Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of technical pentachlorophenol in drinking water (20 mg/l) to male Wistar rats caused significant liver concentration of tetrachlorophenol which remained stable during the exposure of 14 weeks. Pentachlorophenol and tetrachlorophenol accumulated to some extent in the perirenal fat whereas only pentachlorophenol could be found in brain. A period of four weeks of chlorophenol-free diet was sufficiently long to allow removal of the major part of the chlorophenol burden. The neurochemical effects included increased acid proteinase activity at the 8th week of exposure. It levelled off while superoxide dismutase activity increased to twice the control level. Glial glutathione peroxidase activity did not change whereas glial glutathione concentration was below the control range at the 12th week of exposure. Cerebral diaphorase activity was below the control range initially, and its activity increased above the control level during the recovery period whereas other biochemical changes levelled off.
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PMID:Neurochemical effects of peroral administration of technical pentachlorophenol. 44 21

After having described in detail the pathophysiology, symptomatology, X-chromosomal inheritance and some laboratory methods in detecting G-6-PD-deficiency by demonstrating a case of favism (Schulz et al. 1977), the authors now discuss the particularities of the enzyme deficiency in the newborn. These are complicated by additional physiological and transient deficiency of the enzymes catalase, NAD-diaphorase, glutathione peroxidase, and glucuronyl transferase. Several chemical substances, acidosis, hypoxia, hypoglycemia, and immaturity may cause a severe hyperbilirubinemia in G-6-PD-deficient newborns. The development of a kern-icterus in these cases may be prevented by early exchange transfusion. From clinical findings and some observations in different regions of Greece an additional factor influencing the liver function has been postulated which favors the development of hyperbilirubinemias in G-6-PD-deficient newborns. The nature of this possible factor is discussed. The authors emphasize the necessity of screening for G-6-PD-deficiency during pregnancy in families of mediterranian descent.
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PMID:[Glucose-6-phosphate dehydrogenase deficiency of the mediterranean type B minus. 2. Etiological basis for severe hyperbilirubinemia in the newborn]. 63 93

Superoxide dismutase and glutathione peroxidase activities were determined in isolated neurons and glial cells as derived from adult male rat brain. Glial enzyme activities were higher than in neurones, and the glial enzymes may be an important source of the enzyme activities in the homogenate, postmicrosomal fractions and in the whole brain microsomes. For comparison, glial cells showed also higher diaphorase activity than neurons which may stress the importance of glial cells in the oxidative metabolism of exogenous chemicals in brain.
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PMID:Superoxide dismutase and glutathione peroxidase activities in rat brain. 68 76

The c14CoS/c14CoS mouse has a homozygous deletion of about 1.2 cM on chromosome 7 that includes the albino (c) locus. The untreated 14CoS/14CoS newborn has been reported to exhibit a marked transcriptional activation of the hepatic NAD(P)H:menadione oxidoreductase (Nmo-1; DT diaphorase; quinone reductase; azo dye reductase) gene, as well as elevated UDP glucuronosyl-transferase (UGT1*06) and glutathione transferase (GT1) activities, when compared with the cch/cch wild-type and the cch/c14CoS heterozygote. We show here that the newborn hepatic activities of seven enzymes that play a role in the oxidative stress response--NMO1, UGT1*06, GT1, copper-zinc superoxide dismutase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase--are increased 1.5- to 25-fold in 14CoS/14CoS, as compared with ch/ch and ch/14CoS mice. The activities of four additional enzymes having no known association with the oxidative stress response--benzo[a]pyrene hydroxylase (CYP1A1, cytochrome P(1)450), acetanilide 4-hydroxylase (CYP1A2, cytochrome P(3)450), lactate dehydrogenase (LDH), and NADPH-cytochrome c reductase--are not significantly different among the three genotypes. These data suggest that there exists an "oxidative stress" response in the untreated 14CoS/14CoS newborn. We postulate that a chromosome 7 regulatory gene, which we have named Nmo-1n, might encode a trans-acting negative effector of the Nmo-1 gene, and genes corresponding to the other elevated enzymic activities described above. When both copies of Nmo-1n are deleted, as is the case in 14CoS/14CoS mice, a battery of genes involved in oxidative stress is released from negative control and becomes activated--despite the absence of any apparent oxidative insult by foreign chemicals.
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PMID:"Oxidative stress" response in liver of an untreated newborn mouse having a 1.2-centimorgan deletion on chromosome 7. 154 Jan 61

Biochemical characteristics relevant to the differential susceptibilities of liver, heart, and intestine to acute Adriamycin toxicity were examined in female CD-1 mice with and without intravenous Adriamycin (dose range 23-30 mg/kg). The liver which, unlike heart and intestine, is relatively resistant to Adriamycin toxicity, had high levels of glutathione and glutathione peroxidase, and exhibited a sharp decline in non-protein thiol concentrations within 1-3 hr with rebound by 6 hr after Adriamycin. Covalent binding to Adriamycin or its metabolites could not account quantitatively for the loss of non-protein thiols, implicating an oxidative mechanism. No lipid peroxidation was observed in the liver, apparently due to effective utilization of antioxidant defenses. Adriamycin caused significant increases in cardiac lipid peroxides, indicative of oxidative tissue damage, which would be expected to exacerbate cardiotoxicity. However, non-protein thiol concentrations did not decrease in heart or in intestine in response to Adriamycin. Both heart and intestine had extremely low levels of glutathione peroxidase activity, which may limit glutathione utilization for protection against oxidative toxicity. The activity of DT diaphorase, which may have an activating role in Adriamycin metabolism, was high in heart and intestine and was induced 4-fold in liver in response to Adriamycin.
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PMID:Biochemical determinants of Adriamycin toxicity in mouse liver, heart and intestine. 154 Feb 37

A 40% reduction of the diameter of the ascending aorta maintained for 60 days induced the formation of a compensate cardiac hypertrophy in rabbits without changing the value of the azide insensitive Ca2+-ATPase activity in comparison to control hearts. The cardiac mitochondria isolated from constricted animals assayed in presence of glutamate and succinate did not show a change in the R.C.I. and ADP/O values in comparison to the controls, whilst the QO2 value enhanced or decreased respectively when determined with glutamate or succinate. The intramuscular injections of CoQ10 (12 mg/kg body weight/48 h) enhanced the mitochondrial CoQ10 concentrations both in the control and in the constricted animals and further increased the QO2 value determined in both groups of animals when glutamate was used as the substrate. The production of O2.- radicals by the level of the complexes I and III of the respiratory chain, did not change in the constricted animals, nor in the animals administered with CoQ10 in comparison to the control. CoQ10 augmented the rate of oxygen consumption by the submitochondrial particles only in the constricted animals. Moreover, the treatment with the coenzyme or the constriction of the aorta, did not modify the cardiac superoxide dismutase activity, but increased the glutathione peroxidase activity only in the banded animals. In addition, in the CoQ10 treated animals there was a reduction of NADH-diaphorase activity both in the control and constricted animals, while the malondialdehyde, generated during the thiobarbituric acid test, and the cardiac content of lipofuscin were decreased.
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PMID:The effect of treatment with coenzyme Q10 on the mitochondrial function and superoxide radical formation in cardiac muscle hypertrophied by mild aortic stenosis. 303 17

Thirty-six wild-caught woodchucks (Marmota monax) were characterized according to sex, weight, trapping locality, liver pathology, and serum or hepatic markers of woodchuck hepatitis virus. Liver subcellular fractions were assayed for microsomal cytochromes P-450, aryl hydrocarbon hydroxylase, glutathione, cytosolic enzymes involved in its metabolism (glutathione S-transferase, glutathione peroxidase, and glutathione reductase), in the hexose monophosphate shunt (glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase), NADH- and NADPH-dependent diaphorases, and DT diaphorase. Moreover, liver postmitochondrial fractions were assayed for their ability to activate procarcinogens [i.e., a tryptophan pyrolysate product, aflatoxin B1, 2-aminofluorene, and trans-7,8-dihydrobenzo(a)pyrene] to mutagenic metabolites in the Ames reversion test and to decrease the activity of direct-acting mutagens [i.e., 4-nitroquinoline N-oxide, 2-methoxy-6-chloro-9-[3-(2-chloroethyl)aminopropylamino]acridine X 2HCl, and sodium dichromate]. A considerable interindividual variability in metabolism was observed among the examined woodchucks. Some of the investigated parameters were more elevated in virus carriers, especially in those suffering from chronic active hepatitis, but only a few of the recorded differences (i.e., oxidized glutathione reductase and NADPH-dependent diaphorase) were statistically significant. The comparison of the monitored activities in woodchucks and in other rodent species (rat and mouse) led to the conclusion that the liver metabolism of mutagens and carcinogens in woodchucks is more oriented in the sense of activation, while detoxification mechanisms are more efficient in rats and mice.
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PMID:Metabolism of mutagens and carcinogens in woodchuck liver and its relationship with hepatitis virus infection. 360 50

Many red cell enzyme defects have been discovered, many of them in patients with hemolytic anemia. In some cases a cause-and-effect relationship between the enzyme deficiency and shortening of red cell life span has been clearly documented. However, some enzyme deficiencies are well tolerated by the erythrocyte, appearing to produce no impairment in function. These include deficiencies in catalase, galactokinase, UDPGlu-4-epimerase, NADPH diaphorase, phosphoglucomutase, acetylcholinesterase, glutathione reductase, glutathione peroxidase, and adenylate kinase. The capacity of the erythrocyte to tolerate deficiencies in these enzymes indicates either that the metabolic pathways which the enzyme serves are not required by the red cell or that redundancies in metabolism exist which allow the erythrocyte to compensate for the enzyme deficiency.
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PMID:Red cell enzyme deficiencies as non-disease. 623 25

Polymethylmethacrylate was thermally degraded in air at 300 degrees C and the volatile decomposition products studied with gas chromatography-mass spectrometry. The main product was monomeric methacrylate, although many other compounds existed among the products. Electron spin resonance spectroscopy revealed the presence of free radicals. Wistar rats were exposed to the fumes of the plastic (300 degrees C) and their lungs and brain studied for biochemical effects. In the lung, the activity of 7-ethoxycoumarin O-deethylase decreased and an initial inhibition of glutathione peroxidase and superoxide dismutase was observed. The contents of reduced nonprotein sulfhydryl groups were decreased in the lung and brain. The exposures enhanced the activities of acetylcholine esterase, creatine kinase and NADPH-diaphorase in the brain. Scanning electron microscopy of the exposed lungs showed disorganization of ciliated cells, and the epithelial serous cells (Clara cells) were damaged.
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PMID:Toxicity of polymethylmethacrylate thermodegradation products. 647 26

Male Wistar rats were exposed to 200, 1000 or 2000 ppm of 1,1,2-trichloro-1,2,2-trifluoroethane vapour for 2 weeks, 5 day/week, 6 h daily and showed a dose-dependent accumulation of the compound in perirenal fat and brain. In the first week increased NADPH-diaphorase activity was observed and there was decreased cerebral glutathione at the highest dose. During the second week these effects disappeared while RNA tended to increase, and glutathione peroxidase activity to decrease at the highest dose. After a withdrawal period of 7 days, no fluorohydrocarbon was detected and the neurochemical effects had disappeared except that brain RNA at the highest exposure was below the control range.
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PMID:Dose-dependent neurochemical effects of 1,1,2-trichloro-1,2,2-trifluoroethane inhalation exposure in rats. 742 44


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