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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

DHC-1, a multiherbal formulation, was tested for its antioxidant activity in rats. DHC-1 was investigated at dose levels of 100 mg/kg, p.o. and 200 mg/kg, p.o., once daily, for 30 days in normal rats. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), lipid peroxidation, membrane bound enzymes like Ca2+ ATPase, Mg2+ ATPase, Na+K+ ATPase, lipids like phospholipid, cholesterol, triglyceride and total proteins were estimated in liver, kidneys and heart. Liver glucose-6-phosphate-dehydrogenase (G-6-P-D) was also determined. The serum levels of GOT, GPT, alkaline phosphatase, lactate dehydrogenase and bilirubin were also estimated. The decrease in the serum enzymes may be due to the membrane stabilising action of DHC-1. The inhibition of lipid peroxidation and enhancement of antioxidant enzymes (SOD and CAT) along with reduced GSH by DHC-1 may be attributed to the antioxidant potential of various ingredients present in the formulation. Thus, it can be concluded that DHC-1 exhibits an antioxidant activity and could prove beneficial in the treatment of various disorders associated with the involvement of reactive oxygen species.
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PMID:Antioxidant activity of DHC-1--a herbal formulation. 1526 74

A hydroalcoholic (50%) extract of Emblica officinalis (fruit) (EO-50) reduced the severity of hepatic fibrosis induced by carbon tetrachloride (CCl4) and thioacetamide (TAA). Improved liver function was observed by measuring the levels of aspartate aminotransaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and bilirubin in serum. Hepatic parameters monitored were the levels of glutathione (GSH), lipid peroxidation (LPO) and hydroxyproline and the activities of catalase, glutathione peroxidase (GPx), Na+,K+-ATPase and cytochrome P450 (CYP 450 2E1) (aniline hydroxylation). The results suggested that EO-50 effectively reversed profibrogenic events possibly due to its promising antioxidative activity.
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PMID:Reversal of fibrogenic events in liver by Emblica officinalis (fruit), an Indian natural drug. 1599 20

The effect of ten phytotherapeutic products on CCl(4) intoxicated liver in albino male Wistar rats was investigated. Biochemical parameters, including serum transaminase activity (GPT and GOT), histoenzymological measurements (lactate dehydrogenase, LDH; succinate dehydrogenase, SDH, cytochromoxidase, CyOx; Mg(2+)-dependent adenosine triphosphatase, ATP-ase) and histochemical (Sudan black) and histological examinations (haematoxylin-eosin staining) of the liver were investigated. Some positive effects such as the reduction of hepatocytolysis and steatosis, and a return to normal values of the activity of some enzymes in the following plants: Chrysanthemum balsamita, Echinacea pallida, Calendula officinalis and Corylus avelana were obtained.
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PMID:The hepatoprotective action of ten herbal extracts in CCl4 intoxicated liver. 1622 May 65

Disease caused by viruses, especially white spot syndrome virus (WSSV), present the greatest challenge to shrimp aquaculture worldwide. Massive tissue disintegration occurs in WSSV-infected ectodermal and mesodermal tissues of penaeid shrimp. The activities of membrane bound phosphatases (Na(+)K(+)ATPase, Ca(2+)ATPase, Mg(2+)ATPase and Total ATPase), transaminases (alanine transaminase (ALT) and aspartate transaminase (AST)) and mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), alpha-ketoglutarate dehydrogenase (KGDH), NADH dehydrogenase, cytochrome C oxidase) in WSSV-infected tissues (hemolymph, hepatopancreas, gills and muscle) of Fenneropenaeus indicus were determined at intervals after WSSV infection (0, 24, 48, 72 and after 72 h (moribund)). The activities of phosphatases, transaminases and mitochondrial enzymes in healthy as compared with WSSV-infected hemolymph, hepatopancreas, gills and muscle showed marked divergence throughout the course of infection. WSSV infected hemolymph, hepatopancreas, gills and muscle exhibited significantly reduced activity of membrane bound phosphatases compared with the uninfected animals. Inactivation of these enzymes may occur due to increased production of free radicals, that cause conformational change by oxidation of 'SH' groups present at the active site. Significantly marked elevation in the activities of transaminases (ALT and AST) was observed in WSSV-infected hemolymph, hepatopancreas, gills and muscle compared to the uninfected tissues. This may be due to leakage of these enzymes from the damaged tissues. The activities of mitochondrial enzymes in WSSV-infected tissues were significantly decreased compared to the activities in uninfected animals. WSSV-infected animals showed reduced feeding that may have led to decreased oxidation of glucose via the TCA cycle. Excessive production of free radicals in WSSV-infected animals may have affected aerobic oxidation leading to lower production of ATP. It is concluded that membrane dynamics play a major role in the pathogenesis of WSSV infection.
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PMID:Activities of membrane bound phosphatases, transaminases and mitochondrial enzymes in white spot syndrome virus infected tissues of Fenneropenaeus indicus. 1641 26

Acute effects of mercuric chloride (HgCl2) were evaluated on mice. Mice received a single dose of HgCl2 (4.6 mg/kg, subcutaneously) for three consecutive days. Thirty minutes after the last injection with HgCl2, mice received one single injection of 2,3-dimercapto-1-propanesulfonic acid (DMPS) or N-acetylcysteine (NAC) or diphenyl diselenide (PhSe)2. DMPS, NAC and (PhSe)2 were utilized as therapy against mercury exposure. At 24 h after the last HgCl2 injection, blood, liver and kidney samples were collected. delta-Aminolevulinate dehydratase (delta-ALA-D) and Na+, K- (+) ATPase activities, thiobarbituric acid-reactive substances (TBARS), non-protein thiols (NPSH) and ascorbic acid concentrations were evaluated. Plasma aspartate (AST) and alanine (ALT) aminotransferase activities, as well as urea and creatinine levels were determined. The group of mice exposed to Hg + (PhSe)2 presented 100% of lethality. Exposure with HgCl2 caused a decrease on the body weight gain and treatments did not modify this parameter. delta-ALA-D, AST and ALT activities, TBARS, ascorbic acid levels and NPSH (hepatic and erythrocytic) levels were not changed after HgCl2 exposure. HgCl2 caused an increase in renal NPSH content and therapies did not modify these levels. Mice treated with (PhSe)2, Hg + NAC and Hg + DMPS presented a reduction in plasma NPSH levels. Creatinine and urea levels were increased in mice exposed to Hg + NAC, while Hg + DMPS group presented an increase only in urea level. Na+, K- (+) ATPase activity was inhibited in mice exposed to Hg + DMPS and Hg + NAC. In conclusion, therapies with (PhSe)2, DMPS and NAC following mercury exposure must be better studied because the formation of more toxic complexes with mercury, which can mainly damage renal tissue.
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PMID:DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury. 1684 Dec 48

Hepatic injury elicits intracellular stress that leads to peroxidation of membrane lipids accompanied by alteration of structural and functional characteristics of the membrane, which affects the activity of membrane-bound ATPases. We have explored the effect of leptin on hepatic marker enzyme and membrane-bound adenosine triphosphatases in ethanol-induced liver toxicity in mice. The experimental groups were control, leptin (230 microg kg(-1), i.p. every alternate day for last 15 days), alcohol (6.32 g kg(-1), by intragastric intubation for 45 days), and alcohol plus leptin. Ethanol feeding to mice significantly (P < 0.05) elevated the plasma leptin, alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT) and hepatic lipid hydroperoxides (LOOH), and plasma and hepatic total ATPases, Na(+), K(+)-ATPase and Mg(2+)-ATPase. There was a significant decrease in Ca(2+)-ATPase and reduced glutathione (GSH). Leptin injections to ethanol-fed animals further elevated the levels of hepatic LOOH, plasma and hepatic total ATPases, Na(+), K(+)-ATPase and Mg(2+)-ATPase, while the Ca(2)-ATPase and GSH were decreased significantly. In addition, leptin administration was found to increase the plasma levels of leptin, ALT, ALP, GGT, Na(+) and inorganic phosphorous, and decrease the levels of K(+) and Ca(2+) in ethanol-fed mice. These findings were consistent with our histological observations, confirming that leptin enhanced liver ailments in ethanol-supplemented mice.
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PMID:Effect of leptin administration on membrane-bound adenosine triphosphatase activity in ethanol-induced experimental liver toxicity. 1687 59

Heparin and quercetin induce capacitation in spermatozoa through membrane receptor binding and inhibition of Ca-ATPase of the plasma membrane, respectively. Although capacitation is energy intensive, ammonia from amino acid metabolism can inhibit respiration and Krebs cycle activity. The objective was to determine activities of key enzymes in bull spermatozoa that contribute to the redox state and supply energy for capacitation. Malate dehydrogenase (MDH-NAD(+)), alanine and aspartate aminotransferases (ALT, AST), and lactate dehydrogenase-X (LDH-X) were measured spectrophotometrically (340 nm); mean (+/-S.D.) activities in control spermatozoa were 7.65+/-1.67, 0.45+/-0.05 and 0.74+/-0.14x10(-2)U/10(8) spermatozoa for MDH-NAD(+), ALT and AST, respectively, and were 2.83+/-0.66U/10(8) spermatozoa for LDH-X. Heparin decreased (P<0.05) activities of MDH-NAD(+), ALT, AST and LDH-X (78, 53, 66 and 66% of control levels, respectively); we inferred that amino acid catabolism was decreased. Quercetin decreased (P<0.05) activities of MDH-NAD(+) and ALT (60 and 49% of control levels), but activities of AST and LDH-X were not significantly different from controls; apparently maintenance of LDH-X activity supplied pyruvate for cellular metabolism. The proportion of capacitated spermatozoa in controls (8.5+/-1.73%) was substantially increased (P<0.05) by treatment with either heparin (36.2+/-4.5%) or quercetin (32.8+/-4.7%), there was no significant difference among groups for acrosomal integrity and sperm viability. In conclusion, heparin- or quercetin-induced capacitation affected different metabolic pathways that modulated the redox state and oxidative metabolism in cryopreserved bovine spermatozoa.
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PMID:Heparin and quercitin generate differential metabolic pathways that involve aminotransferases and LDH-X dehydrogenase in cryopreserved bovine spermatozoa. 1708 43

Hyperlipidemia is a major risk factor for the premature development of coronary heart disease and it has been shown to increase the incidence of myocardial ischemia and cardiac events. Pentacyclic triterpenes possess antiatherosclerotic, antioxidant, anti-inflammatory and cytoprotective effects. To study the effect of plant derived triterpene, lupeol and its ester lupeol linoleate, on lipid status and biochemical changes on heart tissue, male albino Wistar rats were fed high-cholesterol diet (normal rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days. There was a significant (p<0.001) increase in the levels of total cholesterol, triglycerides and phospholipids along with augmented activities of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in the heart tissue. Triterpenes treatment reduced the above alterations produced in hypercholesterolemic rats. The transmembrane enzymes, namely Na(+), K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase showed a decrease in their activities. Triterpenes treatment reversed these levels, prevented the hypertrophic cardiac histology and restored the normal ultrastructural architecture. In conclusion, lupeol and lupeol linoleate intervention minimized the lipid abnormalities and abnormal biochemical changes induced by HCD fed rats. This shows that triterpenes possess cardioprotective effects which will be beneficial in hypercholesterolemic condition. Out of these two triterpenes tested, lupeol linoleate appeared to be even more effective than lupeol.
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PMID:Protective effect of lupeol and its ester on cardiac abnormalities in experimental hypercholesterolemia. 1733 64

This study was designed to investigate the protective effect of oleanolic acid (OA) against isoproterenol-induced myocardial ischemia in rat myocardium. Wistar strain rats were pretreated with OA (20, 40, and 60 mg/kg, s.c) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, sc for 2 consecutive days). Heart were excised from the experimental animals and assessed for the activities of marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP) and conjugated dienes (CD)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFA) and phospholipids (PL)], and membrane-bound ATPase enzymes (total ATPase, Na(+)K(+) ATPase, Ca(2 +) ATPase, and Mg(2 +) ATPase). Troponin T and I were estimated in plasma. Leakage of cardiac markers, elevated lipid peroxidation with increased lipid profiles and decreased activities of membrane-bound ATPase enzymes were confirmed the severe myocardial damage occurring as a consequence of isoproterenol-induced ischemia, and they also showed the significant improvement effected by oleanolic acid pretreatment. These findings provided evidence that oleanolic acid was found to be protecting rat myocardium against ischemic insult and the protective effect could attribute to its anti-oxidative, anti-hyperlipedemic, and anti-arrhythmic properties as well as its membrane-stabilizing action.
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PMID:Cardioprotective effect of oleanolic acid on isoproterenol-induced myocardial ischemia in rats. 1745 91


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