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)

The disposition of bromosulfophthalein was studied in chronically bile duct obstructed rats. In this model a catheter was inserted into the common bile duct and the distal tip was sealed. Resumption of bile flow was achieved with great ease. Obstruction of bile duct for 18 days in rats resulted in elevated bilirubin, ALT, AST, and alkaline phosphatase levels. Portal hypertension developed within this period (11.6 +/- 0.5 in obstructed rats vs. 8.6 +/- 0.6 mm Hg in sham-operated group). After the bile duct obstruction was opened, the half-life time for elimination of bromosulfophthalein (42.30 +/- 6.47 min) was longer than in sham-operated rats (21.23 +/- 3.34 min). Plasma clearance was reduced by 70% in bile duct obstructed rats. In spite of increased bile flow rate, biliary excretion of the dye was reduced by 40% in chronically bile duct obstructed rats. Hepatic glutathione levels were significantly reduced by 20% in this model. The specific activity of glutathione S-transferase with chlorodinitrobenzene and styrene oxide, as substrates, was reduced by 50% and 30%, respectively. However, the percent of conjugated bromosulfophthalein in bile was similar to that of sham-operated rats.
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PMID:Bromosulfophthalein disposition in chronically bile duct obstructed rats. 150 59

The rabbit hemorrhagic disease virus (RHDV) (isolate AST/89) RNA-dependent RNA-polymerase (3Dpol) coding region was expressed in Escherichia coli by using a glutathione S-transferase-based vector, which allowed milligram purification of a homogeneous enzyme with an expected molecular mass of about 58 kDa. The recombinant polypeptide exhibited rifampin- and actinomycin D-resistant, poly(A)-dependent poly(U) polymerase. The enzyme also showed RNA polymerase activity in in vitro reactions with synthetic RHDV subgenomic RNA in the presence or absence of an oligo(U) primer. Template-size products were synthesized in the oligo(U)-primed reactions, whereas in the absence of added primer, RNA products up to twice the length of the template were made. The double-length RNA products were double stranded and hybridized to both positive- and negative-sense probes.
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PMID:Expression of enzymatically active rabbit hemorrhagic disease virus RNA-dependent RNA polymerase in Escherichia coli. 952 22

The study aimed to evaluate the behavior of alpha-glutathione S-transferase (alpha-GST) in the serum of hemodialysis patients with hepatitis C virus (HCV) infection following treatment with high-dose IFN-alpha-2b. Ten patients with detected anti-HCV antibodies and HCV RNA by RT-PCR were selected and treated with high-dose interferon (IFN)-alpha-2b, 10 million units s.c. daily for 2 weeks followed by 3 times per week for 6 additional weeks. Blood samples were obtained from these patients at baseline for plasma alpha-GST and hepatic aminotransferases. Patients were monitored with weekly blood counts and monthly liver enzymes. Biochemical (normal alpha-GST and ALT) and virologic (negative HCV RNA by RT-PCR) responses were observed in 3 (30%) of the 10 patients. At the end of the follow-up (follow-up duration 44 weeks), 3 patients demonstrated long-term biological and virologic responses and 7 had relapses. In the nonresponders plasma AST and ALT approached normal levels on some occasions despite persistent viral RNA. In contrast to transaminases alpha-GST remained distinctly elevated in nonresponders and provided a more clear distinction between the responders and nonresponders. In conclusion, plasma alpha-GST, as a sensitive and reliable marker of response, may have a role in the monitoring of hemodialyzed patients undergoing IFN-alpha-2b therapy.
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PMID:The role of alpha-glutathione S-transferase in the monitoring of hemodialysis patients with hepatitis C virus infection undergoing high-dose interferon-alpha-2b therapy. 1022 80

The virus genome-linked protein (VPg) coding region from rabbit hemorrhagic disease virus (RHDV) (isolate AST/89) was expressed in Escherichia coli by using a glutathione S-transferase-based vector. The recombinant polypeptide could be purified in good yields and was uridylylated in vitro from [alpha-32P]UTP in a reaction catalyzed by the recombinant RNA-dependent RNA polymerase from RHDV in the absence of added template RNA. The use of deletion and point mutants allowed the identification of Tyr-21 as the residue involved in uridylylation and consequently in the linkage between VPg and the viral genome. These data constitute the first report on the identity of the amino acid residue involved in VPg uridylylation in a member of the Caliciviridae family.
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PMID:Identification of the amino acid residue involved in rabbit hemorrhagic disease virus VPg uridylylation. 1136 64

Recent studies have reported on the toxicity and related oxidative stress of selenium and mercury. The present study compares the effects of Se as sodium selenite (Na2SeO3) and Hg as mercuric chloride (HgCl2) separately and in combination. Rats received repeated oral doses of Se (0.5 micromol/ml), Hg (0.5 micromol/ml), or Se in combination with Hg (0.5 micromol/ml of each) for 5 consecutive days. Rat serum, brain and liver samples were collected for biochemical assays. The following biochemical alterations occurred in response to Hg treatment: protein content (brain and liver), acetylcholinesterase (AChE) (brain and serum), acid and alkaline (AcP and AlP) phosphatases (plasma and liver) and glutathione S-transferase (GST) (plasma and liver) activities were significantly (P<0.05) decreased, while lactate dehydrogenase (LDH) (plasma, brain and liver), aspartate and alanine aminotransferase (AST, ALT) (serum and liver) activities were significantly increased. Thiobarbituric acid reactive substances (TBARS) was significantly increased in brain and liver. Effect of Se alone included decreased AcP, AlP and GST (serum and liver) activities. However, LDH (serum, brain and liver) and AST (liver) and TBARS (brain and liver) increased. Selenium in combination with Hg partially or totally alleviated the toxic effects of Hg on different studied enzymes. It is concluded that Se could be able to antagonize the toxic effects of mercury.
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PMID:Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. 1149 25

Laparoscopic surgery causes a reduction in hepatic blood flow due to a number of factors, including raised intra-abdominal pressure, the neurohumoral response to surgical stress and the effect of patient position. The clinical significance of the phenomenon is not fully understood. Plasma concentrations of alcohol dehydrogenase (AD) and glutathione S-transferase (GST), which are concentrated in the centrilobular acinus of the liver, sensitively reflect hepatic hypoperfusion, and can be used to monitor reductions in hepatic blood flow. We compared perioperative AD, GST, aspartate aminotransferase (AST, normal range 14-32 IU litre(-1)) and alanine aminotransferase (ALT, normal range 8-41 U litre(-1)) concentrations in patients undergoing laparoscopic cholecystectomy or laparoscopic colectomy to study how patient position and surgical manipulation of the liver affect hepatocellular integrity during laparoscopy. There were significant postoperative increases in AD and GST in the cholecystectomy group [mean (SD) peak concentration 10.8 (4.7) U litre(-1) and 113 (55) microg litre(-1) respectively]. Although the duration of pneumoperitoneum was longer in the colectomy group, there were no comparable perioperative increases in AD and GST in this group [peak concentration 4.0 (4.0) U litre(-1) and 33 (35) microg litre(-1) respectively]. AST and ALT on the first postoperative day were significantly higher in the laparoscopic cholecystectomy group (41 and 34 U litre(-1) respectively) than in the laparoscopic colectomy group (24 and 18 U litre(-1); P<0.05 for each). These results indicate that patient position and the effects of surgical manipulation of the liver affect perioperative hepatic perfusion significantly.
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PMID:Subclinical hepatic dysfunction in laparoscopic cholecystectomy and laparoscopic colectomy. 1187 31

A rare outbreak of acute hepatic damage in workers exposed to dichloropropanols was reported in 1992. As there are no detailed reports of dichloropropanols (DCPs) toxicity and its mechanism, we reviewed the toxicity of dichloropropanols using our results. 1) A marked elevation of serum AST and ALT with massive necrosis of the liver was noted in the 1/2 x, the 1 x and 2 x LD50 (0.149 mg/kg) of 1, 3-dichloro-2-propanol(DC 2 P). Hepatic malondialdehyde level was significantly increased, and associated with a decrease in liver glutathione S-transferase activity and reduced glutathione content. It is suggested that the free radical is associated with DCPs. 2) A reduction of leukocytes, platelets and fibrinogen, and prolonged prothrombin time were observed in the 1 x LD50 of DC 2 P. 3) In the CA1 area of the hippocampus, inhibition of population spikes was reduced by the 1 x LD50 of DC 2 P. This research was completed with the assistance of several other papers concerning dichloropropanols toxicity.
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PMID:[Toxicity of dichloropropanols]. 1223 57

Low-dose acetylsalicylic acid (ASA) treatment is a standard therapeutic approach in diabetes mellitus for prevention of long-term vascular complications. The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). Blood glucose, glycated hemoglobin, as well as plasma ALT and AST activities increased in rats with streptozotocin-induced experimental diabetes. The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. We did not observe increased accumulation of membrane lipid peroxidation products or altered levels of reduced glutathione in livers. The linear correlation between blood glucose and glycated hemoglobin in diabetic animals was distorted upon ASA treatment, which was likely due to a chemical competition between nonenzymatic protein glycosylation and protein acetylation. The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. Otherwise, some decrease in these parameters was noted in ASA-treated nondiabetic animals. Increased ASA-induced G6PDH activity was recorded in both diabetic and nondiabetic rats. While both glycation due to diabetic hyperglycemia and ASA-mediated acetylation had very similar effects on the activities of all studied enzymes but G6PDH, we conclude that non-enzymatic modification by either glucose or ASA may be a common mechanism of the observed convergence.
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PMID:Antioxidative enzyme and glutathione S-transferase activities in diabetic rats exposed to long-term ASA treatment. 1681 74

Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0mg Vit. E and 0mg deltamethrin/kg body weight (BW) (control); 100mg Vit. E/kg BW; 1.28mg deltamethrin/kg BW; 100mg Vit. E plus 1.28mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats.
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PMID:Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E. 1697 60

In the present work, we investigated the protective effects of the ethanol extract of Aralia continentalis roots (AC) on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in a cultured Hepa1c1c7 cell line and in mouse liver. Pretreatment with AC prior to the administration of t-BHP significantly prevented the increase in serum levels of hepatic enzyme markers (ALT, AST) and lipid peroxidation and reduced oxidative stress, as measured by glutathione content, in the liver. Histopathological evaluation of the livers also revealed that AC reduced the incidence of liver lesions. The in vitro study showed that AC significantly reduced t-BHP-induced oxidative injury in Hepa1c1c7 cells, as determined by cell cytotoxicity, intracellular glutathione content, lipid peroxidation, reactive oxygen species (ROS) levels, and caspase-3 activation. Also, AC up-regulated phase II genes including heme oxygenase-1 (HO-1), NAD(P)H:quinone reductase, and glutathione S-transferase. Moreover, AC induced Nrf2 nuclear translocation and ERK1/2 and p38 activation, pathways that are involved in inducing Nrf2 nuclear translocation. Taken together, these results suggest that the protective effects of AC against t-BHP-induced hepatotoxicity may, at least in part, be due to its ability to scavenge ROS and to regulate the antioxidant enzyme HO-1 via the ERK1/2 and p38/Nrf2 signaling pathways.
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PMID:Protective mechanisms of Aralia continentalis extract against tert-butyl hydroperoxide-induced hepatotoxicity: in vivo and in vitro studies. 1882 57


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