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)

Captafol fed at concentrations of 0, 0.075, 0.15, 0.3, and 0.6% to both sexes of F344 rats for 13 weeks produced dose-related decreases in body weight in males and females given 0.15% or higher concentrations. A dose-dependent decrease in urinary pH was observed in males receiving 0.3 or 0.6% and in females given 0.15% or higher concentrations of captafol. The 0.3 and 0.6% doses produced slight increases in leukocyte count and glutamic-pyruvic transaminase activity in females, along with a mild increase in alkaline phosphatase activity in the 0.6% case. The liver- and kidney-to-body weight ratios were increased in both male and female rats. Histopathological changes were observed in the forestomach, liver, and kidney. Squamous cell hyperplasia and edema accompanied by polynuclear leukocyte infiltration and dilation of vessels in the lamina propria were observed in the forestomach of both sexes given 0.15% or higher concentrations. Oval cell proliferation was apparent around Glisson's sheath in the livers of females given 0.3 and 0.6% captafol. Multifocal appearance of karyocytomegaly and tubular cell atypia in the proximal tubules of the kidney was found in the 0.3 and 0.6% groups of both sexes.
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PMID:13-Week oral toxicity study of captafol in F344/DuCrj rats. 176 26

Hepatic dysfunction is a frequent finding in sepsis and peritonitis. In the present study, hepatic function in experimental peritonitis in the rat was determined by measuring serum levels of bilirubin, alkaline phosphatase (ALP), glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT), together with antipyrine (AP) clearance as a determinant of microsomal function. Peritonitis was induced by intraperitoneal injection of 3 x 10(8) colony-forming units of E. coli together with either 1.0 ml bile or saline. E. coli + bile peritonitis rats had significantly elevated levels of bilirubin, ALP, GOT and GPT as compared with both controls and rats with peritonitis induced by E. coli alone. The derangements gradually increased with time over the 10-hour period studied. In contrast, no reduction of AP clearance was observed in the peritonitis models. On the contrary, AP clearance was enhanced at 10 hours after induction of peritonitis by E. coli alone. In conclusion, hepatic dysfunction as revealed by routine laboratory tests is seen early in experimental peritonitis in the rat, but this is not accompanied by a reduced AP clearance rate.
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PMID:Effect of bile on liver function tests in experimental E. coli peritonitis in the rat. 176 53

The pulmonary biochemical response, particularly the effects on mixed-function oxidases, was investigated in rats exposed to 40 ppm furfural for 1 h daily, 5 days per week, for periods of 7, 15 and 30 days. This concentration is ca. 22% of the acute LC50 dose. Exposure to furfural increased the activities of acid and alkaline phosphatases and glutamic-pyruvic transaminase, inhibited the activities of arginase and succinic dehydrogenases and elevated the concentration of lactic acid in the lungs. In the group of mixed-function oxidases, the activities of aminopyrene-N-demethylase and aniline hydroxylase (phase I, cytochrome P-450b specific) significantly increased and the activity of Benzo[a]pyrene hydroxylase (phase I, cytochrome P-450c specific) decreased. The activity of glutathione-S-transferase (phase II component) also was increased concurrently with a decrease in the concentration of glutathione. The magnitude of biochemical alterations in most cases was related directly to the duration of exposure. Our observations indicate that furfural caused pulmonary irritation, parenchymal injury and the regenerative proliferation of type II pneumocytes. Selective (cellular and/or cytochrome P-450 isozyme specific) enhancement of pulmonary mixed-function oxidases by furfural appears to stimulate its own pulmonary biotransformation, and the excretion of oxidative metabolites was facilitated by their enzymatic conjugation with glutathione.
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PMID:Inhalation toxicity of furfural vapours: an assessment of biochemical response in rat lungs. 178 39

In an open, pilot study, the efficacy and safety of ursodeoxycholic acid (UDCA) in the treatment of intrahepatic cholestasis of pregnancy was investigated. Four patients received 1 g/day of UDCA during 20 days and another 2 patients received 2 identical periods of treatment separated by a 14-day interval free of drug. Pruritus and serum levels of total bile salts and glutamic-pyruvic transaminase improved significantly during treatment with UDCA. Although pruritus and the laboratory alterations had a relapse in the second week after UDCA was discontinued, they improved again in the 2 patients who received a second treatment with UDCA. No adverse reactions were detected in the mothers or in their babies. All newborns are thriving normally, in a follow-up that lasted 3 to 6 months after delivery. It is concluded that UDCA appears to be safe when administered in late pregnancy; its promising efficacy in the treatment of intrahepatic cholestasis of pregnancy should now be confirmed in controlled clinical trials.
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PMID:[Effects of ursodeoxycholic acid in patients with cholestasis of pregnancy]. 182 60

The whole livers of rats were exposed intraoperatively to graded doses (0 to 75 Gy) of 137Cs gamma radiation. At various times (0 to 155 days) after liver irradiation, minimally invasive, nondestructive tests (rose bengal retention and plasma alkaline phosphatase, glutamic-oxaloacetic acid transaminase, glutamic-pyruvic transaminase) were performed on at least half the surviving animals in each dose group to assess developing liver injury. Liver histology was done on animals sacrificed 96 to 100 days after irradiation. Radiation damage to the stomach killed approximately 50% of the animals 30 to 60 days after exposure to doses of 25 Gy or higher. These deaths were significantly reduced when care was taken to shield the stomach during irradiation. Stomach injury did not, however, appreciably affect liver function as measured by rose bengal retention. Whole-liver irradiation to 15 Gy resulted in reduced liver size and minimal histological changes, but did not result in increased rose bengal retention or plasma alkaline phosphatase concentration. The next highest dose group studied (25 Gy) showed significant histological abnormalities and liver injury as measured by increased rose bengal retention and liver enzymes. The latent period for development of hepatic injury, as measured by increased rose bengal retention, was 35 to 42 days and was relatively invariant over the 25- to 75-Gy dose range. Hepatic vein lesions and cellular necrosis were the most prominent histological lesions observed in 25-Gy-irradiated liver.
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PMID:Hepatic radiation injury in the rat. 182 25

The effect of bucillamine (BA) on glutathione (GSH) and GSH-related enzymes was investigated in C57 mouse. Administration of high doses of BA (150-400 mg/kg) produced a dose-dependent depletion (20-44%) of hepatic GSH, which was similar in magnitude to that produced by equimolar doses of other sulphydryl drugs studied previously. GSH depletion after acute BA administration correlated well with the elevation of serum glutamic-pyruvic transaminase (SGPT) (6-9-fold increase above control). The increase in SGPT after chronic administration (7 days), although significantly higher than the controls, was however much less than after acute administration. The hepatic GSH concentrations of mice given 7 days of BA were similar to the controls, again correlating well with SGPT activity. Administration of BA (150-400 mg/kg) caused also a significant dose-dependent increase in the oxidized glutathione (GSSG) in blood by 2-7-fold, as well as a dose-dependent increase in blood glutathione S-transferase (GST) activity (2-13-fold). In an in vitro experiment, hepatic GST activity was activated by various concentrations of BA (1 microM-1mM). There was little or no effect on GSSG reductase and on glutathione peroxidase (GSH-Px) after acute administration of BA. Chronic administration of BA had no effect on hepatic GSSG reductase and GSH-Px, but GSSG reductase activity in blood was increased significantly by 4-fold. It is possible that BA may affect the redox status through auto-oxidation and oxidation with endogenous thiols such as glutathione, affecting GSH concentrations and the GSH/GSSG ratio in tissues and, thus, having both metabolic and toxicological consequences. Whether or not the induction of GST activity in vivo in blood and in vitro in liver enzyme preparations shared the same underlying mechanism(s) requires further investigation.
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PMID:The effects of bucillamine on glutathione and glutathione-related enzymes in the mouse. 186 40

1. The effects of nitrates and nitrites on growth, erythrocytic count, liver and kidney functions, humoral and cell mediated immune responses in cockerels were investigated. 2. Sodium nitrate (4.2 g/kg diet) and sodium nitrite (1.7 g/kg) retarded growth, caused methaemoglobinaemia and changes in erythrocytic count, serum concentrations of glutamic-pyruvic transaminase, creatinine and urea. 3. Cockerels given nitrate or nitrite in the food had reduced haemagglutination responses after injection of sheep erythrocytes and a reduced delayed hypersensitivity reaction to purified protein derivative tuberculin following sensitisation to Bacille Calmette Guerin. 4. Nitrates and nitrites are environmental pollutants present in food and water and they may contribute to the aetiology of liver and kidney diseases and problems related to failure of immunity in domestic fowls.
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PMID:Pharmacotoxicological aspects of nitrate and nitrite in domestic fowls. 186 78

Plasma components of 6 to 12-month-old beagles were examined using a Technicon auto-analyzer. Age-related changes were noted for 8 of the 21 components: the levels of total protein (T. Pro) and iron (Fe) gradually increased while those of alkaline phosphatase (ALP), creatine phosphokinase (CPK) and inorganic phosphorus (Pi) persistently decreased in both sexes. Triglyceride (Trigly) in female dogs, glutamic-pyruvic transaminase (GPT) and urea nitrogen (Urea-N) in male dogs tended to increase. The following thirteen components showed no significant variation during the period of observation: glucose (Glu), lactic dehydrogenase (LDH), albumin (Alb), creatinine (Crea), glutamic-oxaloacetic transaminase (GOT), leucine aminopeptidase (LAP), total bilirubin (T. Bil), amylase (Amy), total cholesterol (T. Chol), sodium (Na), potassium (K), chloride (Cl) and calcium (Ca). Our results generally agree with the reported findings on beagles from various institutions.
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PMID:Plasma biochemistry values of young beagle dogs. 188 72

Effects of chronic ethanol consumption and one day food deprivation on the hepatotoxicity of low dose carbon tetrachloride (CCl4; 0 to 100 ppm inhalation for eight hours) in rats were investigated by using biochemical and histopathological methods. Liver malondialdehyde (MDA) contents were significantly increased by exposure to 5 ppm to 50 ppm CCl4 in ethanol treated rats or by exposure to 25 ppm to 50 ppm CCl4 in food deprived rats but not in rats without ethanol or food deprivation. The MDA concentrations reached a maximum at 10 ppm and 50 ppm CCl4 in ethanol treated and food deprived rats, respectively, and decreased to the non-exposed concentration at 100 ppm CCl4. At greater than or equal to 50 ppm CCl4 plasma MDA contents increased significantly only in ethanol treated rats. None of the exposure concentrations influenced plasma glutamic-oxaloacetic transamidase (GOT) and glutamic-pyruvic transaminase (GPT) activities in rats that were only exposed to CCl4 whereas exposure to 10 ppm or higher concentrations combined with ethanol increased both activities. To a lesser extent food deprivation combined with exposure to greater than or equal to 25 ppm CCl4 had the same effect. No histopathological changes were found in the liver of rats exposed to less than or equal to 10 ppm CCl4, and only a few ballooned hepatocytes were seen in centrilobular areas when exposure was 25 ppm or higher. The presence of ballooned and hepatocytes became a regular feature of mid-zonal areas in ethanol treated rats and in the centrilobular areas of food deprived rats after exposure to </= 10 and </=25 ppm CC1(4) respectively. Necrotic hepatocytes were seen in centrilobular areas in liver from ethanol treated and food deprived rats when exposure CC1(4) was >/=25 ppm and >/=50 ppm respectively. These results indicate that consumption of ethanol and food deprivation potentiate CCl(4) induced hepatic damage even at low concentrations of CCl(4) by promoting lipid peroxidation. Thus heavy drinking may be a risk factor for CCl(4) induced hepatic damage even though the CCl(4) concentration is as low as the threshold limit value.
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PMID:Ethanol and food deprivation induced enhancement of hepatotoxicity in rats given carbon tetrachloride at low concentration. 191 7

Twenty obese and 20 lean LA/N-cp male rats and 20 male Sprague-Dawley rats were fed a diet containing either 54 percent sucrose or starch for six weeks. After a 14-16 hour fast, rats were killed. Liver and kidney enzyme activities were determined in the LA/N-cp rats while plasma urea and selected amino acids were determined in all rats. Liver glucose-6-phosphatase (G6PASE), fructose-1,6-bisphosphatase (FBPASE), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), glucokinase (GK), pyruvate kinase (PK), phosphofructokinase (PFK), glutamic-oxaloacetic-transaminase (GOT), glutamic-pyruvic transaminase (GPT), arginase (ARGASE), arginine-synthase (ARG-SYN) and ornithine transcarbamylase (OTC) levels were significantly affected by phenotype (obese greater than lean). All the above changes in enzyme levels were exaggerated by sucrose-feeding with the exception of PK, PFK, GOT, GPT, ARGASE and ARG-SYN. Kidney cortex G6PASE, PEPCK and ARGASE activities were higher in the obese rats as compared to the lean littermates. Sucrose feeding resulted in higher cortex G6PASE, FBPASE and PEPCK as compared to starch-fed rats. A phenotype effect was noted with plasma glutamate, urea, leucine, isoleucine and valine (obese greater than lean) and a diet effect was seen with aspartate, phenylalanine, leucine and valine (sucrose greater than starch) concentration. Sprague-Dawley rats had higher plasma urea and lower alanine than lean LA/N-cp males. Metabolic obesity in the LA/N-cp rat appears to involve an elevated capacity for pathways of glycolysis, gluconeogensis, lipogenesis and amino acid catabolism in the liver.
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PMID:Effect of dietary carbohydrate on liver and kidney enzyme activities and plasma amino acids in the LA/N-cp rat. 204 12


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