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)

Solanum alatum Moench. has been shown to have a protective effect against carbon tetrachloride (CCl4)-induced liver injury. Solanum alatum treatment (100 mg/kg, p.o.) decreased the elevation of serum alanine aminotransferase (ALT; GPT) and aspartate aminotransferase (AST; GOT) induced by acetaminophen (paracetamol) (600 mg/kg, i.p.) administration. It also decreased the extent of visible necrosis in liver tissue. In addition, Solanum alatum treatment restored hepatic glutathione (GSH) depletion induced by acetaminophen (600 mg/kg, i.p.) administration. Microsomal enzyme levels such as P-450, reductase, and aniline hydroxylation enzyme were also restored to normal levels after Solanum alatum administration. The hepatoprotective mechanism may function through direct binding with acetaminophen toxic metabolites, decreasing the attraction of acetaminophen metabolites for other cellular GSH or thiol protein. Additionally, Solanum alatum treatment increased the concentration of hepatic GSH and maintained a high level activity of GSTase, which led to acceleration of the excretion of toxic acetaminophen metabolites.
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PMID:The hepatoprotective effects of Solanum alatum Moench. on acetaminophen-induced hepatotoxicity in mice. 1079 22

Isoproterenol, upon oxidation, produces quinones which react with oxygen to produce superoxide anions (O2.-) and H2O2. In the present study, isoproterenol was administered to rats in two doses so as to evaluate its beta adrenergic and toxicological action in terms of lipid peroxidation (LPO) and antioxidant enzymes in erythrocytes. Isoproterenol (30 mg/100 g body wt.) was administered to rats and the animals were followed up to 7 days after administration. Some of these animals were treated with a second dose of isoproterenol 24 h after the first dose and the animals were followed up to 12 h. The result showed increased lipid peroxidation (LPO) and superoxide dismutase (SOD) activity in erythrocytes in response to isoproterenol. Catalase (CAT) activity in erythrocytes decreased with isoproterenol between day 2-7 as compared to control. The second injection of isoproterenol showed increased CAT activity in erythrocytes which decreased at 12 h as compared to control. The erythrocyte GSH content and glutathione-S-transferase (GST) activity decreased with isoproterenol treatment as compared to control. However, erythrocyte GSH content as well as GST activity both recovered towards control with time. Elevated serum lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and glutamate oxaloacetate transaminase (GOT) activity was observed after isoproterenol treatment. The results show increased LPO and altered antioxidant system in erythrocytes in response to isoproterenol induced oxidative stress.
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PMID:Lipid peroxidation and antioxidant enzymes in isoproterenol induced oxidative stress in rat erythrocytes. 1084 29

Activities of hepatic xanthine oxidase (XO) and xanthine dehydrogenase (XD), serum liver enzymes, and reduced glutathione (GSH) were determined in livers of chronic cholestatic rats. The common bile duct was ligated (CBDL) and rats were randomized to either an untreated group or to treatment with allopurinol, a competitive XO inhibitor, or received a tungsten-supplemented diet to inactivate XO and XD, or received antioxidants vitamin C and vitamin E. One group underwent only sham laparotomy. After 4 weeks, in untreated CBDL animals serum aspartate aminotransferase and bilirubin concentrations were significantly elevated and hepatic GSH was significantly decreased when compared with the sham-operated group. Histochemical and enzymatic determinations of XD and XO showed a significant increase in hepatic XO activity after CBDL. Treatment with allopurinol and a tungsten-supplemented, molybdenum-free diet significantly attenuated serum liver enzymes, hepatic XO activity, and improved hepatic GSH levels, whereas vitamins C and E had a positive effect only on hepatic GSH levels. Our results support the hypothesis that cholestasis-induced hepatocellular injury is partially triggered by oxidative processes derived from increased hepatic XO activity. Inhibition and inactivation of XO exerts a hepatocellular protective effect in chronic cholestasis.
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PMID:The impact of hepatic xanthine oxidase and xanthine dehydrogenase activities on liver function in chronic cholestasis. 1089 33

Exposure of human plasma in vitro to gas-phase cigarette smoke (CS) causes a marked modification of plasma proteins as measured by protein carbonyl assay. Aldehydes present in CS may cause this elevation of protein carbonyls by reacting with sulfhydryl groups of proteins. Saliva is the first body fluid to confront the inhaled CS. Thus, in vitro exposure of saliva to nine "puffs" of CS also showed a distinct increase in protein carbonyls. Ascorbate and desferrioxamine mesylate had little effect on protein carbonyl formation, while GSH and N-acetylcysteine considerably inhibited the accumulation of protein carbonyls due to CS exposure. Following the exposure to CS, the activities of several salivary enzymes-amylase, lactic dehydrogenase (LDH), and acid phosphatase-were found to be significantly reduced (34, 57, and 77%, respectively). However, CS had no effect on the activities of aspartate aminotransferase and alkaline phosphatase. Addition of 1 mM of GSH and N-acetylcysteine considerably protected LDH and amylase activities, suggesting that sulfhydryl groups are affected in LDH and amylase. On the other hand, addition of 1 mM ascorbate caused a further loss of LDH and amylase activities, which could be partially prevented by the addition of desferrioxamine mesylate, implicating metal-catalyzed oxidation processes. Finally, loss of acid phosphatase activity was completely unaffected by any of the above antioxidants. It is concluded that the loss of salivary enzyme activities may be due to various agents in the CS that affect the enzyme activities via different mechanisms.
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PMID:Effect of cigarette smoke on salivary proteins and enzyme activities. 1089 39

An attempt was made to study the effect of dietary taurine on the toxicity of oxidized fish oil in male Wistar rats. The rats were fed different diets with or without supplement of 5% taurine and 3% oxidized fish oil. After feeding diet with 3% oxidized fish oil and 5% taurine at the same time, taurine could improve the decrease of body weight and the glutathione (GSH) level in the liver, and the increase of relative ratios of liver and kidney weight to body weight and thiobarbituric acid-reactive substances (TBARS) level in the liver of rats caused by oxidized fish oil It also could reduce the activities of aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) in the plasma of rats caused by oxidized fish oil. It was also found that taurine possessed a good recovering effect and a short-term preventing effect from the toxicity of oxidized fish oil in rats. Judging from these data, this indicates that taurine may play an important role in reducing the toxic effect of oxidized fish oil in rats.
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PMID:Effect of taurine on toxicity of oxidized fish oil in rats. 1094 19

This study examined the effects of black tea (Camellia sinensis L.) on lipid peroxidation and glutathione levels in carbon tetrachloride (CCl4)-treated male Wistar rats. Three groups of rats formed two control groups and one treatment group. The control groups were fed with a standard diet, while the black tea group were fed the standard diet plus 6% by weight dried black tea leaves. After two months, the rats in the black tea group and in one control group were administered a single dose of CCl4 (1 ml/kg, i.p.) and sacrificed two hours later. Rats in the other control group were administered olive oil in a similar fashion. Lipid peroxide levels in liver and plasma, glutathione (GSH) levels in liver and alanine transaminase (ALT) and aspartate transaminase (AST) activities in plasma were measured. Rats in the black tea group were found to have significantly decreased liver lipid peroxide levels, and ALT and AST activities compared with the rats in the CCl4-treated control group. In addition, liver glutathione levels were decreased in the black tea group. These data suggest that black tea attenuates CCl4-induced hepatic injury.
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PMID:Effect of black tea on lipid peroxidation in carbon tetrachloride treated male rats. 1096 44

The protective effect of N-[(3, 5-di-tertiobutyl-4-hydroxy-1-thiophenyl)]-3-propyl-N'-(2,3, 4-trimethoxybenzyl)piperazine (S-15176) on liver injury induced by warm ischemia-reperfusion was investigated using a rat model. Animals were subjected to 2 h of ischemia followed by different reperfusion times. Hepatocyte integrity was assessed by measuring plasma alanine and aspartate aminotransferase activities, and by determining reduced and oxidized glutathione in plasma and bile. Hepatocyte function was quantitated by determining bile flow and liver ATP content. Ischemia-reperfusion resulted in severe hepatic injury involving a huge increase in alanine and aspartate aminotransferase activities, a drop in ATP content, and a decrease in bile flow. Plasma and bile reduced (GSH) and oxidized (GSSG) glutathione concentrations were inversely related: plasma levels increased when biliary levels decreased. This was associated with a decrease in animal survival (-34%). S-15176 pretreatment (1.25, 2.5, 5 or 10 mg kg(-1) day(-1)) improved the survival rate and limited tissue damages in a dose-dependent manner. The pretreatment also reduced the aminotransferase leakage from hepatocytes and the increase in plasma glutathione levels. In addition, normalization of the plasma GSSG/GSH ratio, a good index of an oxidative stress, was observed in groups treated with the higher dosage, suggesting that the antioxidant properties demonstrated for the compound in vitro (IC(50)=0.3 microM towards lipid peroxidation) could play a role in its protective effect. S-15176 pretreatment also protected the organ from the drop in ATP levels. At the higher dose, ATP content was maintained at a level almost 86% of the sham-operated group after 60 min of reperfusion. This was associated with a restoration of the biliary flow. These data suggest that S-15176 may be a useful drug in liver surgery to prevent ischemia-reperfusion injury.
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PMID:S-15176 reduces the hepatic injury in rats subjected to experimental ischemia and reperfusion. 1102 Apr 92

The hepatoprotective effects of acetylbergenin were examined against D -galactosamine (GalN)-induced liver damage in rats, compared with that of bergenin reported previously. Acetylbergenin was synthesized from acetylation of bergenin, isolated from Mallotus japonicus, to increase lipophilic and physiological activities. Acetylbergenin was administered orally once daily for 7 days and then GalN (400 mg kg(-1), i.p.) was injected at 24 h and 96 h after the final administration of acetylbergenin. Acetylbergenin reduced the elevated serum enzyme activities of alanine/aspartate aminotransferase, sorbitol dehydrogenase and gamma -glutamyltransferase and the formation of hepatic malondialdehyde induced by GalN. Acetylbergenin also significantly restored towards normalization the decreased levels of glutathione and the decreased activities of glutathione S-transferase and glutathione reductase induced by GalN. Therefore, these results suggest that acetylbergenin has hepatoprotective effects against GalN-induced hepatotoxicity by inhibiting lipid peroxidation and maintaining an adequate level of GSH for the detoxification of xenobiotics as underlying hepatoprotective mechanisms. In addition, lipophilic acetylbergenin showed more activity in the hepatoprotection than that of the much less lipophilic bergenin reported previously.
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PMID:Effects of acetylbergenin against D -galactosamine-induced hepatotoxicity in rats. 1102 10

In the present study, the genotoxic, hematoxic effects, and their relation with pathological and biochemical parameters of hexane were investigated. Cytogenetic evaluation performed on the bone marrow indicated that chromosome aberrations increased at both hexane doses in relation to the negative controls. Decreased hematocrit, hemoglobin concentrations, and mean corpuscular volume were observed on the whole blood counts. Conjugated dienes (CD), glutathione (GSH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and catalase (CAT) were increased. Histological examinations showed intracytoplasmic vacuolisation, nuclei with lower chromatin, and parenchymatous degenerations in the dose groups. In the bone marrow slides, depletion of the erythroid series were observed. In conclusion, hexane seems to be a genotoxic and hematoxic agent leading to degeneration and lipid peroxidation in exposed groups.
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PMID:Genotoxic, hematoxic, pathological, and biochemical effects of hexane on Swiss albino rats. 1107 17

The effects of black tea (Camellia sinensis L.) on lipid peroxidation and glutathione (GSH) levels in carbon tetrachloride (CCl4)-treated female Wistar rats were examined. Two control groups and one treatment group were tested. The control groups were fed with a standard diet, while the black tea group was fed the standard diet plus 6% by weight dried black tea leaves. At the end of 2 months, a single dose of CCl4 (1 ml/kg, i.p.) in olive oil was administered to rats in one of the control groups and the black tea group. They were sacrificed after 2 hours. Rats in the other control group were administered olive oil in a similar fashion. Measurements were made of lipid peroxide levels in liver and plasma, glutathione levels in liver, and alanine transaminase (ALT) and aspartate transaminase (AST) activities in plasma. Liver lipid peroxide levels, plasma ALT and AST activities were significantly decreased in the black tea group compared with the CCl4-treated control group, while plasma lipid peroxide levels were not. These results are parallel to those previously found with Wistar male rats. Glutathione levels, however, were not significantly affected, in contrast to the data relating to male rats, either after CCl4 or black tea treatments. The results of our study add to the findings that black tea attenuates CCl4-induced hepatic injury but also indicates the susceptibility of glutathione levels to endocrinological effects.
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PMID:Effect of black tea on lipid peroxide and glutathione levels in female rats. 1120 8


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