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)

Pollution, industrial solvents, concentrations of metals and other environmental agents are widely related to biochemicals values which are used in disease diagnosis of environmental toxicity. A rat bioassay validated for the identification of toxic effects of eutrophication revealed increased serum activities of amylase, alanine transaminase (ALT) and alkaline phosphatase (ALP) in rats that received algae, filtered water and nickel or cadmium from drinking water. Serum Cu-Zn superoxide dismutase activity decreased from its basal level of 40.8 +/- 2.3 to 26.4 U/mg protein, at 7 days of algae and at 48 hr of nickel and cadmium water ingestion. The observation that lipoperoxide concentration was not altered in rats treated with filtered water, while amylase, ALT and ALP were increased in these rats and in those treated with nickel or cadmium, indicated that pancreatic, hepatic and osteogenic lesions by eutrophication were not related to superoxide radicals, and might be due to a novel toxic environmental agent found in filtered and non-filtered algae water.
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PMID:Toxic effects of water eutrophication on pancreatic, hepatic and osteogenic tissues of rats. 753 73

The effects of N-benzyl-D-glucamine dithiocarbamate (BGD), diethyldithiocarbamate (DDTC), and N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD) on the enzymatic activities in mice were studied. The mice were given i.v. injections of these chelating agents (1 mmol/kg) and 3 h later the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (gamma-GTP), alkaline phosphatase (ALP), leucine aminopeptidase (LAP), and cholinesterase (ChE) in the liver, kidney, and blood were determined. These enzymatic activities were little changed by treatment with these chelating agents. Cadmium (Cd) administration markedly decreased the activities of AST and ALT in the liver and kidney and greatly increased these enzymatic activities in blood. The changes in the enzymatic activities by treatment with Cd were prevented by injection of BGD (1 mmol/kg). These results indicate that BGD, DDTC, and HBGD were not toxic to the liver or kidney of mice and that BGD treatment protected against the acute hepatic and renal toxicity induced by Cd.
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PMID:Effects of dithiocarbamates and cadmium on the enzymatic activities in liver, kidney and blood of mice. 762 88

The purpose of this study was to compare the hepatoprotective effects of seven Chinese herbal compounds/mixtures on four known hepatotoxicants in mice. These compounds include fulvotomentosides oleanolic acid, total saponins of Panax japonicus (Jgs), total saponins of Panax notoginseng (Ngs), sweroside, oxymatrine, and dimethyl dicarboxylate biphenyl (DDB). All have previously been reported to exhibit hepatoprotective effects. Acute liver injury was produced in male CF-1 mice by CCl4, acetaminophen, cadmium chloride and allyl alcohol. Liver damage was assessed by quantifying serum activities of sorbitol dehydrogenase and alanine aminotransferase, as well as by histopathological examination. Fulvomentosides markedly decreased the toxicity produced by all four hepatotoxicants; oleanic acid also remarkably decreased acetaminophen, CCl4 and Cd-induced hepatotoxicity, but had no effect on allyl alcohol; total saponins of Panax japonicus and Panax notoginseng had moderate hepatoprotective effects on these models except that total saponins of Panax japonicus markedly decreased allyl alcohol toxicity; sweroside decreased Cd and CCl4 toxicity but had no effect on the other two hepatotoxicants; oxymatrine only decreased allyl alcohol toxicity; whereas DDB did not protect against any of the hepatotoxicants. The mechanism(s) by which these compounds/mixtures protect against different types of hepatotoxicants requires further investigation. In conclusion, of the seven compounds examined, fulvotomentoside and oleanolic acid appear to be the most effective in protecting against chemical-induced liver injury.
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PMID:The effect of Chinese hepatoprotective medicines on experimental liver injury in mice. 793 88

The purpose of this study was to compare the hepatoprotective effects of 10 oleanane-type triterpenoid compounds on three known hepatotoxicants in mice. These compounds include oleanolic acid, ursolic acid, uvaol, alpha-hederin (alpha-H), hederagenin, glycyrrhizin, 18 alpha-glycyrrhetinic acid (alpha-GA), 18 beta-glycyrrhetinic acid (beta-GA), 19 alpha-hydroxyl asiatic acid 28-O-beta-D-glucoside (HAG), and 19 alpha-hydroxyl asiatic acid (HA). They were administrated sc for 3 days at 200 mumol/kg, except for alpha-H, which was given at 100 mumol/kg for 2 days. Acute liver injury was produced in male CF-1 mice by CCl4 (15 microliters/kg, ip), acetaminophen (500 mg/kg, ip), and cadmium chloride (3.7 mg/kg, iv). Liver damage was assessed by serum activities of alanine aminotransferase and sorbitol dehydrogenase, as well as by histopathological examination. alpha-Hederin, ursolic acid, and oleanolic acid markedly decreased the toxicity produced by all three hepatotoxicants. Uvaol significantly decreased CCl4- and Cd-induced hepatotoxicity, but had no effect on acetaminophen toxicity. Glycyrrhizin, alpha-GA, and beta-GA decreased acetaminophen-induced liver injury, whereas hederagenin, HAG, and HA did not protect against any of the hepatotoxicants. In addition, alpha-hederin, ursolic acid, oleanolic acid, and uvaol increased hepatic metallothionein levels by 87-, 48-, 28-, and 10-fold, respectively, as determined by the Cd/hemoglobin assay. In conclusion, among the 10 triterpenoid compounds examined, alpha-hederin, ursolic acid, and oleanolic acid appear to be the most effective in protecting against CCl4-, acetaminophen-, and Cd-induced liver injury.
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PMID:The effects of 10 triterpenoid compounds on experimental liver injury in mice. 812 11

Oleanolic acid (OA) is a triterpenoid compound that has been shown to protect against some hepatotoxicants and is used in China to treat hepatitis. This study was conducted to examine the protective effects of OA against cadmium (Cd)-induced liver injury in mice and the mechanism of protection. OA (100 mg/kg x 3 days) pretreatment dramatically decreased Cd (3.7 mg/kg i.v.)-induced liver injury as indicated by decreased serum activities of alanine aminotransferase and sorbitol dehydrogenase, as well as by histopathological observation. To examine the mechanism of protection, the distribution of Cd to major organs and the hepatic subcellular distribution of Cd were determined 2 hr after 109Cd injection (3.5 mg/kg of Cd and 10 microCi/mg of Cd i.v.). OA did not reduce the amount of Cd in liver, but significantly altered the hepatic subcellular distribution of Cd, with more Cd in hepatic cytosol bound to metallothionein (MT), and with less Cd in other organelles and proteins. OA produced an approximately 30-fold increase in hepatic MT, but had no appreciable effects on MT levels of five other organs. Furthermore, OA increased both hepatic MT-I and MT-II levels, as determined by high-performance liquid chromatography/atomic absorption spectrophotometry. Northern blot analysis revealed that OA increases MT mRNA expression. In summary, OA pretreatment protects against Cd-induced hepatotoxicity by inducing MT. MT bound Cd in the cytosol, and thus decreased the amount of Cd in other critical organelles and proteins. OA is a hepatic MT inducer for both MT-I and MT-II isoforms, and this effect is due, at least in part, to an increased MT mRNA accumulation.
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PMID:Oleanolic acid protects against cadmium hepatotoxicity by inducing metallothionein. 833 68

alpha-Hederin (alpha-Hed) is a triterpenoid saponin that has been shown to protect against some hepatotoxicants. This study examined the protective effect of alpha-Hed against cadmium (Cd) hepatotoxicity and the mechanism of protection. alpha-Hed pretreatment (100 mumol/kg, sc) dramatically decreased Cd (3.7 mg/kg, iv) hepatotoxicity as indicated by a reduction of serum alanine aminotransferase and sorbitol dehydrogenase, as well as by histopathological examination. alpha-Hed did not produce protection by decreasing the distribution of Cd to the liver, as higher amounts of Cd were found in the liver of alpha-Hed-pretreated mice. However, there was a marked alteration in subcellular distribution of Cd in the alpha-Hed-pretreated mice, with much less Cd distributing to nuclei, mitochondria, and microsomes and more in the cytosol. The increased cytosolic Cd was found primarily bound to a low-molecular-weight protein, metallothionein (MT). alpha-Hed (10-300 mumol/kg, sc) produced a dose-dependent increase in hepatic MT with a 100-fold increase over controls 24 hr after a single injection of 100 mumol/kg, as determined by the Cd/hemoglobin assay. The hepatic MT increase produced by alpha-Hed is relatively long lasting, in that it is still eight times control values 6 days after a single administration. The induction of MT was also relatively specific for the liver, as little or no increase in MT was observed in other tissues. Furthermore, alpha-Hed increased both hepatic MT-I and MT-II levels. Northern blot analysis revealed that alpha-Hed rapidly increased MT mRNA levels. In conclusion, alpha-Hed decreases the hepatotoxicity of Cd by inducing MT, which binds Cd in the cytosol, and thus reduces the amount of Cd in the critical cellular organelles. alpha-Hed is an effective inducer of both MT-I and MT-II in liver, and this effect is associated with an increase in MT mRNA.
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PMID:Induction of metallothionein by alpha-hederin. 833 95

The toxicity of cadmium (Cd) chloride was studied in ovariectomized (OX) female rats and non-OX female rats after intravenous administration of the compound at doses of 2.0 and 3.0 mg/kg for 14 days. Mild hypochromic microcytic anemia developed in all rats treated with Cd, but growth retardation in the OX rats was more prominent than that in the non-OX rats. There was an increase of AST and ALT and a decrease of total cholesterol and the A/G ratio in both OX and non-OX rats treated with Cd. The hepatic and renal Cd concentrations increased in a dose-dependent manner, and the concentrations in both organs on Day 14 were comparable in the 3.0 mg/kg OX group (liver, 270.0 +/- 39.6 micrograms/g; kidney, 121.3 +/- 10.1 micrograms/g) and non-OX group (liver, 277.0 +/- 29.9 micrograms/g; kidney, 100.8 +/- 1.3 micrograms/g). Hepatocyte necrosis developed only in OX rats treated with Cd, and the nephrotoxicity of Cd was also notably enhanced by ovariectomy, since Cd nephropathy affected the proximal convoluted epithelium more severely and more frequently in OX rats than in non-OX rats. BrdU-labeled cells in the renal cortex were increased by approximately 2.7-fold in OX rat (7.4 cells/mm2) over those in the renal cortex in non-OX rat (2.7 cells/mm2). In conclusion, the present study demonstrated that ovariectomy enhanced Cd-induced nephrotoxicity and hepatotoxicity in rats.
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PMID:Ovariectomy enhances cadmium-induced nephrotoxicity and hepatotoxicity in rats. 848 Mar 35

The purpose of this study was to determine whether metallothionein-I (MT-I) transgenic female mice (MT-TG) are resistant to cadmium (Cd) hepatotoxicity. Female MT-TG mice have 10- to 20-fold higher MT concentrations in liver than control mice and are more resistant to Cd-induced lethality than control mice. CdCl2 (3.7 mg Cd/kg, iv) was lethal to 73% of control mice, but only to 13% of MT-TG mice. Cd administration (3.1 mg/kg, iv) to control mice produced extensive liver injury as evidenced by 20- and 70-fold increases in serum enzyme activities of sorbitol dehydrogenase and alanine aminotransferase, respectively. MT-TG mice are considerably more resistant to Cd-induced hepatotoxicity than control mice, as evidenced by only about one-tenth the elevation in serum enzymes observed in control mice and a lower incidence of hepatocyte necrosis in MT-TG mice. To ascertain the mechanism of this protection, the distribution of Cd to various organs and the subcellular distribution of Cd in liver were determined 2 hr after Cd injection (109CdCl2, 3.5 mg Cd/kg, iv). The hepatic subcellular distribution of Cd was altered markedly in MT-TG mice, with much less Cd distributing to nuclei, mitochondria, and microsomes (25, 42, and 24% of controls, respectively), and more Cd to the cytosol (240% of controls). The increased cytosolic Cd was bound primarily to MT, as determined by G-75 gel chromatography. In addition, primary hepatocyte cultures from MT-TG mice maintained higher levels of MT than hepatocytes from control mice and were more resistant to Cd cytotoxicity than control hepatocytes. In conclusion, studies using MT-I transgenic mice demonstrate that MT protects against Cd lethality and hepatotoxicity, and this hepatoprotective effect of MT is also observed in hepatocyte cultures from MT-TG mice.
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PMID:Transgenic mice that overexpress metallothionein-I are protected from cadmium lethality and hepatotoxicity. 854 31

Sodium arsenite and cadmium chloride, were administered orally to adult female rats at 21 and 4 h prior to sacrifice. Liver, lung, skin and urinary bladder were the tissues studied. DNA damage, cytochrome P450, glutathione content (GSH), ornithine decarboxylase (ODC), serum alanine aminotransferase and heme oxygenase activity were measured. Sodium arsenite increased rat hepatic ODC activity at 1.6 and 24.6 mg/kg and hepatic heme oxygenase activity at 8.2 and 24.6 mg/kg, but did not cause any DNA damage. Cadmium chloride did not affect any of the six parameters tested. These findings suggest that sodium arsenite may be a promoter rather than an initiator of carcinogenesis.
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PMID:Arsenite, but not cadmium, induces ornithine decarboxylase and heme oxygenase activity in rat liver: relevance to arsenic carcinogenesis. 855 13

Selected serum parameters of metabolic profile and distribution of cadmium in reproductive organs in rabbits were studied after an acute and subchronic administration. After an i.p. application of cadmium (1.5 mg.kg-1) a significant increase of glucose (5.90 mmol.l-1) and cholesterol (2.22 mmol.l-1) was observed. There were no significant differences in these parameters after the subchronic (5 month) p.o. application. The concentration of AST and ALT significantly decreased after a subchronic p.o. administration (1.0 mg.kg-1) but not after an acute i.p. application. There were no significant differences in the level of total proteins and total lipids. The highest accumulation in reproductive organs (testis, ovary, uterus) was observed after i.p. administration. The level in the testis was 40 times higher than in the control group (0.04 mg.kg-1; 1.93 mg.kg-1), 174 times higher in the ovary (0.03; 5.21) and 65 times higher in the uterus (0.04; 2.59). After a subchronic p.o. application, the concentration was only 2.5 times higher in the testis (0.04; 0.10), 16 times higher in the ovary and 6 times higher in the uterus than in the control group.
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PMID:Evaluation of selected parameters of a metabolic profile and levels of cadmium in reproductive organs of rabbits after an experimental administration. 885 52


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