Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Measurement of the serum enzyme activity is generally used as a screening test for hepatic and biliary diseases. The purpose of this study is to examine the use of serum enzyme activity as indices of health by analyzing relationships to changes in nutrient intakes. The results obtained were as follows: In cross-sectional studies gamma-GTP (1) and LDH-4 and -5 isozyme levels had a significant negative correlation to dietary intakes of vitamin C and protein, but total serum gamma-GTP and LDH activities had no correlation. Intake trials of these nutrients showed that high intake levels of vitamin C related to decrease in isozymes levels while low protein intake resulted in increases. Serum GPT activity had a negative relationship to vitamin C intake in men, but was not correlated with nutrient intakes in women. Serum ALP activity was affected positively with vitamin B intake in 40-79 year old men and women. There were statistically significant correlations between serum cholinesterase activity and energy, and food intake patterns.
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PMID:[Relationship of nutrient intake to serum enzyme activity]. 824 33

Cross-sectional interactions by malaria status were investigated between plasma alpha-tocopherol, retinol, and several carotenoids (lutein, beta-cryptoxanthin, lycopene, and alpha- and beta-carotene) and indicators of disease severity (blood parasite count, hemoglobin concentration), acute-phase response (plasma albumin and ceruloplasmin concentrations), hepatic involvement (plasma alanine aminotransferase), oxidant status and antioxidant status (plasma thiobarbituric acid-reactive material and ascorbate), nutritional (weight-for-age) and carrier protein [retinol binding protein (RBP)] status, and cholesterol concentration (as a proxy for lipoprotein) in 100 consecutively admitted children with malaria. There were 50 children with severe and 50 with mild malaria and 50 age- and sex-matched control subjects. alpha-Tocopherol, retinol, and all the carotenoid concentrations were lower in the patients than in the control subjects (P < 0.001). The differences were greater in severe than in mild malaria, except for lutein. In severe malaria only, both retinol and alpha-tocopherol correlated with albumin, ceruloplasmin, and RBP concentrations whereas in all three groups retinol correlated with RBP and alpha-tocopherol correlated with cholesterol (all P < 0.01)). Using multivariate analysis on data from all patients combined, cholesterol was the most significant factor explaining the variance in alpha-tocopherol (29%) whereas RBP was responsible for 95% of the variance in retinol. Plasma cholesterol and RBP values in turn (in the absence of alpha-tocopherol and retinol, respectively) were influenced primarily by acute-phase markers (mainly albumin and ceruloplasmin). Alanine aminotransferase (r = -0.17) and thiobarbituric acid-reactive material (r = -0.17) also showed a small contribution to the variance of RBP but 60-70% remained unexplained. In conclusion, low plasma lipid-soluble micronutrient concentrations in malaria are strongly influenced by the reductions in their carrier molecules, which, in turn, are low as a consequence of the acute-phase response.
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PMID:Plasma alpha-tocopherol, retinol, and carotenoids in children with falciparum malaria. 866 21

The hepatoprotective effect of the shark bile salt 5beta-scymnol has been studied in the model of acute hepatotoxicity induced by administration of acetaminophen (APAP, paracetamol). 5beta-Scymnol at doses of 20, 35, and 70 mg/kg intraperitoneally (ip) decreased significantly the serum activity of alanine aminotransferase, sorbitol dehydrogenase, and lactate dehydrogenase (p < 0.05) caused by APAP treatment (350 mg/kg ip) alone. The highest dose of 5beta-scymnol remained hepatoprotective when administered 4 hr after the APAP overdose. N-Acetylcysteine (NAC) is protective against APAP-induced hepatotoxicity at 250 and 500 mg/kg (ip) when administered up to 3 hr after APAP overdose, as shown by a significant reduction in serum enzyme activity. Coadministration of 5beta-scymnol (70 mg/kg) and NAC (250 mg/kg) also reduced serum enzyme levels and histopathological effects; however, a similar level of hepatoprotection was conferred by 5beta-scymnol treatment alone. In addition, 5beta-scymnol has potent hydroxyl radical quenching activity as it markedly inhibited deoxyribose degradation in a ferrous/ascorbate Fenton reaction system. These results indicate a possible role for the use of 5beta-scymnol, either alone or concomitant with NAC, in the prevention of hepatic necrosis following toxic doses of APAP.
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PMID:Hepatoprotective effects of the shark bile salt 5beta-scymnol on acetaminophen-induced liver damage in mice. 881 14

An experiment was conducted to study the efficacy of two tomato pastes and aronia nectar (fruit juice + pulp from the black chokeberry, Aronia melanocarpa Elliot) as inhibitors of nitrosamine production in cancer prophylaxis programmes. White male rats of the Wistar strain were employed in an acute trial. Aminopyrin+sodium nitrite (APSN) were used as precursors for generation of endogenous nitrosamine. The animals were allocated to different dietary groups and fed by intubation with APSN or APSN + food products. Introduction of tomato paste (TP), high-beta-carotene tomato paste (HCTP) and aronia nectar (AN) as inhibitors of N-nitrosamine formation exerted a positive effect on blood and liver variables which was demonstrated by decreased concentrations of glutamic-oxaloacetic transaminase (EC 2.6.1.1), glutamic-pyruvic transaminase (EC 2.6.1.2) and uric acid in serum and lipid content in hepatocytes. Animals treated with APSN developed dystrophic changes in liver such as centrolobular necrosis, intense exangia, and enlarged cells with two, often large, pyknotic nuclei, while the structure of livers of rats fed with TP, HCTP or AN was well protected and almost normal. TP had a particularly beneficial effect on serum total protein and albumin concentrations as had AN on the urea value. The inhibitory effect of the food products used is explained by their chemical nature including pH, ascorbic index (ascorbate:nitrate), lycopene and beta-carotene contents.
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PMID:Effect of food products on endogenous generation of N-nitrosamines in rats. 930 22

Thymoquinone (TQ) is the major active component of the volatile oil of Nigella sativa seeds. The effects of TQ on carbon tetrachloride (CCl4)-induced hepatotoxicity was investigated in male Swiss albino mice. Carbon tetrachloride (20 microliters/Kg, i.p.) injected into mice, induced damage to liver cells and was followed by the increase in serum alanine aminotransferase (ALT) activity after 24 h. Oral administration of TQ in a single dose (100 mg/Kg) resulted in significant (p < 0.001) protection against the hepatotoxic effects of CCl4. TQ was tested as a substrate for mice hepatic DT-diaphorase in the presence of NADH. TQ appears to undergo reduction to dihydrothymoquinone (DHTQ). Reduction rates as a function of protein (liver homogenate) and substrate (TQ) concentrations are reported. An apparent K(m) of 0.1 mM and an apparent Vmax of 74 mumol/min/g liver were measured. TQ and DHTQ inhibited the in vitro non-enzymatic lipid peroxidation in liver homogenate (induced by Fe(3+)-ascorbate) in a dose dependent manner. In this in vitro model DHTQ was more potent in comparison with TQ and butylated hydroxytoluene (BHT). The IC50 for DHTQ, TQ and BHT were found to be 0.34, 0.87 and 0.58 microM respectively. The data suggest that the in vivo protective action of TQ against CCl4-induced hepatotoxicity may be mediated through the combined antioxidant properties of TQ and its metabolite DHTQ.
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PMID:Thymoquinone protects against carbon tetrachloride hepatotoxicity in mice via an antioxidant mechanism. 1009 55

The protective action of thymol (paramethyl-isopropyl-phenol) was investigated against carbon tetrachloride (CCl(4))-induced hepatotoxicity in male Swiss albino mice. The CCl(4)at a dose of 20 microl kg(-1)produced damage to liver cells and was followed by the significant increase (P<0.001) in serum alanine aminotransferase (ALT) activity and hepatic lipid peroxidation after 24 h. The hepatocellular necrosis was further confirmed by histopathological examination of liver section. Oral administration of thymol in a single dose (300 mg kg(-1)) resulted in significant (P<0.05) amelioration of CCl(4)-induced hepatotoxicity. Thymol also inhibited lipid peroxidation induced by CCl(4)in vivo. The protection offered by thymol was also evident from histopathology photomicrograph. In a separate in vitro assay, thymol inhibited the non-enzymatic lipid peroxidation of normal mice liver homogenate induced by Fe(3+)-ascorbate. The present study suggests that thymol protects the liver against CCl(4)-induced toxicity and the protection may be mediated through its ability to inhibit lipid peroxidation. However, other interactions between thymol and CCl(4)remains to be elucidated. 1999 Academic Press.
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PMID:The protective action of thymol against carbon tetrachloride hepatotoxicity in mice. 1043 75

The effects of thymoquinone (TQ) and desferrioxamine (DFO) against carbon tetrachloride (CCl4)-induced hepatotoxicity were investigated. A single dose of CCl4 (20 microl/kg, i.p.) induced hepatotoxicity, manifested biochemically by significant elevation of activities of serum enzymes, such as alanine transaminase (ALT, EC: 2.6.1.2) , aspartate transaminase (AST, EC: 2.6.1.1) and lactate dehydrogenase (LDH, EC: 1.1.1.27). Hepatotoxicity was further evidenced by significant decrease of total sulfhydryl (-SH) content, and catalase (EC: 1.11.1.6) activity in hepatic tissues and significant increase in hepatic lipid peroxidation measured as malondialdhyde (MDA). Pretreatment of mice with DFO (200 mg/kg i.p.) 1 h before CCl4 injection or administration of TQ (16 mg/kg/day, p.o.) in drinking water, starting 5 days before CCl4 injection and continuing during the experimental period, ameliorated the hepatotoxicity induced by CCl4, as evidenced by a significant reduction in the elevated levels of serum enzymes as well as a significant decrease in the hepatic MDA content and a significant increase in the total sulfhydryl content 24 h after CCl4 administration. In a separate in vitro assay, TQ and DFO inhibited the non-enzymatic lipid peroxidation of normal mice liver homogenate induced by Fe3+/ascorbate in a dose-dependent manner. These results indicate that TQ and DFO are efficient cytoprotective agents against CCl4-induced hepotoxicity, possibly through inhibition of the production of oxygen free radicals that cause lipid peroxidation.
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PMID:Protective effects of thymoquinone and desferrioxamine against hepatotoxicity of carbon tetrachloride in mice. 1088 36

In a prospective, randomized, double-blind therapeutic trial, 191 patients with non-alcoholic steatohepatitis were treated for 8 weeks daily b.i.d. orally either with betaine glucuronate combined with diethanolamine glucuronate and nicotinamide ascorbate (Ietepar) (96 patients) or with undistinguishable placebo capsules (95 patients). The verum treatment effectively reduced by 25% hepatic steatosis (p < 0.01) and by 6% hepatomegaly (p < 0.05), while placebo did not significantly reduce the disorders. Verum was also more effective than placebo on discomfort in abdominal upper right quadrant. The global efficacy of treatment was rated by the doctor "very good" or "good" in 48% of verum treated patients and only in 17% after placcbo (P of difference = 9 x 10(-6)). 52% of patients self-rated efficacy as "very good" or "good" after verum and only 34% after placebo (P of difference = 0.017). The verum treatment provoked a significant reduction of the increased liver transaminases (ALT, AST and gamma-GT) while placebo was ineffective. Adverse events were recorded in 10% of verum-treated patients and in 7% under placebo (no significant difference). In both groups the adverse events were mild and transient, did not require treatment discontinuation and were undistinguishable from common symptoms of liver disorders. In conclusion, the 8-week treatment with betaine glucuronate combined with diethanolamine glucuronate and nicotinamide ascorbate was found effective in non-alcoholic steatohepatitis, a disorder for which the hitherto pharmacological interventions were poorly and inconsistently effective.
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PMID:Efficacy and safety of oral betaine glucuronate in non-alcoholic steatohepatitis. A double-blind, randomized, parallel-group, placebo-controlled prospective clinical study. 1099 56

Piper betle L. is a commonly used masticatory in Asia. This study was carried out to investigate the hepatoprotective and antioxidant properties of P. betle, using ethanol intoxication as a model of hepatotoxic and oxidative damage. Ethanol-treated rats exhibited elevation of hepatic marker enzymes and disturbances in antioxidant defense when compared with normal rats. Oral administration of P. betle extract (100, 200, or 300 mg/kg body weight) for 30 days significantly (P <.05) decreased aspartate aminotransferase (AST), alanine aminotransferase (ALT), thiobarbituric acid reactive substances (TBARS), and lipid hydroperoxides in ethanol treated rats. The extract also improved the tissue antioxidant status by increasing the levels of nonenzymatic antioxidants (reduced glutathione, vitamin C, and vitamin E) and the activities of free radical-detoxifying enzymes such as superoxide dismutase, catalase, and glutathione peroxidase in liver and kidney of ethanol-treated rats. The highest dose of P. betle extract (300 mg/kg body weight) was most effective. The results were comparable with the known hepatoprotective drug, silymarin. These results indicate that P. betle could afford a significant hepatoprotective and antioxidant effect.
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PMID:Influence of Piper betle on hepatic marker enzymes and tissue antioxidant status in ethanol-treated Wistar rats. 1263 94

Previous studies have implied a relationship between Se-deficiency and oxidative stress. In the present study, the occurrence of oxidative stress due to Se-deficiency was investigated by evaluating the age dependence of growth and indices of oxidative damage for the liver of Se-deficient (SeD) rats. The ratios of liver weight to body weight of the SeD rats were greater than those of the normal rats. The values of AST and ALT (clinical indices of liver damage) were higher in the SeD rats than the normal ones especially in the young (6-12 weeks of age). The TBARS level of the 4-week-old SeD group were higher than the normal group while the level decreased with age. Conversely, the TBARS level of the normal group gradually increased and became higher than SeD group in older rats (12-20 weeks of age). Vitamin E rather than vitamin C may be consumed during oxidative stress due to Se-deficiency. Damage induced by Se-deficiency may be related to growth and the mechanisms of this damage may alter with age.
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PMID:Evaluation of oxidative damage in the liver of selenium-deficient rats. 1268 28


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