UNIPROT:P17174 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the effects of natural distomatosis infections on sheep liver malondialdehyde (MDA) concentration, activities of enzymatic antioxidants (glutathione peroxidase (GPx), superoxide dismutase (Cu, Zn-SOD), catalase (CAT)) and concentrations of non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C, and beta-carotene). Eighteen Akkaraman sheep naturally infected with Fasciola sp and Dicrocoelium dentriticum (D. dentriticum) and ten healthy Akkaraman sheep were included in the study Liver samples for the analysis of MDA, GPx, Cu, Zn-SOD, CAT, GSH, vitamin C, and beta-carotene and blood samples for the measurement of alanine aminotransferase and aspartate aminotransferase were collected immediately after sheep in the two groups were slaughtered. The concentration of MDA and activity of GPx in the group with distomatosis were higher than in the control group (P < 0.001). However, the Cu, Zn-SOD, CAT activities and the GSH, vitamin C concentrations in the infected group were significantly lower than in the control group (P < 0.001). The serum beta-carotene was not found to be statistically different in the two groups (P > 0.05). ALT and AST serum activities of the group with distomatosis were significantly higher in comparison to the control group (P < 0.001). In this study it was demonstrated that lipid peroxidation increased and activities or/and concentrations of antioxidant compounds were significantly changed in the liver of sheep with distomatosis.
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PMID:Lipid peroxidation and antioxidant potential of sheep liver infected naturally with distomatosis. 1835 46

Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats.
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PMID:Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats. 1840 91

Oxidative stress is a general mechanism whereby free radicals induce oxidative damages and reduce the antioxidant defences of the biological systems. The aim of the present study was to determine plasma malondialdehyde levels as a biomarker of lipid peroxidation and its relation to the antioxidants status (plasma ascorbate and blood glutathione concentrations), liver function tests and anaemia in spontaneous ovine fascioliasis. For this purpose, jugular blood samples and livers of 27 infected ewes with Fasciola hepatica along with blood samples of 20 healthy (control) ewes were collected from animals slaughtered in a F. hepatica endemic area (Kharga oasis, Egypt). An increase (P<0.001) in plasma malondialdehyde (141.1%) accompanied by decreased levels (P<0.001) of albumin (29.3%) and ascorbate (36.2%) in plasma and glutathione in blood (31.6%) of infected sheep was noticed when compared with control values. In the infected group, malondialdehyde values were positively correlated with liver fluke burden (r=0.57, P=0.002) and the activity of plasma aspartate aminotransferase (r=0.39, P=0.0.046) and gamma-glutamyltransferase (r=0.64, P=0.0003) and negatively correlated with the concentrations of albumin (r=-0.53, P=0.004), ascorbate (r=-0.46, P=0.0.17) and glutathione (r=-0.41, P=0.034). In conclusion, oxidative stress is a significant feature of chronic F. hepatica infection in grazing sheep.
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PMID:Circulating oxidative stress status in desert sheep naturally infected with Fasciola hepatica. 1843 62

Chromium (VI) compounds are genotoxic and carcinogenic in a variety of experimental systems. Garlic and its derivatives possess antioxidant properties to scavenge the toxic radicals. The mechanism by which garlic induces the antioxidant and phase II enzymes during oxidative stress-induced apoptosis is not known. This study aims to evaluate the protective role of aqueous garlic extract (AGE; 200 mg kg(-1) b.w.) and S-allylcysteine (SAC; 100 mg kg(-1) b.w.) on potassium dichromate-induced apoptosis and oxidative stress in the hepatocytes of Wistar rats. Activities of liver marker enzymes such as aspartate transaminase, alanine transaminase and lactate dehydrogenase were found to be increased in the serum of chromium-induced group, whereas administration of garlic extract and SAC restored the enzymes to near normal status. The activities of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase), non-enzymic antioxidants (vitamin C and vitamin E) and the levels of reduced glutathione were found to be decreased, while an increase in lipid peroxidation (LPO) and reactive oxygen species were observed in the liver tissues of chromium-induced group. Administration of AGE and SAC reversed the status of these parameters substantially. Histological and transmission electron microscopic studies support our findings. Confocal microscopic analysis using annexin-V showed the involvement of apoptosis. Further, the expression of a novel transcription factor, nuclear factor-E2 related factor 2 (Nrf2) was investigated using Immunofluorescence and Western blotting. The results show the promising role of Nrf2-mediated antioxidant defense of AGE and SAC against chromium toxicity.
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PMID:Chromium (VI)-induced oxidative stress and apoptosis is reduced by garlic and its derivative S-allylcysteine through the activation of Nrf2 in the hepatocytes of Wistar rats. 1854 44

Cyclosporine A (CsA) is an immunosuppressor, which is most frequently used in the transplant surgery and in the treatment of autoimmune diseases. It has been shown that CsA is able to generate reactive oxygen species and lipid peroxidation, which are directly involved in the CsA nephrotoxicity, hepatotoxicity and cardiotoxicity. This study was undertaken to investigate the protective effect of ellagic acid (EA), a polyphenolic compound against CsA-induced liver injury in male Wistar rats. In this study, CsA was administered orally (25 mg/kg body weight) for 21 days to induce toxicity. EA was administered orally (12.5, 25 and 50 mg/kg body weight) for 21 days along with oral administration of CsA. CsA-induced liver damage was evidenced by increased activities of serum hepatic enzymes namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase with a significant elevation of lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS) and hydroperoxides in the liver. The levels of enzymic antioxidants such as superoxide dismutase, catalase and glutathione-S-transferase and non-enzymic antioxidants (vitamin C, vitamin E and reduced glutathione) were also decreased in CsA-treated rats. Administrations of EA at 50 mg/kg body weight significantly decreased the activities of hepatic marker enzymes compared with other doses of EA (12.5, 25 mg/kg body weight). In addition, the levels of TBARS and hydroperoxides were significantly decreased and the levels of enzymic and non-enzymic antioxidants significant increased on treatment with EA in the liver. The biochemical observation was supplemented by histopathologic examination of liver section. The results of this study indicate that EA might play an important role in protecting CsA-induced oxidative damage in the liver.
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PMID:Effect of ellagic acid on cyclosporine A-induced oxidative damage in the liver of rats. 1870 50

Carbon tetrachloride (1 ml/kg body weight as a 1:1 mixture of CCl(4) and mineral oil) was orally administered to rats. After 12 h, the activity of plasma ALT (alanine aminotransferase) was significantly higher than that of the control group, and plasma ALT and AST (aspartate aminotransferase) activities significantly increased 24 h after CCl(4) administration. These results indicated that the necrotic process had initiated at about 12 h and developed thereafter. After 6-24 h of CCl(4) administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 6 h after CCl(4) intoxication and thereafter. Oral administration of vitamin E (1 ml/kg body weight as a 1:1 mixture of alpha-tocopherol and mineral oil) 12 h before CCl(4) administration caused a significant elevation of liver vitamin E level and ameliorated liver necrosis 24 h after CCl(4) intoxication based on plasma AST and ALT. Vitamin E also significantly restored the hepatic vitamin C concentration 12 and 24 h after CCl(4) intoxication, demonstrating that vitamin E functioned as an antioxidant. The liver vitamin E concentration was not changed by vitamin E supplementation to rats that did not receive CCl(4). This result indicated that vitamin E accumulated in the damaged liver. The activation of JNK, ERK1/2 and p38 MAPK took place 1.5 h after CCl(4) administration. Co-administration of alpha-tocopherol with CCl(4) did not affect these early changes in MAPKs.
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PMID:Effect of alpha-tocopherol on carbon tetrachloride intoxication in the rat liver. 1906 52

Currently there has been an increased interest globally to identify antioxidant compounds that are pharmacologically potent and have low or no side effects for use in preventive medicine. This study was designed to evaluate the protective effect of gallic acid on cardiac marker enzymes, troponin-T, LDH-isoenzyme pattern, lipid peroxidation products and antioxidant status in isoproterenol (ISO)-induced myocardial infarction in male Wistar rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, ISO (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days. ISO-induced myocardial damage was indicated by increased activities of marker enzymes such as creatine kinase, creatine kinase-MB, aspartate transaminase, alanine transaminase and lactate dehydrogenase in serum and the levels of troponin-T in the serum. Increased LDH-isoenzyme bands (LDH-1 and LDH-2) were also observed in serum of ISO-induced rats. In addition to these diagnostic markers, the levels of lipid peroxidation products in plasma and the heart were significantly (P<0.05) increased and the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione, vitamin C and E in plasma and the heart were significantly (P<0.05) decreased in ISO-induced rats. The level of uric acid in plasma was significantly (P<0.05) increased in ISO-treated rats. Gallic acid pretreatment showed significant protective effect on all the biochemical parameters studied. Histopathological findings of gallic acid pretreated myocardial infarcted heart confirmed the biochemical findings of this study. Thus, gallic acid protects the myocardium against isoproterenol-induced oxidative stress.
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PMID:Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats. 1914 39

This experiment pertains to the protective role of naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5mg/kg) was administered orally for 4 weeks to induce hepatotoxicity. Liver damage induced by cadmium was clearly shown by the increased activities of serum hepatic marker enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and serum total bilirubin (TB) along with the increased level of lipid peroxidation indices (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) and protein carbonyl contents in liver. The toxic effect of cadmium was also indicated by significantly decreased levels of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C and vitamin E). Administration of naringenin at a dose of (50mg/kg) significantly reversed the activities of serum hepatic marker enzymes to their near-normal levels when compared to Cd-treated rats. In addition, naringenin significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. The histopathological studies in the liver of rats also showed that naringenin (50mg/kg) markedly reduced the toxicity of cadmium and preserved the normal histological architecture of the tissue. The present study suggested that naringenin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of rats.
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PMID:Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin. 1940 69

The present study was undertaken to examine the protective effects of an anthocyanin fraction (AF) obtained from purple-fleshed sweet potato on acetaminophen (paraceptamol [APAP])-induced hepatotoxicity in mice and to determine the mechanism involved. Mice pretreated with AF prior to APAP administration showed significantly lower increases in serum alanine aminotransferase and aspartate aminotransferase activities and hepatic malondialdehyde formation than APAP-treated animals without AF. In addition, AF prevented hepatic glutathione (GSH) depletion by APAP, and hepatic GSH levels and GSH S-transferase activities were up-regulated by AF. APAP-induced hepatotoxicity was also prevented by AF, as indicated by liver histopathology findings. In addition, the effects of AF were examined on cytochrome P450 (CYP) 2E1, the major isozyme involved in APAP bioactivation. Treatment of mice with AF significantly and dose-dependently reduced CYP2E1-dependent aniline hydroxylation and CYP2E1 protein levels. Furthermore, AF had an antioxidant effect on FeCl(2)/ascorbate-induced lipid peroxidation in mouse liver homogenates and had superoxide radical scavenging activity. These results suggest that AF protects against APAP-induced hepatotoxicity by blocking CYP2E1-mediated APAP bioactivation, by up-regulating hepatic GSH levels, and by acting as a free radical scavenger.
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PMID:Hepatoprotective effects of an anthocyanin fraction from purple-fleshed sweet potato against acetaminophen-induced liver damage in mice. 1945 32

Carvacrol (2-methyl-5-(1-methylethyl)-phenol) is a predominant monoterpenic phenol which occurs in many essential oils of the family Labiatae including Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. This study was designed to investigate the hepatoprotective and antioxidant properties of carvacrol on D-galactosamine (D-GalN)-induced hepatotoxicity and oxidative damage in male albino Wistar rats. D-GalN hepatotoxic rats exhibited elevation in the activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and lipidperoxidative markers such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides. Activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and the levels of non-enzymatic antioxidants (vitamin C, vitamin E, and reduced glutathione) in the plasma, erythrocytes, liver, and kidney decreased in the hepatotoxic rats. Oral administration of carvacrol for 21 days brought these parameters towards normal. The biochemical observations were supported by histological studies of rat liver and kidney tissues. These results suggest that carvacrol could afford a significant hepatoprotective and antioxidant effect against D-GalN-induced rats.
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PMID:Effect of carvacrol on hepatic marker enzymes and antioxidant status in D-galactosamine-induced hepatotoxicity in rats. 1965 Aug 54

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