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)

The present study investigated the effect of ethanol extracts of seeds, pericarp and leaves of Eugenia Jamolana (E. Jamolana) on inflammation, gastric ulcer, anti-oxidants and hepatoprotective in rats. The acute inflammation was induced by intra-plantar injection of carrageenan (100 microl of 1 %) in the rat hind paw. Gastric ulcer was evoked by indomethacin (25 mg/kg) oral administration. Liver damage was induced by given CCL4 (2.5 ml/kg) orally. The median lethal (LD(50)) of the ethanol extract of both seeds and pericarp were determined and revealed that the investigated extracts of seeds and pericarp were non toxic up to 5 g/kg. The anti-inflammatory results showed that the oral administration of ethanol extract of E. Jamolana seeds (250, 500 mg/kg) showed significant inhibition of oedema formation in dose-dependent manner by -27.86, -41.23, -44.73, -51.78 % and by -63.16, -37.77, -47.04, -55.36 % at 1, 2, 3 and 4 h at 1, 2, 3 and 4 h, respectively. While the pericarp given at dose (500 mg/kg) exhibited significant inhibition of the oedema formation by -34.64, -21,8, 19.23 and -33.47 % at 1, 2, 3 and 4 h, respectively post carrageenan injection as compared with saline control group. E. Jamolana leaves fraction 1 given orally at dose of 25 mg/kg, induced non significant change on oedema, while the oedema response was significantly inhibited by -25.14, -33.4, -20.57 and -26.46 % at 1, 2, 3 and 4 h, respectively in group of rats that received leaves fraction 2 at the same dose. Rats were given leaves fraction 3 extract showed inhibition of oedema formation by -4.48 % at 1(st) h post- carrageenan injection, while at 2(nd), 3(rd) and 4(th) h showed non significant change on oedema formation. The acute gastric mucosal lesions was significantly reduced by given ethanol extract of E. Jamolana seeds, pericarp (250, 500 mg/kg) and leaves fractions 1, 2 and 3 (25 mg/kg) respectively in dose dependent manner, as compared with indomethacin treated group (control group). All tested extracts showed significant reduction in elevated serum ALT, AST and ALP levels as compared with CCl4 treated group. The ethanol extract of E. Jamolana seeds, pericarp and leaves fractions 1, 2, 3 showed significant elevation of blood GSH level and significant reduction in elevated plasma lipid peroxides (MDA) as compared with CCl4 treated group. In conclusion we can see that the ethanol extracts of E. Jamolana of seeds, pericarp and leaves fractions showed anti-inflammatory, anti-ulcer, hepatoprotective and anti-oxidants activity.
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PMID:Evaluation of some pharmacological activities of ethanol extracts of seeds, pericarp and leaves of Eugenia Jamolana in rats. 1911 87

Cisplatin-induced oxidative stress can cause liver and kidney damage, thus limiting therapeutic efficacy. Thus, in the present study, since Rhus verniciflua Stokes (RVS) containing flavonoids has antioxidant effects, we investigated whether it can protect cisplatin-induced toxicity in vitro and in vivo, The in vitro effects of RVS on the cell viability and reactive oxygen species (ROS) production were investigated using cisplatin-treated Madin-Darby Canine kidney (MDCK)-I renal cells. Its in vivo effects were also studied in BALB/c mice inoculated with CT-26 colon adenocarcinoma cells and treated with cisplatin with or without RVS. Liver and renal functions were assessed together with indices of tissue oxidation. RVS prevented cisplatin-induced cytotoxicity and ROS release against MDCK-I cells. RVS alone exerted modest antitumor activity against CT-26 cells. When used concurrently with cisplatin, RVS prevented the increases in serum blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and NO, while reducing liver and kidney tissue MDA content, and increasing catalase, glutathione (GSH), and superoxide dismutase (SOD) activities. Moreover, the antitumor efficacy of cisplatin was not altered by concurrent administration of RVS. These findings demonstrate that RVS prevents cisplatin-induced toxicity in vitro and in vivo via an antioxidant activity without hurting its antitumor effectiveness, suggesting that RVS can be usefully applied to the neoplastic patients as a combined chemopreventive agent with cisplatin.
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PMID:Rhus verniciflua Stokes prevents cisplatin-induced cytotoxicity and reactive oxygen species production in MDCK-I renal cells and intact mice. 1915 Feb 36

Comparative toxicity of nitrogen mustards (HN-1, HN-2 and HN-3) and sulphur mustard was carried out in mice. Based on LD50, the toxicity pattern was HN-2 < HN-1 < HN-3 < sulphur mustard by percutaneous route whereas, by subcutaneous route the toxicity pattern was sulphur mustard < HN-3 < HN-2 < HN-1. Single dose of 1 LD50 of nitrogen mustards and sulphur mustard was administered percutaneously and various oxidative stress parameters were also evaluated. The weight loss was more in HN-2 on day 3 and in sulphur mustard on day 7. There was a drastic fall of WBC count on day 3 in all groups with a recovery in nitrogen mustard groups on day 7. The RBC count and haemoglobin content showed a significant increase on day 7 in sulphur mustard group. The plasma enzymes (ALT, AST and ALP) showed an increase in all groups on day 3 and day 7. The hepatic GSH and GSSG contents were reduced and MDA content increased in all groups, with a further change in sulphur mustard on 7 day. Extensive DNA fragmentation was observed in all the nitrogen mustard groups compared to sulphur mustard group, on day 3. However, on the day 7 the DNA fragmentation was same in all groups. This study showed that the nitrogen mustards and sulphur mustard were extremely toxic by percutaneous route and caused oxidative stress. Sulphur mustard was more toxic by the percutaneous route and the effects were delayed and progressive.
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PMID:Comparison of toxicity of selected mustard agents by percutaneous and subcutaneous routes. 1924 79

The research was conducted to investigate the toxic effects of cadmium chloride (CdCl2), administered during gestation period on female Wistar rats. Pregnant rats received CdCl2 (20 mg/l, orally) from Day 6 to Day 19 of pregnancy. Results showed that Cd treatment induced a decrease in body weight gain. The relative liver weight increased significantly, with a marked decrease of glycogen and total lipids content. The administration of Cd induced hepatotoxicity as indicated by elevations in plasma alanine aminotransferase (ALT), aspartate aminotransferase and lactate dehydrogenase (LDH) activities (p < 0.05). Treatment with CdCl2 caused a significant (p < 0.05) increase in glucose. A significant increase was observed in the level of MDA and 8-oxodGuo tissues in the cadmium-exposed group compared to the control group (p < 0.05). Results showed that cadmium given to dams led to an oxidative stress and DNA damage in tissues of pregnant rats.
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PMID:Changes in antioxidant status and biochemical parameters after orally cadmium administration in females rats. 1937 26

The present study was designed to evaluate the protective effect of some local medicinal plants against liver and kidney toxicity induced by cadmium chloride. Methanolic extracts of Acacia nilotica and Retama raetam were used in this study. Furthermore, histopathological and histochemical investigations were done. Cadmium chloride caused a significant increase in serum AST, ALT, ALP, bilirubin, urea, and creatinine, cholesterol, LDL, triglycerides, and HDL levels Administration of Acacia nilotica and Retama raetma significantly inhibit that increase. Cadmium chloride induced a significant decrease in serum total protein, albumin, globulin levels, albumin/globulin ratio, blood SOD, and GPx, while Acacia nilotica and Retama raetam increase. Cadmium chloride caused a significant increase in MDA and NO, while a significant decrease in MDA and NO after Acacia nilotica and Retama raetam administration. These results suggested a beneficial effect of these plant extracts against experimentally-induced hepato- and nephro-toxicity of cadmium, and the possible mechanism of the protective effects may be partly due to the antioxidant activity of these plants.
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PMID:Role of some Egyptian medicinal plants against liver and kidney toxicity induced by cadmium chloride. 1981 61

Recently, we showed that L-arginine (L-Arg) supplementation could attenuate acute exercise-induced oxidative and inflammatory stress in aging rats. In this study, we investigate whether L-Arg supplementation protects cellular oxidative stress, inflammation, or the mitochondrial DNA 4834-bp large deletion (mtDNA4834 deletion) in 14-week-old young rats tissues during exhaustive exercise. Rats were randomly divided into four groups: sedentary control (SC); SC with L-Arg treatment (SC+Arg); exhaustive exercise (E); and exhaustive exercise with L-Arg treatment (E+Arg). Rats in the SC+Arg and E+Arg groups received supplemental 2% L-Arg diet. Rats in groups E and E+Arg performed an exhaustive running test on a treadmill. The results showed a significant increase in xanthine oxidase (XO) and myeloperoxidase (MPO) activities and lipid peroxide (malondialdehyde; MDA) levels of muscular, hepatic, and renal tissues in exercised rats as compared with sedentary rats. The increased XO, MPO, and MDA levels of these tissues significantly decreased in exercised rats supplemented with L-Arg. However, exhaustive exercise had no effect on mtDNA4834 deletions of muscular and hepatic tissues. The activities of creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine (CRE), lactate, uric acid, non-esterified fatty acid (NEFA), and D-3-hydroxybutyrate in the plasma significantly increased in the exercised rats compared with the sedentary rats, while the CK, lactate and uric acid levels in the plasma significantly decreased in L-Arg-supplemented exercised rats. These findings suggest that L-Arg supplementation reduces the oxidative damage to and inflammatory response in skeletal muscles, the liver, and kidneys caused by exhaustive exercise in young rats.
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PMID:Protective effects of L-arginine supplementation against exhaustive exercise-induced oxidative stress in young rat tissues. 2003 35

The emergence of silymarin (SMN) as a natural remedy for liver diseases, coupled with its entry into NIH clinical trial, signifies its hepatoprotective potential. SMN is noted for its ability to interfere with apoptotic signaling while acting as an antioxidant. This in vivo study was designed to explore the hepatotoxic potential of Doxorubicin (Dox), the well-known cardiotoxin, and in particular whether pre-exposures to SMN can prevent hepatotoxicity by reducing Dox-induced free radical mediated oxidative stress, by modulating expression of apoptotic signaling proteins like Bcl-xL, and by minimizing liver cell death occurring by apoptosis or necrosis. Groups of male ICR mice included Control, Dox alone, SMN alone, and Dox with SMN pre/co-treatment. Control and Dox groups received saline i.p. for 14 days. SMN was administered p.o. for 14 days at 16 mg/kg/day. An approximate LD(50) dose of Dox, 60 mg/kg, was administered i.p. on day 12 to animals receiving saline or SMN. Animals were euthanized 48 h later. Dox alone induced frank liver injury (>50-fold increase in serum ALT) and oxidative stress (>20-fold increase in malondialdehyde [MDA]), as well as direct damage to DNA (>15-fold increase in DNA fragmentation). Coincident genomic damage and oxidative stress influenced genomic stability, reflected in increased PARP activity and p53 expression. Decreases in Bcl-xL protein coupled with enhanced accumulation of cytochrome c in the cytosol accompanied elevated indexes of apoptotic and necrotic cell death. Significantly, SMN exposure reduced Dox hepatotoxicity and associated apoptotic and necrotic cell death. The effects of SMN on Dox were broad, including the ability to modulate changes in both Bcl-xL and p53 expression. In animals treated with SMN, tissue Bcl-xL expression exceeded control values after Dox treatment. Taken together, these results demonstrated that SMN (i) reduced, delayed onset, or prevented toxic effects of Dox which are typically associated with hydroxyl radical production, (ii) performed as an antioxidant limiting oxidative stress, (iii) protected the integrity of the genome, and (iv) antagonized apoptotic and necrotic cell death while increasing antiapoptotic Bcl-xL protein levels and minimizing the leakage of proapoptotic cytochrome c from liver mitochondria. These observations demonstrate the protective actions of SMN in liver, and raise the possibility that such protection may extend to other organs during Dox treatment including the heart.
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PMID:Silymarin modulates doxorubicin-induced oxidative stress, Bcl-xL and p53 expression while preventing apoptotic and necrotic cell death in the liver. 2014 34

Forty-eight male BALB/c mice, weighing 30-35 g, were used in the study, and were divided into groups of 12 each. The four groups established in the study included one control group and three experimental groups. The first group served as the control group, while Groups 2, 3 and 4 were administered 1g/kg bw/day pine honey, 180 mg/kg bw/day trichlorfon ( approximately 1/5LD(50)) and 1g/kg bw/day pine honey plus 180 mg/kg bw/day trichlorfon, respectively, by the oral route using a catheter for 21 days. At the end of 21 days post-administration, blood and tissue (liver, kidney, brain and heart) samples were collected. Serum levels/activities of total protein, albumin, glucose, cholesterol, triglyceride, BUN, creatine, uric acid, magnesium, sodium, potassium, chloride, total bilirubin, GGT, LDH, AST, ALT and ALP were determined. Furthermore, tissue MDA levels and CAT, SOD and GSH-Px activities were analyzed. According to the data obtained, when administered at the indicated dose and for the indicated time period, trichlorfon was determined to lead to negative alterations in most of the biochemical parameters investigated. The administration of pine honey was determined to alleviate this effect.
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PMID:Beneficial effect of pine honey on trichlorfon induced some biochemical alterations in mice. 2030 75

The aim of this study is to investigate effects of Flos lonicera extract (FLE) on acute liver injury model rats which induced by 35 mg/kg dimethylnitrosamine (DMN). Model rats were divided into hepatic injury control group (administrated with water), FLE group (administrated with FLE) and silymarin group (administrated with silymarin which is hepatotherapeutic drug) as positive control. They were examined including ALT, AST, ALP, gamma-GT, ALB and TP levels in serum, and MDA, GPx levels in liver tissue. In addition, pathologic changes, particularly fibrosis, were examined by Azan staining. The results revealed that the ALT, AST, ALP, gamma-GT, MDA GPx and liver fibrosis degree in the LJE group were lower than the silymarin group and control group, ALB and TP were higher than the silymarin group and control group. These results suggested that LJE may help in inhibiting of acute liver injury greater than silymarin.
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PMID:Protective effects of Flos lonicera extract on acute liver injury by dimethylnitrosamine-induced in rats. 2030 46

The purpose of this study was to study the hepatoprotective effects of the most promising extract of the root from Rubus aleaefolius Poir. and to isolate and identify the active components. Various crude forms of Rubus aleaefolius have been evaluated for their effects on CCl(4)-induced acute liver injury in mice vivo experimental model. Treatment groups contained 5 sub-groups that were ethanol crude extract; the high/low dosage ethyl acetate or n-butanol fraction; extracted with ethyl acetate or n-butanol after the residues and major constituent; intragastrically administrated with 35 mg/kg; 35, 4.6 mg/kg; 35, 5.8 mg/kg; 35 mg/kg and 3.5 mg/kg for 7 days. The serum samples were collected for biological analysis and also carried out histopathological studies. The low-dosage ethyl acetate fraction was the most active when the fractions were compared. It was found to decrease AST, ALT; to prevent formation of hepatic MDA, NO and intensify the activity of SOD. The histopathological changes induced by CCl(4) were also significantly reduced. The separation revealed the presence of six constituents by a bioassay-guided fractionation, beta-Sitosterol (1), 1beta-Hydroxyeuscaphic acid (2), Oleanolic acid (3), Myrianthic acid (4), Euscaphic acid (5), and Tomentic acid (6). Among them, compounds 2, 4, 5 in Rubus aleaefolius root is reported here for the first time. 1beta-Hydroxyeuscaphic acid (major constituent) showed a tremendous activity and the results confirm the traditional uses of Rubus aleaefolius in treating hepatitis.
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PMID:Hepatoprotective effects of Rubus aleaefolius Poir. and identification of its active constituents. 2036 54


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