (hippocampus) of rats with high and low motor activity. After L-DOPA (madapar) cessation significant changes were revealed in the formation of motor system of the brain, primarily in the group of rats with low motor activity. It is suggested that a decrease in MAO activity after madapar cessation may be responsible for dyskinesia arising after cessation of L-DOPA preparations treatment.
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PMID:[Pathochemical changes in the motor structures of the brain under the influence of the administration of L-DOPA preparations and their withdrawal (experimental research)]. 790 Apr 46

Changes in superoxide dismutase (SOD), catalase (C), and peroxidase (P) blood activity, as well as the activity of glucose-6-phosphate dehydrogenase (G-6-PDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH), and peroxide resistance of erythrocytes (PRE) have been studied in 45 gastroenterologic patients under different types of general anesthesia. A significant increase in G-6-PDH, SOD, K, P activity and an increase in ICDH and MDH activity, as well as a drop in PRE which tends to return to baseline postoperatively have been established during general anesthesia. SOD expressed the greatest intergroup differences. A fragment of mechanism of energy transfer in the erythrocyte aimed at hemoglobin oxygenation and tissue hypoxia compensation has been suggested.
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PMID:[Effects of general anesthesia on the regulation of hydrogen peroxide metabolism in erythrocytes]. 801 May 17

Incubation of glucose-6-phosphate dehydrogenase (Glu-6-PDH) from Leuconostoc mesenteroides with the lipid peroxidation product 4-hydroxy-2-nonenal leads to the formation of cross-linked protein. This is accompanied by the appearance of protein-associated fluorescence with excitation and emission maxima of 340 and 415 nm, respectively, and with the disappearance of histidine and lysine residues. Cross-linked protein is less susceptible than native Glu-6-PDH to proteolysis by the multicatalytic protease, a multienzymic proteolytic complex involved in the intracellular degradation of damaged proteins. In addition, 4-hydroxy-2-nonenal-modified Glu-6-PDH inhibits the multicatalytic protease and can therefore prevent the efficient degradation of oxidized protein. These findings may have important implications for the accumulation of altered protein and fluorescent material in vivo, processes that are believed to be involved in age- and disease-related impairment of cellular function.
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PMID:Modification of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal. Formation of cross-linked protein that inhibits the multicatalytic protease. 806 6


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