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)

Sesame oil is regarded as a daily nutritional supplement to increase cell resistance to lipid peroxidation. The aims of this study were to examine the effects of parenteral sesame oil on oxidative stress and hepatic disorder induced by lipopolysaccharide and to determine the defense mechanisms involved in sesame oil-associated anti-oxidative effects in rats. Oxidative stress was induced by lipopolysaccharide (5 mg/kg, intraperitoneally) and assessed by determination of lipid peroxidation. Sesame oil (8 ml/kg, subcutaneously) was given 3 h after lipopolysaccharide, and lipid peroxide levels, hydroxyl radical, superoxide anion, the enzyme activities of superoxide dismutase and catalase as well as the levels of glutathione and nitrite were examined 6 h after lipopolysaccharide. Hepatic function was assessed by determining the activities of serum aspartate aminotransferase and alkaline phosphatase. Sesame oil reduced lipid peroxidation and hydroxyl radical, but failed to affect superoxide anion. Superoxide dismutase and catalase were increased, but glutathione was not affected, and the levels of nitrite were reduced. Further, sesame oil-treated groups showed attenuated hepatic disorder in lipopolysaccharide-treated rats. Thus, parenteral sesame oil can be used to attenuate oxidative stress and relieve hepatic disorder after lipopolysaccharide intoxication in rats.
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PMID:Parenteral sesame oil attenuates oxidative stress after endotoxin intoxication in rats. 1503 64

This study was conducted to investigate the effect of a 7-day treatment as well as the influence of gender on cocaine hepatotoxicity (CH). Lipopolysaccharide (LPS) potentiation of CH was also investigated. Male and female CF-1 mice were orally administered 20 mg/kg body weight cocaine hydrochloride once daily for 7 days. Four hours after the last cocaine administration, the mice were administered 12 x 10(6) EU LPS (or equal volume of sterile saline) intraperitoneally. Plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were evaluated as indices of liver injury. Blood and liver glutathione (GSH), glutathione reductase (GRx), and catalase (CAT) activities were also determined to investigate the oxidation stress induced by the treatment. Plasma ALT and AST concentrations were elevated in all males receiving cocaine alone or cocaine + LPS. Furthermore, blood GSH and CAT were decreased and GRx activity was elevated in the same males. Histological analysis revealed a high degree of focal necrosis in the male cocaine group, and severe necrosis in the male cocaine + LPS group. Unlike males, females showed no effect of either cocaine alone or cocaine + LPS treatments. These results indicate that gender plays a significant role in CH and its potentiation by LPS and lengthening the administration by two treatments increased the severity of cocaine + LPS hepatotoxicity dramatically in male mice.
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PMID:Cocaine hepatotoxicity and its potentiation by lipopolysaccharide: treatment and gender effects. 1520 19

This study was designed to examine the effects of squalene on tissue antioxidant status in isoproterenol-induced myocardial infarction in male albino rats. Levels of diagnostic marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)] in plasma, lipid peroxides, reduced glutathione, and the activities of glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and antiperoxidative enzymes [catalase (CAT) and superoxide dismutase (SOD)] in the heart tissue of experimental groups of rats were determined. The prior administration of squalene at 2% level along with feed for 45 days significantly prevented the isoproterenol-induced elevation in the levels of diagnostic marker enzymes in plasma of experimental rats. Squalene also exerted an antioxidant effect against isoproterenol-induced myocardial infarction by blocking the induction of lipid peroxidation. A tendency to prevent the isoproterenol-induced alterations in the level of reduced glutathione and in the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. The cardioprotective effect of squalene might be ascribable to its antioxidant property and membrane stabilizing action.
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PMID:Effect of squalene on tissue defense system in isoproterenol-induced myocardial infarction in rats. 1522 64

Deltamethrin toxicity was studied in broilers and vitamin E was evaluated for therapeutic management. Day old male broiler chicks were randomly divided into 3 groups consisting of 6 chicks in each. Group 1 was maintained as control for 6 wks, group 2 was fed on deltamethrin (100 mg/kg feed) for 6 wks and group 3 was fed on deltamethrin for the first 4 wks and during the subsequent 2 wks with vitamin E (300 mg/kg feed) with out deltamethrin. Weekly body weights, feed conversion ratio, glutathione (GSH) concentration and high density lipoproteins (HDL) were significantly (P < 0.05) reduced, while the activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSH-R), catalase, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), and the lipid profile and renal biomarkers were increased significantly (P < 0.05) in group 2 and 3 at the end of 4th wk as compared to group 1. Following treatment with vitamin E during the last 2 wks in group 3, all the parameters in study revealed improvement. From this study, it is concluded that deltamethrin induces toxicity by oxidative damage in biological system and supplementing vitamin E in feed is useful in treating accidental toxicity.
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PMID:Evaluation of vitamin E against deltamethrin toxicity in broiler chicks. 1526 58

Salinomycin was studied for its toxicity and zinc (80 mg/kg) was assessed for prophylactic and therapeutic management in broiler chicks. Male broiler chicks were randomly divided into 7 groups consisting of 6 chicks in each. Group 1, 2 and 3 were maintained as control, therapeutic dose control (60 mg/kg feed) and toxic dose control (120 mg/kg feed), respectively. Group 4 was fed on feed containing salinomycin therapeutic dose and zinc. Group 5 received feed containing toxic dose of salinomycin. Group 6 and 7 were fed on feed containing toxic dose of salinomycin for the first 4 weeks for induction of ionophore toxicity and for the subsequent 2 weeks, group 6 received zinc and group 7 was fed on feed containing toxic dose of salinomycin along with zinc. Weekly body weights revealed a significant (P<0.01) decrease in toxic controls as compared to group 1, 2, 4 and 5. The activity of glutathione peroxidase, glutathione reductase and catalase, and the values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total proteins, total cholesterol, triglycerides, low density lipoproteins (LDL), urea, creatinine and blood urea nitrogen (BUN) were significantly (P<0.01) elevated in toxic controls, whereas glutathione (GSH) and high density lipoproteins (HDL) were significantly (P<0.01) lowered as compared to group 1, 2, 4 and 5. Following toxicity, zinc supplementation in group 6 and 7, all serobiochemical parameters were revived to normal. Thus, it is enunciated that salinomycin toxicity is due to oxidative damage and use of zinc in feed tends to cure and avoid any accidental toxicity.
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PMID:Evaluation of zinc against salinomycin toxicity in broilers. 1527 Mar 74

Cocaine (COC) produces hepatotoxicity by a mechanism, which remains undefined, but has been linked to its oxidative metabolism. Ketamine (KET) is also a potentially hepatotoxic agent. The abuse of KET with COC is currently popular among young abusers therefore; this study was conducted to investigate the possible potentiation of COC-mediated hepatotoxicity (CMH) by KET. Male Sprague Dawley (SD) rats were administered oral KET hydrochloride for three consecutive days at a dose of 100 mg/kg with and without a single dose of COC (5 mg/kg, i.v.) administered 18 h after the last KET dose. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured as markers of liver injury. Liver reduced glutathione (GSH) levels were determined as well as the activities of glutathione peroxidase (GPx) and catalase (CAT). In addition, the activity of liver glutathione reductase (GRx) was measured. The results demonstrate that KET pretreatment potentiated the hepatotoxicity of COC. Serum ALT and AST were significantly elevated with the combined KET and COC treatment versus all other treatments. While COC alone resulted in focal inflammatory cell infiltration, COC administration after KET pretreatment produced sub-massive hepatic necrosis. Hepatic GSH content was significantly reduced in KET-pretreated COC group compared to the other treatment groups, rendering the liver more susceptible to oxidative stress. Moreover, there was a significant decrease in the activities of hepatic GPx and CAT, particularly with the KET-pretreated COC group. In addition, norcocaine (NC) was only detected in the plasma of rats received COC after KET pretreatment. In conclusion, this study demonstrates that KET pretreatment potentiates the hepatotoxicity of COC as revealed by an array of biochemical and morphological markers most probably due to increase in COC oxidative metabolism.
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PMID:Effect of ketamine pretreatment on cocaine-mediated hepatotoxicity in rats. 1533 Nov 30

The aim of the present study was to investigate the effects of daily intragastric administration of bullfrog oil (oleic, linoleic and palmitoleic acid-rich oil), corresponding to 0.4% of body weight for four weeks, on fatty acid composition and oxidative stress (lipid peroxidation and catalase activity) in mouse liver. The activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT), biomarkers of tissue injury, were determined in liver homogenates and serum. The proportions of 18:2n-6, 20:4n-6, 20:5n-3, and 22:6n-3 (polyunsaturated fatty acids, from 37 to 60%) in the total fatty acid content were increased in the liver of the bullfrog oil-treated group (P < 0.05) compared to control. At the same time, a significant decrease in the relative abundance of 14:0, 16:0, and 18:0 (saturated fatty acids, from 49 to 25%) was observed. The hepatic content of thiobarbituric acid reactive substances (TBARS) was increased from 2.3 +/- 0.2 to 12.3 +/- 0.3 nmol TBA-MDA/mg protein and catalase activity was increased from 840 +/- 32 to 1110 +/- 45 micromol reduced H2O2 min-1 mg protein-1 in the treated group. Bullfrog oil administration increased AST and ALP activities in the liver (from 234.10 +/- 0.12 to 342.84 +/- 0.13 and 9.38 +/- 0.60 to 20.06 +/- 0.27 U/g, respectively) and in serum (from 95.41 +/- 6.13 to 120.32 +/- 3.15 and 234.75 +/- 11.5 to 254.41 +/- 2.73 U/l, respectively), suggesting that this treatment induced tissue damage. ALT activity was increased from 287.28 +/- 0.29 to 315.98 +/- 0.34 U/g in the liver but remained unchanged in serum, whereas the GGT activity was not affected by bullfrog oil treatment. Therefore, despite the interesting modulation of fatty acids by bullfrog oil, a possible therapeutic use requires care since some adverse effects were observed in liver.
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PMID:Effect of bullfrog (Rana catesbeiana) oil administered by gavage on the fatty acid composition and oxidative stress of mouse liver. 1544 69

Antioxidative property and tumor inhibitive property of B. monniera (20mg/kg body wt, sc) was examined in 3-methylcholanthrene induced fibrosarcoma rats. Antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and the levels of glutathione (GSH) and the rate of lipid peroxidation (LPO) in the liver and kidney tissues were assessed. A significant increase was noted for the rate of LPO with a corresponding decrease in the antioxidant enzyme status in fibrosarcoma bearing rats. In fibrosarcoma bearing rats, the tumor markers like lactate dehydrogenase (LDH), creatine kinase (CK), alanine transaminase (ALT), aspartate transaminase (AST) and sialic acid (SA) were increased in the serum. Treatment with B. monniera extract significantly increased the antioxidant enzyme status, inhibited lipid peroxidation and reduced the tumor markers. It can be concluded that B.monniera extract promotes the antioxidant status, reduces the rate of lipid peroxidation and the markers of tumor progression in the fibrosarcoma bearing rats.
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PMID:Bacopa monniera Linn. extract modulates antioxidant and marker enzyme status in fibrosarcoma bearing rats. 1557 26

Cyclophosphamide (CP), one of the most widely prescribed antineoplastic drugs could cause a lethal cardiotoxicity. The present study is aimed at evaluating the role of DL-alpha-lipoic acid (LA) in oxidative cardiac damage induced by CP. Adult male Wistar rats were divided into four treatment groups. Two groups received single intraperitoneal injection of CP (200 mg/kg BW) to induce cardiotoxicity, one of these groups received LA treatment (25 mg/kg BW for 10 days). A vehicle treated control group and a LA drug control were also included. Cardiotoxicity, evident from increased activities of serum creatine phosphokinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase in CP administered rats, was reversed by LA treatment. CP administered rats showed abnormal levels of enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymic antioxidants (glutathione, vitamin C and vitamin E) along with high malondialdehyde levels. However, normalized lipid peroxidation and antioxidant defenses were reported in the LA treated rats. These findings highlight the efficacy of LA as a cytoprotectant in CP induced cardiotoxicity.
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PMID:Protective effect of DL-alpha-lipoic acid on cyclophosphamide induced oxidative cardiac injury. 1560 58

We previously reported that, as compared with selenite, nano red elemental selenium (Nano-Se) had lower acute toxicity in mice and similar bioavailability in terms of up-regulating seleno-enzymes. The short-term toxicity of both selenite and Nano-Se in mice was further compared in this study. At an oral dose of 6 mg/kg bw per day administered for consecutive 12 days, selenite and Nano-Se completely and partially suppressed mice growth respectively. Abnormal liver function was more pronounced with selenite treatment than Nano-Se as indicated by the increase of both alanine aminotransferase and aspartate aminotransferase in serum. Selenite inhibited liver catalase and superoxide dismutase activities, whereas, Nano-Se did not affect these two antioxidant enzymes. Selenite increased the malondialdehyde content of liver, but Nano-Se decreased it. Both Se forms had similar effects on depletion of reduced glutathione and up-regulated glutathione peroxidase. Nano-Se was more potent than selenite in the induction of glutathione S-transferase. At oral doses of 2 or 4 mg/kg bw per day for consecutive 15 days, selenite was more active than Nano-Se in supressing growth, deleting reduced glutathione, and inhibiting superoxide dismutase activities. Taken together, these results indicate that over a short-term, a high-dose of selenite caused more pronounced oxidative stress, greater liver injury, and prominent retardation of growth as compared to Nano-Se.
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PMID:Comparison of short-term toxicity between Nano-Se and selenite in mice. 1562 May 74


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