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)

The present study was carried out to examine whether nitrofurantoin-induced pulmonary toxicity in normal rats was mediated via oxidant stress mechanisms. The relative importance of the cellular antioxidant enzymes in nitrofurantoin toxicity was also assessed. For this, the pulmonary toxicity induced by nitrofurantoin in rats was evaluated at various time intervals after a single subcutaneous injection. Data from this study showed that nitrofurantoin (200 mg/kg, s.c.) resulted in transient but measurable lung damage as evidenced by the increases in wet lung weight/body weight ratio and decreases in lung angiotensin converting enzyme activity. A transient decrease in GSH concentrations with a concurrent increase in GSSG concentrations as well as an increase in lipid peroxidation levels (measured by the formation of diene conjugates and thiobarbituric acid reactants) were also evident in lungs of nitrofurantoin-treated rats. In addition, nitrofurantoin did not alter the pulmonary superoxide dismutase and glutathione peroxidase activities, but it did produce transient decreases in catalase and glutathione reductase activities. These data indicate that impairment of the ability of the lung to detoxify reactive oxygen species may play an important role in the development of nitrofurantoin-induced pulmonary toxicity. The results of the present study suggest that nitrofurantoin can damage the lungs of rats, probably through oxidative stress-mediated mechanisms. Also, our data have provided in vivo evidence for substantiating lipid peroxidation as a possible cause of lung damage.
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PMID:Nitrofurantoin-induced pulmonary toxicity. In vivo evidence for oxidative stress-mediated mechanisms. 131 37

Overall 94 patients with different patterns of pulmonary tuberculosis were examined for glutathione peroxidase (GP), glutathione reductase, glucose 6-phosphate dehydrogenase (G 6-PDH) and superoxide dismutase activity in neutrophils and lymphocytes. Chemiluminescence was used to study the capacity of neutrophils to generate free oxygen forms. Neutrophils showed functional deficiency of GP and G 6-PDH. The decrease of the oxygen-producing capacity of neutrophils, unbalance of glutathione-conjugated enzymes in lymphocytes were revealed either. The role of the alterations enumerated in the reduction of function of phagocytizing and immunocompetent cells in patients with pulmonary tuberculosis is discussed.
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PMID:[The oxidative metabolic indices of phagocytizing and immunocompetent cells in patients with pulmonary tuberculosis]. 209 92

Maximal activities of antioxidant enzymes involved in oxygen free radical metabolism in skeletal muscle and liver were investigated in 4-, 26-, and 31-mo-old male Wistar-Furth rat at rest and after a single bout of treadmill exercise. In skeletal muscle, cytosolic (Cu-Zn) and mitochondrial (Mn) superoxide dismutase (SOD) specific activities were significantly higher in the aged rats and at 31 mo reached 135 and 218%, respectively, of those at 4 mo. Resting catalase activity was doubled at 31 mo compared with that at 4 mo. Glutathione peroxidase (GPX) activity increased twofold in muscle cytosol and by 47% in mitochondria of aged rats. Glutathione S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G-6-PDH) activities in muscle were also significantly elevated. Hepatic antioxidant enzymes were altered differentially with aging. Cytosolic SOD and GST activities were decreased, whereas mitochondrial GPX, GR, and G-6-PDH activities were increased. Lipid peroxidation was greater in skeletal muscle homogenate and mitochondria but lower in liver homogenate in the aged rats. An acute exercise bout had little effect on muscle or liver antioxidant enzymes regardless of the animal's age. It is concluded that aging is accompanied with an elevation of antioxidant enzyme activities and lipid peroxidation in skeletal muscle probably due to the increased oxygen free radical production and reaction.
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PMID:Alteration of antioxidant enzymes with aging in rat skeletal muscle and liver. 233 Oct 35

As many as 160 patients with acute virus hepatitis B (AVHB) were examined over time. Spectroscopy was used to study the activity of glucose-6-phosphate dehydrogenase (G-6-PDH), glutathione peroxidase-1 (GP1), glutathione peroxidase-2 (GP2), glutathione reductase (GR), glutathione transferase (GT) and to measure the concentration of reduced glutathione (GSH) in the blood serum and in red blood cells. Within the first days of the icteric period, the activity of all the enzymes rose, followed by reduction of the activity of G-6-PDH, GP1, GP2, GR and the concentration of GSH at the height of the disease. The GT activity remained high throughout the entire disease period.
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PMID:[The functioning of the glutathione system in patients with acute viral hepatitis B]. 233 29

The effect of manganese exposure (Mn2+ 4 mg Mn/kg intraperitoneally) on certain bioantioxidants in brain, liver, kidney and testes in growing rats maintained on 21% and 8% casein diet were investigated. Manganese administration for 30 days caused significant reduction in the level of GSH (reduced glutathione) in liver and testes and GR (glutathione reductase) and G-6-PDH (glucose-6-phosphate dehydrogenase) in brain, liver and testes. The magnitude of alteration was greater in 8% casein diet fed animals compared to rats maintained on 21% casein diet. These results indicate that protein deficient animals are more susceptible to the manganese induced biochemical changes in various tissues. The mechanism of such changes is discussed.
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PMID:Effect of manganese on some bioantioxidants in various organs of protein-deficient rats. 278 47

The acinar distribution of glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G-6-PDH) was examined by analyzing periportal (p.p.) and perivenous (p.v.) rat hepatocytes selectively isolated by the digitonin-collagenase perfusion. The cytosolic GST activity was higher in p.v. cells, but the microsomal GST and cytosolic GR were found to be evenly distributed in the acinus. In contrast, the activity of both the Se-dependent GPx and the microsomal (Se-independent) GPx, as well as G-6-PDH, was much lower in the p.v. than in the p.p. cells. The heterogeneous distribution of GST, GPx and G-6-PDH was confirmed by analyzing liver perfusion effluents collected after ante- or retrograde digitonin infusion. The relatively low activities of GPx and G-6-PDH in the p.v. cells could partly explain the susceptibility of this region to chemical injury.
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PMID:Acinar distribution of glutathione-dependent detoxifying enzymes. Low glutathione peroxidase activity in perivenous hepatocytes. 359 5

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

Alteration in the antioxidant defence mechanism of erythrocytes with rise in serum unconjugated bilirubin level in neonates has been observed. The cellular glutathione level was found to be significantly low. The activity of glutathione reductase in erythrocyte increased to combat the cellular loss of reduced glutathione in neonatal jaundice. In plasma fraction the level of glutathione (reduced) was found to be significantly higher with lowering of glutathione reductase level. Glutathione peroxidase was reduced in cellular level whereas an increase was observed in plasma fraction. Gamma glutamyl transpeptidase level was barely detectable in erythrocyte whereas an increase was observed in plasma fraction. In all the cases erythrocyte G-6-PDH activity level was found within normal limits.
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PMID:Jaundice in new born and erythrocyte and plasma antioxidant defence system. 755 88

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

Utilization of highly enriched preparations of steroidogenic Leydig cells have proven invaluable for studying the direct effects of various hormones and agents on Leydig cell function in vitro. However, recent work indicates that isolated Leydig cells are often subjected to oxygen (O2) toxicity when cultured at ambient (19%) oxygen concentrations. Because intracellular antioxidants play an important role in protecting cells against oxygen toxicity, we have investigated the intracellular antioxidant defense system of isolated Leydig cells. The cellular levels of several antioxidants including catalase, glucose-6-phosphate dehydrogenase (G-6-PDH), superoxide dismutase (SOD) of the Cu/Zn & Mn variety, glutathione peroxidase, glutathione reductase and total glutathione were quantitated using enriched populations of Leydig cells isolated from adult male guinea pig testes. Compared to whole testicular homogenates, Leydig cells contained significantly (P < 0.01) less G-6-PDH, total SOD, glutathione reductase and total glutathione, but significantly (P < 0.001) more glutathione peroxidase. Compared to hepatic values previously reported in the guinea pig, Leydig cells contain nearly 400 times less catalase, about 14 times less glutathione peroxidase and almost 11 times less glutathione reductase. Since G-6-PDH and glutathione reductase are both necessary to regenerate reduced glutathione (GSH) which couples with glutathione peroxidase to breakdown hydrogen peroxide (H2O2) under normal conditions, it is plausible that the oxygen toxicity observed in isolated Leydig cells is due to the intracellular accumulation of H2O2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The antioxidant defense system of isolated guinea pig Leydig cells. 810 85


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