Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Azathioprine (AZA) is an important drug used in the therapy of autoimmune system disorders. It induces hepatotoxicity that restricts its use. The rationale behind this study was the proven efficacy of N-acetylcysteine (NAC; a replenisher of sulfhydryls) and reports on the antioxidant potential of aminoguanidine (AG; an iNOS inhibitor), that might be useful to protect against the toxic implications of AZA. AG (100 mg/kg; i.p.) or NAC (100 mg/kg; i.p.) were administered to the Wistar male rats for 7 days and after that AZA (15 mg/kg, i.p.) was given as a single dose. This caused an increase in the activity of hepatic aminotransferases (AST and ALT) in the serum 24 h after AZA treatment. AZA (7.5 or 15 mg/kg, i.p.) also caused an increase in rat liver lipid peroxides and a lowering of reduced glutathione (GSH) contents. In the other part of experiment, protective effects of AG and NAC were observed on AZA induced hepatotoxicity. NAC significantly protected against the toxic effects produced by AZA. Pretreatment with NAC prevented any change in the activities of both the aminotransferases after AZA. This pretreatment also resulted in a significant decline in the contents of lipid peroxides and a significant elevation in GSH level was evident after AZA treatment. In the group with AG pretreatment the activities of AST and ALT did not increase significantly after AZA when compared to control. However, the lipid peroxides and GSH levels did not have any significant difference when compared to AZA group. These observations also indicate that the improvement in the GSH levels by NAC is the most significant protective mechanism rather than any other mechanistic profile. The protective effect of AG against the enzyme leakage seems to be through the liver cell membrane permeability restoration and is independent of any effects on liver GSH contents.
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PMID:A comparison of hepatoprotective activities of aminoguanidine and N-acetylcysteine in rat against the toxic damage induced by azathioprine. 1272 94

Tetracera loureiri is one of the most valued herbs in Thai traditional medicine. In this study, we describe its in vitro and in vivo antioxidant and hepatoprotective activities. The ethanol extract of T. loureiri possessed potent antioxidant and strong free radical scavenging properties assayed using ferric reducing antioxidant power (FRAP) and 2,2-diphenyl-1-picrylhydrazyl (DPPH), respectively. The cytoprotective effects of T. loureiri were demonstrated in ethanolic extracts of freshly isolated rat hepatocytes against the chemical toxicants paracetamol and tertiary-butylhydroperoxide. The cells pretreated with the extract maintained the GSH/GSSG ratio and suppressed lipid peroxidation in a dose dependent manner. Pretreating rats with the ethanol extract orally, one hour prior to intraperitoneal injection of toxic doses of paracetamol, significantly prevented elevations of plasma ALT and AST. These results suggest that T. loureiri may be of potential therapeutic value in some liver disorders.
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PMID:Hepatoprotective and antioxidant activities of Tetracera loureiri. 1291 65

This study evaluated the effects of dehydroepiandrosterone (DHEA) on the oxidant [malondialdehyde (MDA)] and antioxidant [superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and glutathione (GSH)] systems in liver after renal ischemia-reperfusion (IR) injury in rabbits. Thirty rabbits were randomly assigned to 3 groups of 10: group I (sham operation), group II (renal IR group), and group III (DHEA, 25 mg/kg, s.c., 15 min pre-ischemia). Renal IR injury in group II caused a decrease of SOD (25%), GPx (36%), and CAT (26%) activities and GSH levels (32%), and increases of MDA (30%) in liver and of ALT and AST activities in serum, compared to group I. DHEA administration decreased the hepatic MDA level (19%) and serum ALT activity (30%) (p <0.01 and p <0.05, respectively), and considerably increased hepatic GSH levels and GPx activities (p <0.01 for both) in group III, compared to group II. These results suggest that DHEA treatment has beneficial effects on antioxidant defenses against hepatic injury after renal IR in rabbits, possibly by augmenting GSH levels and lowering MDA production.
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PMID:Dehydroepiandrosterone improves hepatic antioxidant systems after renal ischemia-reperfusion injury in rabbits. 1458 61

Ribonuclease inhibitor (RI) is an acidic cytosolic glycoprotein with molecular weight of about 50 kDa, which contains 32 cysteine residues. It is possibly that RI may have antioxidant effect by thiol-disulfide exchange reaction. We studied the effects of RI over-expression on the rat glial cell line C6 injured with H2O2. The transfected C6 cells with RI cDNA (C6') had higher viability, less LDH leakage and MDA contents, but more GSH contents compare that in the control C6 cells. In transfected C6 cells, the activities of CAT and GST were higher than that in the control C6 cells. Without H202 stress, the activities of CAT and GST in the C6' cells were 1.73 and 3.62 times that in the control C6 cells, respectively; With 1.00 mmol/L H2O2 stress, the activities of CATand GSTin the C6' cells were 3.38 and 2.11 times that in the C6 cells, respectively. These results suggest that the over-expression RI has antioxidant activity and it is able to protect cells from per-oxidative injuries. Moreover, we investigated whether RI has a protective role against mouse hepatic damage in vivo. The mice pretreated with different doses of human RI were injected by CC14. The results show that the SOD activities of therapy groups were significantly higher than that of the control group (p < 0.01), while the contents of MOD and activities of ALT and AST in blood were remarkably lower than that of the control group (p < 0.01). Pathological examination shows that the degree of damage was alleviated with RI therapy. These results suggest that RI has the protective role against mouse hepatic damage induced by CC14. The anti-oxidative effects of RI may play an important role in cell protection from per-oxidative injuries.
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PMID:The antioxidant effects of ribonuclease inhibitor. 1470 97

Prostaglandins are synthesized ubiquitously in the body from unsaturated fatty acids and they act as paracrine messengers. We have studied the influence of a prostaglandin analogue on experimental induced hepatopathy. The tested compound is a synthetic isopropyl ester of PGF2 alpha (IPEF) and as hepato-toxic agent we used CCl4. We worked on four groups of 4 adult male rats each. Group I received no substance; Group II received CCl4 0.1 ml/bw/per os, single dose, for three days; Group III received CCl4 as series I and IPEF 15 micrograms/bw i.p., single dose daily, one hour before CCl4 administration; Group IV received CCl4 as series I and IPEF 50 micrograms/bw i.p., single dose daily. Twenty-four hours after the last administration, samples of blood were taken and ALT, AST, LDH as well as conjugate and unconjugate bilirubin were determined. We also determined MDH, GSH and glutathion peroxidase, in liver homogenate. Our data show that MDH levels are increased in Group I (20.81 +/- 3.15 microM/microgram protein) as compared with both Group III (8.44 +/- 1.32 microM/microgram protein) and IV (7.31 +/- 1.92 microM/microgram protein) which might suggest that prostaglandin analogue IPEF decreases the polyunsaturated fatty acids degradation, at both low and high level. ALAT levels for group that received CCl4 (782 +/- 20.8 U/L) are significantly higher than those for group III (264 +/- 15.4 U/L) and IV (227 +/- 8.4 U/L) which received IPEF at low, respectively high dose. Our data suggest that the synthetic prostaglandin analogue presents stabilizing membrane effects (plasmatic and membrane of some cellular organelles) and reduces peroxide radicals production.
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PMID:The role of some prostaglandin analogues in experimental intoxication produced by carbon tetrachloride in rats. 1475 47

Hepatotoxic effect of (+)usnic acid, the active constituent of Usnea siamensis Wainio was studied in rats, isolated rat hepatocytes and isolated rat liver mitochondria. In rats, after treatment with high dose of (+)usnic acid (200 mg/kg per day, i.p.) for 5 days, there was no significant change in serum transaminase activity (serum AST, ALT) while the electron micrographs showed apparent morphological damage of mitochondria and endoplasmic reticulum. (+)Usnic acid at high dose (1 mM) as well as carbon tetrachloride (CCl4, the reference hepatotoxin) induced loss of cell membrane integrity in isolated rat hepatocytes by increasing the release of cellular transaminases (AST, ALT). Increase in lipid peroxidation, decrease in glutathione (GSH) content and increase in aniline hydroxylase activity (CYP 2E1) were also found. Combination of (+)usnic acid and CCl4 showed the additive results. (+)Usnic acid (0.15-6 microM) possessed uncoupling activity in isolated rat liver mitochondria. It stimulated respiration by mitochondria respiring with glutamate plus malate or succinate as substrates and activated ATPase activity. Increasing concentration of (+)usnic acid (>6 microM) exhibited loss of respiratory control and ATP synthesis. In conclusion, hepatotoxic effect of high dose (+)usnic acid may involve its reactive metabolite(s), causing loss of integrity of membrane like structures, resulting in destruction of mitochondrial respiration and oxidative phosphorylation.
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PMID:Hepatotoxic effect of (+)usnic acid from Usnea siamensis Wainio in rats, isolated rat hepatocytes and isolated rat liver mitochondria. 1501 5

The plant Mentha piperita, or peppermint, is commonly used in the treatment of loss of appetite, common cold, bronchitis, sinusitis, fever, nausea and vomiting, and indigestion as a herbal agent. In this study, we aimed to investigate biochemical and histological effects of M. piperita Labiatae, growing in the Yenisar Bademli town of Isparta city, and Mentha spicata Labiatae, growing in the Anamas high plateau of the Yenisar Bademli town, on the rat liver tissue. Forty-eight male Wistar albino rats weighing 200-250 g were used for this study. Rats were divided into four groups of 12 animals: Group I received no herbal tea (control group); Group II received 20 g/L M. piperita tea; Group III received 20 g/L M. spicata tea; and Group IV received 40 g/L M. spicata tea. Herbal teas were prepared daily and provided at all times to the rats during 30 days as drinking water. Liver function tests, including aspartate aminotransferase (AST/GOT) and alanine aminotransferase (ALT/GPT) activities were measured. To evaluate liver antioxidant defences, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thiobarbituric acid reactive substance (TBARS) activities were determined in the homogenates of liver tissue. In addition, liver tissues were submitted for histopathologic examination. AST and ALT activities were increased in Group II, Group III and Group IV gradually when compared with the control group. The difference between Group II and the control group was not statistically significant (P > 0.016). Increases in AST and ALT activities of Group III and Group IV were statistically significant when compared with the control group. SOD, GSH-Px and CAT activities were increased in Group II when compared with the control group but the difference was not statistically significant (P > 0.016). However, SOD, GSH-Px activities and the TBARS level were significantly increased, and CAT activity was significantly decreased in Group III when compared with the control group. In Group IV, while SOD, GSH-Px and CAT activities were decreased, the TBARS level was increased as compared with the control group (P < 0.0016). Histopathological evaluation of experimental groups revealed a mild to severe degree of hepatic damage when compared to the control group. In Group II, there was only minimal hepatocytes degeneration. In Groups III and IV, there were granular or ballooning hepatocyte degeneration and necrosis, sinusoidal and central vein dilatation. It was concluded that lipid peroxidation and hepatic damage occurs after M. piperita and M. spicata administration in rat liver and the damage seems to be dose dependent.
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PMID:Investigation of biochemical and histopathological effects of Mentha piperita Labiatae and Mentha spicata Labiatae on liver tissue in rats. 1502 12

The relationship among the enzyme activities of cardiac markers, the antioxidant defense system, and erythrocyte membrane malonyldialdehyde (MDA) levels related to vitamin-mineral supplementation in swim exercise was investigated. Swimmers aged 11 - 13 years were divided into 2 separate groups as control and vitamin-mineral supplemented. Swimmers participated in a monthly swimming program (4 times/wk) and swam approximately 2- 2.5 km/d. Cardiac markers such as creatine kinase (CK), creatine kinase-MB (CK - MB), glutamic oxaloacetic transaminase [GOT (AST)], lactate dehydrogenase (LDH), and anti-oxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities in post-training samples were found to be significantly (p<.05) higher than in pre-training samples. Except for GOT (AST), the activity increases in CK, CK-MB, and LDH in female and male supplemented groups were significantly (p<.05) lower than those of control groups during the 1-month period of swim training. Antioxidant enzyme activity increases in the male vitamin-mineral group were significantly (p <.05) higher when compared with the other groups. Post-training MDA levels were significantly (p <.001) higher than pre-training MDA levels in the control groups, whereas no significant (p<.05) differences were found between the vitamin-mineral supplemented groups. Vitamin-mineral supplementation was found to attenuate cardiac and muscle damage markers while also enhancing antioxidant levels and reducing membrane LPO levels in response to 1 month of swim training.
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PMID:Effects of vitamin-mineral supplementation on cardiac marker and radical scavenging enzymes, and MDA levels in young swimmers. 1511 88

This study was planned to determine the protective role of zinc, if any, in attenuating the toxicity induced by nickel sulfate in rat liver. Female Sprague Dawley (SD) rats received either nickel alone in the dose of 800 mg/l in drinking water, zinc alone in the dose of 227 mg/l in drinking water, and nickel plus zinc or drinking water alone for a total duration of eight weeks. The effects of different treatments were studied on various parameters in rat liver which include antioxidant enzymes, levels of nickel and zinc and histoarchitecture at the light microscopic level. Further, the activities of hepatic marker enzymes AST and ALT were also studied in rat serum. Nickel treatment to the normal control animals, resulted in a significant increase in lipid peroxidation and enzyme activities of catalase and glutathione-S-transferase. On the contrary, nickel treatment to normal rats caused a significant inhibition in the levels of reduced glutathione. Superoxide dismutase activity was found to be decreased which however was not significant. Interestingly, when Zn was supplemented to nickel treated rats, the activities of catalase, and glutathione-S-transferase and the levels of GSH and lipid peroxidation came back to within normal limits. Activities of serum AST and ALT were increased significantly following nickel treatment to normal rats. Simultaneous zinc administration to nickel treated rats tended to restore the altered levels of AST and ALT. Normal control and zinc treated animals revealed normal histology of liver. On the other hand, nickel treated animals showed alterations in normal hepatic histoarchitecture which comprise of vacuolization of the hepatocytes and dilatation of sinusoids as well as increase in the number of bi-nucleated cells. Administration of zinc to nickel treated rats resulted in marked improvement in the structure of hepatocytes, thus emphasizing the protective potential of zinc in restoring the altered hepatic histoarchitecture. The nickel administration to normal rats indicated increased concentrations of nickel and decreased concentrations of zinc. However, zinc effectively brought the altered levels of nickel and zinc to within normal range. The study concludes that zinc has the potential in alleviating the toxic effects of nickel in rat liver because of its property to induce metallothionein (S-rich protein) as a free radical scavenger, or its indirect action in reducing the levels of oxygen reactive species.
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PMID:Protective role of zinc in nickel induced hepatotoxicity in rats. 1553 90

In the present study, we investigated the protective effect of Lycium chinense Miller (Solanaceae) fruit (LFE) against CCl(4)-induced hepatotoxicity and the mechanism underlying these protective effects in rats. The pretreatment of LFE has shown to possess a significant protective effect by lowering the serum aspartate and alanine aminotransferase (AST and ALT) and alkaline phosphatase (ALP). This hepatoprotective action was confirmed by histological observation. In addition, pretreatment of LFE prevented the elevation of hepatic malondialdehyde (MDA) formation and the depletion of reduced glutathione (GSH) content and catalase activity in the liver of CCl(4)-injected rats. The LFE also displayed hydroxide radical scavenging activity in a dose-dependent manner (IC(50) = 83.6 microg/ml), as assayed by electron spin resonance (ESR) spin-trapping technique. The expression level of cytochrome P450 2E1 (CYP2E1) mRNA and protein, as measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot analysis, was significantly decreased in the liver of LFE-pretreated rats when compared with that in the liver of control group. Based on these results, it was suggested that the hepatoprotective effects of the LFE might be related to antioxidative activity and expressional regulation of CYP2E1.
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PMID:Protective effect of Lycium chinense fruit on carbon tetrachloride-induced hepatotoxicity. 1561 74


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