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)

Methanol and aqueous leaf extracts of L. hirta demonstrated hepatoprotective activity against carbon tetrachloride induced liver damage in rats. The parameters studied were serum total bilirubin, total protein, alanine transaminase, aspartate transaminase and alkaline phosphatase activities. The hepatoprotective activity was also supported by histopathological studies of liver tissue. Results of the biochemical studies of blood samples of CCl4 treated animals showed significant increase in the levels of serum markers and decrease in total protein level reflecting the liver injury caused by CCl4. Whereas blood samples from the animals treated with methanol and aqueous leaf extracts showed significant decrease in the levels of serum markers and increase in total protein indicating the protection of hepatic cells. The results revealed that methanol leaf extract followed by aqueous extract of L. hirta could afford significant protection against CCl4 induced hepatocellular injury.
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PMID:Hepatoprotective activity of Leucas hirta against CCl4 induced hepatic damage in rats. 1612 14

From the leaves of Viburnum tinus L. (Adoxaceae) two acylated iridoid glucosides (viburtinoside A and B), a coumarin diglucoside scopoletin 7-O-beta-D-sophoroside and a natural occurred dinicotinic acid ester 2,6-di-C-methyl-nicotinic acid 3,5-diethyl ester were isolated. In addition to these, 10 known compounds were isolated, namely two bidesmosidic saponins, a hexamethoxy-flavone and five flavonol glycosides, as well as suspensolide A and oleanolic acid were isolated for the first time in this genus and species, respectively. The structures were determined mainly by spectroscopic methods (UV, IR, ESI-MS, 1H-, 13C NMR and DEPT). Toxicity of the investigated extract was determined (LD50=500 mg/kg). CCl4-induced hepatotoxicity has been evaluated in terms of the determination of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxide and nitric oxide levels in serum and compared using adult male rats weighing 150-180 g. Their highly elevated levels were significantly reduced by treatment with the investigated aqueous methanol extract in dose-dependent manner.
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PMID:Phytochemical constituents and hepatoprotective activity of Viburnum tinus. 1630 55

Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of methanol on antioxidant status and lipid peroxidation in lymphoid organs such as the spleen, thymus, lymph nodes and bone marrow of rats. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.w intraperitoneally) for detecting toxicity levels for one day, 15 d and 30 d, respectively. Administration of methanol at 15 and 30 d significantly (p<0.05) increased lipid peroxidation and decreased the enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic antioxidants (reduced glutathione and vitamin C) in lymphoid organs. However, lipid peroxidation and enzymatic and non-enzymatic antioxidants in the acute methanol exposed group animals were found to be significantly (p<0.05) increased. In one day methanol intoxication, the levels of free radicals initially increased, and to remove these free radicals, antioxidants levels were elevated, which generally prevented oxidative cell damage. But in longer periods of intoxication, when the generation of reactive free radicals overwhelmed the antioxidant defense, lipid peroxidation increased. Further, decreased antioxidants in 15 and 30 d methanol intoxication may have been due to overutilization of non-enzymatic and enzymatic antioxidants to scavenge the products of lipid peroxidation. In addition, the liver and kidney markers of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine significantly increased. This study concludes that exposure to methanol causes oxidative stress by altering the oxidant/antioxidant balance in lymphoid organs of the rat.
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PMID:Methanol-induced oxidative stress in rat lymphoid organs. 1648 59

Kava (Piper methysticum), a perennial shrub native to the South Pacific islands, has been used to relieve anxiety. Recently, several cases of severe hepatotoxicity have been reported from the consumption of dietary supplements containing kava. It is unclear whether the kava constituents, kavalactones, are responsible for the associated hepatotoxicity. To investigate the key components responsible for the liver toxicity, bioassay-guided fractionation was carried out in this study. Kava roots, leaves, and stem peelings were extracted with methanol, and the resulting residues were subjected to partition with a different polarity of solvents (hexane, ethyl acetate, n-butanol, and water) for evaluation of their cytotoxicity on HepG2 cells based on the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase and aspartate aminotransferase enzyme leakage assays. Organic solvent fractions displayed a much stronger cytotoxicity than water fractions for all parts of kava. The hexane fraction of the root exhibited stronger cytotoxic effects than fractions of root extracted with other solvents or extracts from the other parts of kava. Further investigations using bioassay-directed isolation and analysis of the hexane fraction indicated that the compound responsible for the cytotoxicity was flavokavain B. The identity of the compound was confirmed by (1)H and (13) C NMR and MS techniques.
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PMID:In vitro cytotoxicity of nonpolar constituents from different parts of kava plant (Piper methysticum). 1660 46

How to effectively mix small volumes of liquids within microplate wells is a still underestimated and often neglected challenge. The method the authors introduce here relies on violent turbulent motion within a liquid caused by spotting an organic solvent drop onto its surface. The amount needed, less than 1 to 3 microL, is generally small enough not to alter bioactive molecules. Moreover, a solvent may be selected for its compatibility with assay components. The method was tested with layers of aqueous liquids that differ in pH and concentration of a pH-dependent dye, allowing mixing to be monitored optically. Rapid mixing was caused by spotting drops of alcohols, acetone, acetonitrile, and aqueous solutions of these, as long as the difference of surface tension between the drop and the uppermost layer of the bulk liquid surpassed 30 dynes/cm. Along with this difference, position and velocity of spotting, as well as viscosity and geometry of the bulk liquid volume, may influence the turbulence evoked. No significant difference was found for the activity of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase when measured after mixing by shaking and after mixing by spotting 1 microL of methanol onto assays within 96-well microplates.
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PMID:Turbo-mixing in microplates. 1725 92

Orthosiphon stamineus (OS), Benth. (Lamiaceae) is widely used in Malaysia for treatments of various kidney and liver ailments. In the experiment, DPPH* radicals scavenging, Fe(3+)-induced lipid peroxidation inhibiting activities and trolox equivalent antioxidant capacity (TEAC) of methanol/water extract of Orthosiphon stamineus (SEOS) were determined. The results indicated that SEOS exhibited antioxidant, lipid peroxidation inhibition and free radical scavenging activities. The hepatoprotective activity of the SEOS was studied using CCl(4)-induced liver toxicity in rats. The activity was assessed by monitoring liver function tests through the measurement of alanine transaminase (ALT) and aspartate transaminase (AST). Furthermore, hepatic tissues were also subjected to histopathological studies. Pretreatment of SEOS (125, 250, 500 and 1000 mg/kg p.o.) dose-dependently reduced the necrotic changes in rat liver and inhibited the increase of serum ALT and AST activities. The results of the present study indicated that the hepatoprotective effect of Orthosiphon stamineus might be ascribable to its antioxidant and free radical scavenging property.
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PMID:Antioxidant and hepatoprotective effects of Orthosiphon stamineus Benth. standardized extract. 1726 56

In the present study, preventive and protective effects of Ocimum gratissimum in ethanol-induced hepatotoxicity are assessed in albino rats. A methanol extract of O. gratissimum leaves is prepared, with a yield of 3.5% (w/w) of the dry weight of leaves. Graded doses of the extract (10, 20, 40 and 80 mg/kg body weight), together with ethanol (5 gm/kg body weight) are administered orally to experimental groups for 30 days. Normal control rats receive distilled water only, while rats in an alcohol control group (AC) receive ethanol only for 30 days. O. gratissimum reduced the level of thiobarbituric acid reactive substance in all experimental groups (E1-E4). Alanine transaminase and aspartate transaminase levels fell in all experimental groups (E1-E4), but this reduction was significant only in groups E3 and E4 (P < 0.05), indicating inhibition of lipid peroxidation by free radicals generated after ethanol metabolism. Levels of antioxidants also increased. Ascorbic acid and glutathione levels increased in all experimental groups (E1-E4; P < 0.05 and P < 0.01, respectively). A significant increase in catalase (P < 0.05) was noted only in group E4, although an upward trend was noted in all experimental groups. This study shows that O. gratissimum prevents free radical damage to the liver and thus protects the organ from oxidative stress.
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PMID:Preventive and protective effects of wild basil in ethanol-induced liver toxicity in rats. 1744 12

The methanol extract of Raphanus sativus root extract showed a protective effect on paracetamol-induced hepatotoxicity in a dose-dependent manner. Degree of lipid peroxidation caused by paracetamol was measured in terms of thiobarbituric acid reactive substances (TBARS) and protection was measured in reference to serum glutamate oxaloacetate transaminase (SGOT), serum glutamate aspartate transaminase (SGPT), and blood and hepatic levels of antioxidants like glutathione and catalase. Administration of extract along with paracetamol showed significant protection. Levels of TBARS were found to be low, activities of SGOT and SGPT were low, while hepatic glutathione levels were significantly higher in experimental rats that received the mixture of paracetamol and the extract as compared to rats that received paracetamol only. Activities of catalase were also high in all experimental groups. Thus this study indicates the involvement of Raphanus sativus root extract with antioxidants like glutathione and catalase in rendering protection against paracetamol-induced lipid peroxidation and hepatotoxicity.
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PMID:Protective role of Raphanus sativus root extract on paracetamol-induced hepatotoxicity in albino rats. 1768 94

The present study was conducted to evaluate the hepatoprotective effect of Andrographis lineata (Acanthaceae) extracts in carbon tetrachloride-induced liver injury in rats. Male Wistar rats with chronic liver damage, induced by subcutaneous injection of 50% v/v carbon tetrachloride in liquid paraffin at a dose of 3 mL/kg on alternate days for a period of 4 weeks, were treated with methanol and aqueous extracts of A. lineata orally at a dose of 845 mg/kg/day. The biochemical parameters such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, serum bilirubin and alkaline phosphatase were estimated to assess the liver function. Histopathological studies of the liver were also carried out to confirm the biochemical changes. Histopathological examinations of liver tissue corroborated well with the biochemical changes. The activities of extracts were comparable to a standard drug. Hepatic steatosis, hydropic degeneration and necrosis were observed in the carbon tetrachloride treated group, while these were completely absent in the standard and extract treated groups. A. lineata extracts exhibited hepatoprotective action against carbon tetrachloride-induced liver injury. The present investigation established pharmacological evidence to support the folklore claim that it is used traditionally as a hepatoprotective agent.
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PMID:Hepatoprotective effect of leaf extracts of Andrographis lineata nees on liver damage caused by carbon tetrachloride in rats. 1770 41

In the present study, the efficacy of a methanol extract of Raphanus sativus root (RSME) is tested in albino rats that developed hepatic damage due to administration of paracetamol (100 mg/kg body weight) for 30 days. Twenty rats were divided into three experimental groups (E1, E2, E3) and one control group (EC). Two doses of RSME (80 and 120 mg/kg body weight) were administered orally to E1 and E2, respectively, and a mixture of RSME (120 mg/kg) and paracetamol (100 mg/kg) was administered to E3 for 21 days. Group EC and another group of normal rats (EN) that served as controls were administered distilled water. At the end of the experiment rats were bled to assay thiobarbituric acid reactive substances (TBARS), serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate aspartate transaminase (SGPT), reduced glutathione (GSH) and catalase. Results indicated that RSME reduced the levels of TBARS, SGOT and SGPT, and increased the level of GSH and the catalase activity in E1 and E2 as compared to the EC group. Group E3 showed decreases in TBARS, SGOT and SGPT levels, but the results were not statistically significant compared with the EN group. There was also a marked depletion in GSH level and catalase activity in this group. RSME reduced lipid peroxidation induced by paracetamol and brought the levels of SGOT and SGPT to normal, indicating liver recovery. It also brought about repletion of GSH levels and recovery of catalase activity. Results for group E3 indicated that RSME was not able to reverse the effects of paracetamol if administration continued.
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PMID:Efficacy of Raphanus sativus in the treatment of paracetamol-induced hepatotoxicity in albino rats. 1791 Feb 78


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