Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed fluid resuscitation of burn shock may lead to many harmful effects. We investigated the injury of liver and kidney of rats sustaining non-fluid perfusion, immediate perfusion, and delayed perfusion of burn shock. The electron spin reonance (ESR) was used to determine the existence of oxygen free radicals (OFR) successfully. We tested the activity of ATP enzyme in kidney, lactate dehydrogenase isoenzyme 5 (LDH5), GPT and GOT. We also tested the contents of malonaldehyde (MDA) and ATP in liver and kidney, urea nitrogen (BUN) and creatinine (Cr) in blood. We found that OFR plays an important role in the injury of liver and kidney sustaining delayed fluid resuscitation of burn shock. Immediate fluid perfusion can not protect the liver and kidney perfectely. And some OFR scavengers should be added to the fluid resuscitation of burn shock.
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PMID:[The injury of liver and kidney of rats sustaining delayed fluid resuscitation of burn shock]. 876 54

The protective effect of pyoverdins Pa A and Pf, peptidic siderophores secreted respectively by Pseudomonas aeruginosa and fluorescens, was studied in primary cultures of human hepatocytes exposed to iron (50 or 100 microM of iron-citrate). AST, ALT and MDA releases were measured as indexes of cytotoxicity. In order to demonstrate that these chelators were able to decrease iron uptake or increase iron release from the hepatocytes, labelled cells were obtained by maintaining the cultures in the presence of 1 microM 55Fe ferric chloride plus 50 microM iron citrate. One day after iron treatment, an increase in AST, ALT and MDA release was observed with 50 or 100 microM of iron citrate; it appeared that the concentrations 50 and 100 microM of iron were highly toxic for human hepatocytes. In the presence of 50 or 100 microM of iron, the addition of 50 or 100 microM of Pa A or Pf was effective to inhibit the increase observed in the enzyme leakage and the MDA production resulting from iron exposure. In human hepatocytes cultured for 1 day in the presence of 1 microM 55Fe-50 microM iron citrate plus 50 or 100 microM Pa A or Pf, a net decrease of iron uptake by the cells was observed, as demonstrated by the low intracellular iron level. When the hepatocytes were cultured for 1 day in the presence of 1 microM 55Fe-50 microM iron citrate and then for a further day in the presence of 50 or 100 microM Pa A or Pf without additional iron, the chelators increased the extracellular iron level, indicating their iron release from the loaded cells; however, the effects of Pa A and Pf on iron release did not differ significantly. In conclusion, iron loading achieved by adding iron citrate to the culture medium is highly toxic for human hepatocytes. Pyoverdins Pa A and Pf are effective in protecting human hepatocytes against the toxic effect of iron by both decreasing the uptake of the metal and increasing its release from the loaded cells.
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PMID:Inhibition of iron toxicity in human hepatocyte cultures by pyoverdins Pa A and Pf, the peptidic siderophores of Pseudomonas aeruginosa and fluorescens. 913 75

Methylene dianiline (DAPM) causes hepatic damage and bile duct necrosis in rats. This has been detected histologically and biochemically. The toxicity was dose related over the range 0-100 mg/kg but the dose response relationship showed a maximum at about 75-100 mg/kg. This was true for both histopathology and biochemical parameters of liver dysfunction. When animals were depleted of taurine using beta-alanine pretreatment, the toxicity of DAPM was increased. Conversely treatment of rats with taurine, significantly attenuated the rise in alanine transaminase (ALT). However depletion of taurine with guanidinoethanesulphonate (GES) attenuated rises in both transaminases. It is concluded that taurine may play a role in the toxicity of DAPM but that GES, although depleting taurine as does beta-alanine, causes additional effects such as increasing glutathione (GSH), perhaps leading to protection.
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PMID:Modulation of taurine levels in the rat liver alters methylene dianiline hepatotoxicity. 932 19

The aim of this investigation was to determine serum levels of vitamin A, E, beta carotene, glutathione peroxidase (GSHPx), lipid peroxidation (MDA) and biochemical and haematological parameters during enflurane anaesthetised dogs. Ten kangal dogs were used and all animals were anaesthetised with enflurane for two hours and blood samples were taken before and 30, 120 minutes, 24 hours and 7 days during the anaesthesia. Vitamin E and beta carotene content were significantly (p<0.05 and p<0.01) higher before anaesthesia than after whereas serum GSHPx activity was not statistically different. However, serum levels of vitamin A and MDA were significantly (p<0.05) increased during the anaesthesia. In general, serum levels of aspartate aminotransferase, alanine aminotransferase, albumin, glucose, urea and creatinine were significantly (p<0.05 and p<0.01) increased during anaesthesia and returned to near normal values after 7 days of anaesthesia, whereas the white blood cell count was significantly (p<0.05 and p<0.01) decreased during the anaesthesia. However, the red blood cell count, haemoglobin and packed cell volume values, and levels of total cholesterol, triglycerides, total protein and globulin were apparently not influenced by the anaesthesia. In conclusion, we observed that the serum level of vitamin E and beta carotene were significantly decreased, whereas serum MDA and vitamin A levels were significantly increased during the enflurane anaesthesia.
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PMID:The levels of some antioxidant vitamins, glutathione peroxidase and lipoperoxidase during the anaesthesia of dogs. 1045 42

It has been found out that the carbon tetrachloride (CCl4)-induced increase of serum glutamic-pyruvic transaminase (ALT) and elevation of MDA in liver of mice are significantly lowered by Phyllanthus urinaria in vivo, and the coincubation of isolated rat hepatocytes with Phyllanthus urinaria in vitro significantly inhibits CCl4-induced decrease of mobility of membrane of liver cells and increase of intracellular free Ca2+ ([Ca2+]i) concentrations of liver cells. These results suggest that the anti-lipid peroxidation effect and protective action of membrane of Phyllanthus urinaria may be related to its protective action against CCl4-induced liver injuries.
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PMID:[Mechanism of protective action of Phyllanthus urinaria L. against injuries of liver cells]. 1074 6

Pregnyl (hCG), a preparation of human chorionic gonadotropin, was evaluated for its effects on the endocrinological, biochemical and genotoxic changes in female Swiss albino mice. hCG treatment at different doses (25, 50 and 100 I.U./Kg/day) for 5 days was found to significantly increase the plasma levels of hCG, estradiol and progesterone in a dose-dependent manner, while the concentrations of LH and FSH remained below the detection levels. The plasma levels of ALT, CK-MB, creatinine and urea were significantly decreased, whereas the concentrations of AST were significantly increased. The treatment was found to significantly increase and decrease the hepatic concentrations of MDA and NP-SH respectively. The hepatic levels of proteins and DNA were not affected, but there was a significant increase in the concentrations of RNA. In addition, hCG treatment did not show any effect on the frequency of occurrence of micronuclei, whereas the ratio of PCE/NCE was found to be significantly increased. These results demonstrate that the hCG treatment in mice affected the pituitary-ovarian hormones in a similar pattern to that of humans. The treatment increased oxidative stress in hepatic cells without disturbing the functions of the liver as well as other organs. This finding may be of value concerning the safe use of hCG and may contribute to the overall antioxidant balance in the body.
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PMID:Evaluation of the effects of pregnyl on pituitary-ovarian hormones and biochemical markers of tissue injury in female Swiss albino mice. 1085 Mar 79

The liver injury was induced by intestinal ischemia-reperfusion and the protective effect of erigeron injection (EI) was studied in mice. The results showed that serum alanine transaminase (ALT) and glutathione S-transferase (GST) activity increased while the root of superior mesenteric artery was blocked with non-injury artery clap for 20 minute and reperfusion for 1 hour. EI could protect the above changes induced by intestinal ischemia-reperfusion. EI could reduce the activities of serum ALT and GST, decrease the content of hepatic MDA and significantly increase the activity of SOD. The pathological changes of hepatocytes induced by intestinal ischemia-reperfusion were less in EI groups. These results suggested that EI could protect the liver of mice from injury induced by intestinal ischemia-reperfusion. One of the mechanisms of hepatoprotective action was related to the antioxidative function of erigeron.
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PMID:[Protective effect of erigeron injections on hepatotoxicity induced by intestinal ischemia-reperfusion in mice]. 1132 58

Cotreatment of rats with a low hepatotoxic dose (30.7 mg/kg, i.p.) of allyl alcohol (AA) and a higher, but nontoxic, dose (150 mg/kg, oral) of caffeine (CF) potentiated the hepatotoxicity of AA. This was verified by significantly higher levels of plasma alanine aminotransferase (ALT) activity and histopathologically greater severity of lesions in the periportal hepatocytes than those due to AA alone. Treatment of rats with 4-methylpyrazole (4-MP) (0.5 mmol/kg, i.p.) (an inhibitor liver alcohol dehydrogenase) for 30 minutes, followed by similar cotreatment with AA and CF, completely prevented the elevation of plasma levels of ALT and histological damage induced by cotreatment with CF and AA 24 hours following their administration. Severe liver damage induced by cotreatment with CF and AA was further, markedly enhanced by phenobarbital pretreatment (80 mg/kg, i.p., 3 days). Thus, extensive necrosis of periportal hepatocytes was noted, as well as edema and accumulation of inflammatory cells in the necrotic foci caused by such pretreatment. The depression of hepatic nonprotein sulfhydryls resulting from CF plus AA was much more severe than that caused by AA or CF alone and appeared as early as 30 minutes after administration. However, much less marked depletion of protein thiols was observed following similar treatments. Significant increase in lipid peroxidation (as measured by melondialdehyde [MDA] formation) was also observed in rat liver but only 24 hours after administration. The production ofMDA in the rat liver was significantly higher after administration of AA plus CF than after administration of AA alone. Pretreatment of rats with phenobarbital further significantly enhanced the formation of 2,4-dinitrophenylhydrazine (DNP)-reactive metabolite(s) (measured as DNP-acrolein adduct equivalents) in rat liver induced by AA (30.7 mg/kg) plus CF (150 mg/kg) within 1 hour following such treatment. Cotreatment with AA and a higher dose of CF resulted in significantly higher excretion of urinary thioethers or mercapturic acids than in rats treated with AA alone. Thus, these data suggest that an increased bioactivation pathway of acrolein involving a P450 mixed-function oxidase system caused by CF may be involved in such potentiating effects of CF on AA-induced hepatotoxicity in rats.
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PMID:Influence of caffeine on allyl alcohol-induced hepatotoxicity in rats. I. In vivo study. 1139 13

This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd.
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PMID:Effect of cadmium and aluminum intake on the antioxidant status and lipid peroxidation in rat tissues. 1167 49

The protective effects of betaine in ethanol hepatotoxicity were investigated in 24 female wistar albino rats. Animals were divided into three groups: control, ethanol and ethanol + betaine group. Animals were fed liquid diets and consumed approximately 60 diet per day. Rats were fed ethanol 8 kg(- 1) day(- 1). The ethanol + betaine group were fed ethanol plus betaine (0.5% w/v). All animal were fed for 2 months. Reduced glutathione, malondialdehyde and vitamin A were determined in the liver tissue. Alanine aminotransferase activities were also measured on intracardiac blood samples. GSH levels in the ethanol group were significantly lower than these in the control group (p < 0.001). GSH was elevated in the betaine group as compared to the ethanol group (p < 0.001). MDA in the ethanol group was significantly higher than that in the control group (p < 0.05). MDA was decreased in the betaine group as compared to the ethanol group (p < 0.05). Vitamin A in the ethanol group was significantly lower than that in the control group (p < 0.01), but, in the ethanol + betaine group it was high compared with the ethanol group (p < 0.01). ALT in the ethanol group was higher than that in the control group (p < 0.05). Oxidative stress may play a major role in the ethanol-mediated hepatotoxicity. Betaine may protect liver against injury and it may prevent vitamin A depletion. Therefore, it may be a useful nutritional agent in the prevention of clinical problems dependent on ethanol-induced vitamin A depletion and peroxidative injury in liver.
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PMID:Ethanol-induced hepatotoxicity and protective effect of betaine. 1174 10


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