Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Verapamil, a calcium channel blocker, improves myocardial preservation during cold cardioplegia and protects against renal damage during periods of warm and cold ischemia. To determine if verapamil could prevent ischemic damage to livers during and after cold storage, harvested rat livers were flushed with either University of Wisconsin (UW) solution or UW solution with 25 mg/liter verapamil. Twenty rats were used in each group. After 24 hr of storage at 4 degrees C, livers were perfused with oxygenated blood through the portal veins for 2 hr at 37 degrees C and pH 7.4. Liver enzymes, electrolytes, and perfusate flow rate were determined at 30-min intervals. At 90 min of perfusion, the verapamil group of livers had less elevation of AST (110 +/- 17 IU/liter vs 172 +/- 25 IU/liter, P less than 0.05), ALT (115 +/- 21 IU/liter vs 210 +/- 34 IU/liter, P less than 0.05), and LDH (962 +/- 170 IU/liter vs 1452 +/- 253 IU/liter, NS). Verapamil livers produced more bile than controls (6.9 +/- 1.9 microliters/g vs 2.3 +/- 1.7 microliter/g, P less than 0.05) and maintained a higher portal flow rate throughout the perfusion. Both groups showed similar reduction in liver weights after storage (3.9 +/- 0.9% vs 2.8 +/- 0.7%) and required the same amount of bicarbonate for correction of acidosis during perfusion (2.6 +/- 0.2 mM vs 2.8 +/- 0.2 mM). Light microscopic exam after perfusion showed hepatocyte damage in 30% of control livers, but 0% of verapamil livers. We conclude that verapamil-treated rat livers showed less damage and better function upon reperfusion after 24 hr of cold storage. This agent may be clinically useful as an additive to the UW preservation solution for livers.
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PMID:Verapamil improves rat hepatic preservation with UW solution. 205 66

Chronic oral administration of oxodipine, a new calcium channel blocker, resulted in a reduction in the blood enzyme activity of alanine and aspartate aminotransferase. The reductions were both time and dose related. The decline in enzyme activities was accompanied by microscopic hepatic changes, which in the opinion of the authors should have been associated with an increase in the enzyme activities of alanine aminotransferase and aspartate aminotransferase. The effect was only partially reversed one month after the cessation of oxodipine treatment.
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PMID:Drug-induced decrease of serum alanine and aspartate aminotransferase activity in the rat, as a result of treatment with oxodipine, a new calcium channel blocker. 231 33

This study analyzes the effects of intraoperative and postoperative calcium channel blockers on myocardial protection, postoperative arrhythmias, perioperative infarctions, and survival. Thirty-nine women undergoing consecutive coronary artery bypass operations were placed either in a control group (N = 23), in which standard cold potassium cardioplegia was used, or in a verapamil-nifedipine group (N = 16), in which verapamil (1 mg per liter) was added to the standard cardioplegic solution and nifedipine was instituted postoperatively. The verapamil-nifedipine group showed a significant reduction in postoperative levels of creatine phosphokinase (p less than 0.05). Levels of aspartate aminotransferase were also reduced (74 IU/L) compared with those for the control group (114 IU/L). In the control group, there were 3 early deaths secondary to abrupt ventricular fibrillation, but no patient in the verapamil-nifedipine group died or had serious early ventricular arrhythmias. Late hemodynamic variables were similar in both groups. We conclude that calcium channel blockers enhance myocardial protection during ischemic arrest and may diminish the incidence of fatal early postoperative ventricular arrhythmias in women undergoing coronary revascularization.
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PMID:Calcium channel blockers: an intraoperative and postoperative trial in women. 660 28

The effects of calcium channel blockers, verapamil, nifedipine and diltiazem, on CCl4-induced liver damage were determined. A single dose of CCl4 (0.5 ml/kg p.o.) led to a five-fold increase in liver calcium content. The toxic effect of CCl4 was also observed in other hepatic processes: the protein synthesis rate in the liver showed an important decrease, liver glycogen content and bile flow was decreased, and lipid peroxidation was approximately doubled. The plasma levels of cholesterol, triglycerides and transaminases (AST and ALT) also increased. When the calcium channel blockers were administered 2 hr prior to and 7 hr after the administration of the toxic agent at doses of 25 mg/kg (diltiazem) and 10 mg/kg (nifedipine and verapamil), the liver showed a significant reestablishment of several of these parameters: a considerable reduction in liver calcium content, a decrease in AST and ALT levels, and a significant increase in protein synthesis rate. There was also a partial inhibition of lipid peroxidation.
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PMID:Protective effects of calcium channel blockers in carbon tetrachloride-induced liver toxicity. 808 14

This study examines the effects of three calcium channel blockers (verapamil, nifedipine and diltiazem) on isolated rat hepatocytes exposed to ethanol. In the first part of our study, hepatocytes were incubated with increasing concentrations of ethanol (100, 300, 500, 1000 mM) for varying times. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) release were measured to evaluate the cytotoxic effects of ethanol. The concentration of 300 mM and time of incubation of 45 min were chosen for cytoprotection experiments in which calcium channel blockers, at two different concentrations, were added to the medium 30 min prior to the addition of ethanol. ALT, AST and LDH release as well as lipid peroxidation and cellular reduced glutathione (GSH) were measured. Nifedipine and verapamil (25 microM) reduced ALT, AST and LDH activities. The highest dose of diltiazem (50 microM) was more effective than the lowest one (25 microM). Ethanol caused a significant depletion of cellular GSH content as well as a moderate enhancement of lipid peroxidation. While none of the three calcium channel blockers was able to restore the decrease in GSH levels, diltiazem (25 microM) and nifedipine (50 microM) showed the greatest effect, significantly reducing lipid peroxidation.
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PMID:Hepatotoxicity of ethanol: protective effect of calcium channel blockers in isolated hepatocytes. 913 76

We investigated the effect of betaxolol on the decrease of mitochondrial aspartate aminotransferase (mAAT) activity in rat retinas induced by hypoxia in vitro. It is reported that mAAT decreases in ischemic or hypoxic retina and that the decrease is caused by Ca(2+)-dependent proteases such as calpain. Betaxolol is a compound that has beta(1)-adrenergic receptor blocking and voltage-dependent calcium channel blocking properties. The rat eye cups were maintained with Locke's solution saturated with 95% air - 5% CO(2). The eye cups were immersed in glucose-free Locke's solution saturated with 95% N(2) / 5% CO(2) (hypoxic solution). Ninety minutes of hypoxia caused a 20% decrease in mAAT activity. The eye cups incubated with the hypoxic solution containing 1 mM EGTA, 10 micro M MK-801 or 100 micro M betaxolol were protected from the decrease in mAAT activity, so that the residual mAAT activity was 50%, 45% or 40%, respectively, compared to the eye cups incubated in hypoxic solution alone, which had a 100% decrease in mAAT activity. In addition, co-incubation with EGTA and betaxolol had a greater protective effect against the mAAT decrease than a single application. This additive effect of betaxolol was dose-dependent. These results suggested that betaxolol had a protective effect against the decrease of mAAT caused by hypoxia and indicated that betaxolol might inhibit the Ca(2+) release from intracellular Ca(2+) stores.
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PMID:Effect of betaxolol on aspartate aminotransferase activity in hypoxic rat retina in vitro. 1241 81

This study describes the antihypertensive, antispasmodic, bronchodilator and hepatoprotective activities of the aqueous-methanolic extract of Carum copticum Benth. seeds (CSE) to rationalize some of its traditional uses. CSE (3-100 mg/kg) caused a dose-dependent fall in arterial blood pressure in anaesthetized rats. In isolated rabbit aorta and jejunum preparations, CSE (0.1-3.0 mg/ml) caused an inhibitory effect on the K+-induced contractions. The calcium channel blocking (CCB) effect was confirmed when CSE shifted the Ca2+ dose-response curves (DRCs) to right similar to verapamil. In isolated guinea-pig tracheal preparations, it caused inhibition of carbachol and K+-induced bronchoconstriction at 0.1-1.0 mg/ml as well as shifted the dose-response curves (DRCs) of carbachol and histamine to the right with suppression of maximum response suggestive of non-specific bronchodilator effect mediated possibly through CCB. Pretreatment of rats with CSE (500 mg/kg orally for 2 days at 12 h intervals) prevented paracetamol (640 mg/kg) and CCl4 (150 ml/kg)-induced rise in serum alkaline phosphatase (ALP) and aminotransferases (AST and ALT). The same dose of CSE was able to prevent the CCl4-induced prolongation in pentobarbital-induced sleeping time in mice confirming its hepatoprotectivity. These results indicate the presence of calcium antagonist(s) in Carum copticum seeds and thus provides sound mechanistic basis for some of their folkloric uses.
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PMID:Studies on the antihypertensive, antispasmodic, bronchodilator and hepatoprotective activities of the Carum copticum seed extract. 1576 73

The crude extract of Achillea millefolium (Am.Cr) was studied for its possible hepatoprotective effect against d-galactosamine (d-GalN) and lipopolysaccharide (LPS) induced hepatitis in mice and antispasmodic effect in isolated gut preparations to rationalize some of the folklore uses. Co-administration of d-GalN (700 mg/kg) and LPS (25 microg/kg) produced 100% mortality in mice. Pre-treatment of animals with Am.Cr (300 mg/kg) reduced the mortality to 40%. Co-administration of d-GalN (700 mg/kg) and LPS (1 microg/kg) significantly raised the plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared with values in the control group (p < 0.05). Pre-treatment of mice with Am.Cr (150-600 mg/kg) significantly prevented the toxins induced rise in plasma ALT and AST (p < 0.05). The hepatoprotective effect of Am.Cr was further verified by histopathology of the liver, which showed improved architecture, absence of parenchymal congestion, decreased cellular swelling and apoptotic cells, compared with the toxin group of animals. In isolated rabbit jejunum preparations, Am.Cr caused a concentration-dependent (0.3-10 mg/mL) relaxation of both spontaneous and K(+)-induced contractions as well as shifting the Ca(++) concentration-response curves (CRCs) to the right, similar to that caused by verapamil. These results indicate that the crude extract of Achillea millefolium exhibits a hepatoprotective effect, which may be partly attributed to its observed calcium channel blocking activity.
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PMID:Studies on hepatoprotective, antispasmodic and calcium antagonist activities of the aqueous-methanol extract of Achillea millefolium. 1661 41

Hepatic ischemia should be considered in serious liver injury, liver tumor resection and liver transplantation. There are other conditions that decrease hepatic blood flow and cause hepatic ischemia, such as hemorrhagic shock, sepsis, hepatic artery ligation, trauma, and certain vascular lesions. In this study, effects of nimodipine (a calcium channel blocker) and pentoxyfylline (a derivative of methylxanthine) on duration and degree of hepatic ischemia in rats at normothermic and hypothermic conditions are investigated. This study was performed on 6 groups of Wistar Albino type rats, each group consisting of 7 rats. Groups were separated into normothermic (A) and hypothermic (B) conditions AI-Control group, AII-Nimodipine group and AIII-Pentoxyfylline group, B IV-Control group, BV-Nimodipine group and BVI-Pentoxyfylline group respectively. After hepatic pedicle occlusion lasting 45 min, blood samples were drawn from the rats for evaluation of alanine aminotransferase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) values. Moreover, hepatic biopsies were taken to assess pathological changes under electron microscopy. These changes were evaluated through a grading system. As a result; it has been shown that both nimodipine and pentoxyfylline delayed effects of hepatic ischemia in a statistically significant manner in comparison with the control group and these effects were found to be more significant in hypothermic conditions.
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PMID:Effects of nimodipine and pentoxyfylline in prevention of hepatic ischemic damage in rats at normal and hypothermic conditions. 1849 96

The aim of this study was to examine the effect of cyclic adenosine monophosphate (cAMP) and its possible interference/synergism with calcium channel blocker in mice with acute liver injury induced with D-galactosamine (D-GalN) and lipopolysaccharide (LPS). C57Bl/6 mice were given i.p. simultaneously 300 mg/kg D-GalN and LPS 0.01 mg/kg. This treatment induced severe hepatitis, as evidenced by high mortality (80-90%) of control mice and large increase in concentration of aminotransferases in plasma (AST, ALT). Injection of stabile analogue of cAMP (dibutyryl-cAMP, db-cAMP) one hour before hepatotoxic agents increased survival of mice in dose-dependent manner and in medium dose significantly decreased plasma ALT level. Similar (protective) effect had also verapamil, calcium channel blocker, when given in non toxic doses and at the same time schedule as db-cAMP Combination of db-cAMP and verapamil had not synergistic effect in protection from D-GalN+LPS hepatotoxicity; the survival of mice was similar to that seen in protection caused by each agent alone.
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PMID:The effect of cyclic adenosine monophosphate (cAMP) on acute liver toxicity in mice induced by D-galactosamine and lipopolysaccharide. 2040 32


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