Disease relevance of Gpt1

• Glutamic oxalacetic transaminase, glutamic pyruvic transaminase, and guanase activities were found to be significantly elevated in patients with various liver disorders, those with acute myocardial infarction with prominent congestion of the liver, and also in CCl4-treated dogs [1].
• Repeatedly bred spontaneously hypertensive rats (SHR) were found to have severe hypertension, hyperglycemia, hyperlipidemia, elevated creatine phosphokinase (CPK), serum glutamic oxaloacetic and glutamic pyruvic transaminase (SGOT, SGPT), and lactic dehydrogenase (LDH), as well as high circulating corticosterone levels [2].
• Further, additional injections of hydrocortisone into rats with tumors weighing more than 5% of the body weight did not cause any appreciable change in alanine aminotransferase activity in the thymus, although in rats with smaller tumors it slightly increased the enzyme activity in the thymus [3].
• In this study using an experimental rat model, left hepatic lobar ischemia followed by reperfusion resulted in an increase of serum glutamic pyruvic transaminase at 30 min with concomitant histological evidence of hepatocellular necrosis at 24 hr [4].
• Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein [5].

Psychiatry related information on Gpt1

• After sacrifice, serum transaminases (GOT, GPT), triacylglyceride and hepatic triacylglyceride (HTG) concentration were assayed to observe liver injuries induced by chronic alcohol abuse [6].

High impact information on Gpt1

• Eight dag populations and eight clones are characterized as being different from Faof1 cells by the production of serum albumin, aldolase B and in some cases activity of alcohol dehydrogenase and alanine aminotransferase [7].
• Training increased skeletal muscle citrate synthase, cytochrome c oxidase (Cyt-Ox), carnitine palmitoyltransferase (CPT), beta-hydroxyacyl coenzyme A dehydrogenase, mitochondrial malate dehydrogenase (MDH), and alanine aminotransferase (ALT) activities significantly in the TC group, but not in TP [8].
• Binge ethanol exposure caused liver injury in obese fa/fa but not in lean Fa/? rats, as assessed by alanine aminotransferase and H&E staining [9].
• RESULTS: Four hours after an i.v. bolus of TCDC (10 mumol/100 g weight), serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels peaked, hepatic mitochondria showed evidence of increased lipid peroxidation, and serum bile acid analysis was consistent with a cholestatic injury [10].
• Liver damage was determined by aspartate aminotransferase and alanine aminotransferase and by histology [11].

Chemical compound and disease context of Gpt1

• Aortic-ligated S-D rats had elevated creatine phosphokinase, serum glutamic-oxaloacetic transaminase, serum glutamic-pyruvic transaminase, and lactic hydrogenase levels and manifested hyperglycemia, hypercholesterolemia, and elevated blood urea nitrogen (BUN) levels [12].
• Lipo-PGE1 markedly suppressed both the increases in plasma PCOOH (phosphatidyl-choline hydroperoxide) levels and the leakage of GOT, GPT, and LDH from the liver during the ischemia reperfusion [13].
• The severity of the cholestasis and hepatic injury were determined by the changes in the plasma enzyme activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AP), g-glutamyl-transpeptidase (GGT), and levels of albumin, total bilirubin (TB) and direct bilirubin (DB) [14].
• After hepatic reperfusion, the disappearance rate of serum hyaluronic acid in obstructive jaundice was lower, and serum alanine aminotransferase levels were higher than those in the Sham group [15].
• RESULTS: TJ-9 (1% w/w) prevented fibrosis, as indicated by reduced hydroxyproline content in the liver and inhibition of the increase in a serum marker of fibrosis (hyaluronic acid), without reducing the increase in serum alanine aminotransferase and aspartate aminotransferase [16].

Biological context of Gpt1

• Complete amino acid sequence of rat liver cytosolic alanine aminotransferase [17].
• When prostaglandin (PG) E1 was continuously administered to rats from 24 hours before giving a dose of carbon tetrachloride, deranged serum glutamic pyruvic transaminase levels and prothrombin time were significantly reduced 12 hours after intoxication compared with controls [18].
• Analysis of serum glutamic-pyruvic transaminase and histologic observations did not show any sign of cell death at the time points examined [19].
• Liver injury was evaluated by alanine aminotransferase activity in serum, and histological examination and DNA fragmentation in liver [20].
• 3. The increase in alanine metabolism on high-protein diets was associated with an increase in alanine aminotransferase and in pyruvate utilization for gluconeogenesis [21].

Anatomical context of Gpt1

• RESULTS: Serum activities of tumor necrosis factor, purine nucleoside phosphorylase present in both hepatocytes and sinusoidal endothelial cells, and levels of alanine aminotransferase were higher after 30 minutes, 1 hour, and 3 hours, respectively [22].
• At a neutrophil/hepatocyte ratio of 20:1, the alanine aminotransferase activity releases were 53.7% +/- 5.4% (mean +/- 1 S.E.) and 27.4% +/- 4.8% for normal and inflammatory hepatocytes, respectively [23].
• IP before 90 minutes of warm ischemia of rat livers in vivo significantly reduced serum alanine aminotransferase (AST) levels and leukocyte adherence to sinusoids and postsinusoidal venules during reperfusion [24].
• Furthermore, in normal rats, increase in alanine aminotransferase activity in the thymus with involution of the glands was observed with a dose of corticosterone close to the physiological range attained in rats with tumors in an advanced stage [3].
• In contrast, activation of the reticuloendothelial system by glucan increased galactosamine-induced alterations in serum bilirubin, glucose and cholesterol concentrations, glutamic oxalacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention [5].

Associations of Gpt1 with chemical compounds

• Most of the crucial amino acid residues hydrogen-bonding to pyridoxal 5'-phosphate identified in aspartate aminotransferase by X-ray crystallography are conserved in alanine aminotransferase [17].
• RESULTS: The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin (Alb) in EGb-protected group were notably improved as compared with the CCl(4)-treated group (P < 0.01) [25].
• Serum enzymes, creatine phosphokinase, serum glutamic oxalo-pyruvic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, and blood urea nitrogen levels were elevated in breeder rats [26].
• Whole blood LTB4 and serum alanine aminotransferase (ALT), total bilirubin, and bromodeoxyuridine labeling index (LI) were measured before and after hepatectomy [27].
• Time course of serum enzyme elevations (alanine aminotransferase, aspartate aminotransferase, and sorbitol dehydrogenase) indicated that actual infliction of liver injury by APAP peaked between 12 to 24 hours after the administration of APAP, whereas the ultimate outcome of that injury depended on the biological events thereafter [28].

Regulatory relationships of Gpt1

• Intracisternal injection of urocortin dose-dependently enhanced elevation of serum alanine aminotransferase and aspartate aminotransferase levels induced by CCl4 [29].
• COX-2 inhibition with NS-398 as well as iNOS inhibition with aminoguanidine diminished LPS-induced changes in aspartate aminotransferase and alanine aminotransferase levels [30].

Other interactions of Gpt1

• Portal pressure, serum alanine aminotransferase, hepatic nitrate/nitrite, inducible nitric oxide synthase (iNOS), and endothelin-1 markedly increased after T-H [31].
• Portal inflow pressure was measured, and perfusate samples were collected to measure IL-6, alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels [32].
• Ten-day survival rates, serum alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels, liver tissue blood flow, histological findings, and activities of p38 MAPK and p46/p54 c-Jun N-terminal kinase (JNK) in liver grafts were evaluated [33].
• Bile flow, bile salt excretion, liver lipid conjugated diene content, liver glutathione reductase and glutathione peroxidase activities, and serum alanine aminotransferase (ALAT) activity were not affected by the nifurtimox treatment, thus ruling out widespread damage of the liver cell by nifurtimox [34].
• Five hours after CLP, plasma and tissue samples were analyzed for cytokines (IL-6 and IL-10), MPO, neutrophil chemotactic factor (CINC-3), and liver injury (alanine aminotransferase and lactate dehydrogenase) [35].

Analytical, diagnostic and therapeutic context of Gpt1

• RESULTS: Serum alanine aminotransferase release increased from approximately 60 U/L before implantation to 750, 1410, and 2520 U/L after full-size, half-size, and quarter-size transplantation, respectively [36].
• Rat peritoneal PMNs (4 x 10(8] or vehicle (Hank's balanced salt solution [HBSS], pH 7.35) were added, and liver injury was assessed 90 minutes later by release of alanine aminotransferase (ALT) into the perfusion medium and histopathologic analysis of liver sections [37].
• Following LPS and tezosentan administration, serum aspartate aminotransferase and alanine aminotransferase activities were similar to those in the control group while they were increased by more than 700% with LPS alone [38].
• Alanine aminotransferase (ALT) release after liver transplantation was 4.5-fold higher in recipients receiving ethanol-induced fatty grafts than in those receiving normal grafts [39].
• Necrosis was identified only when ligation was > or = 68%, this being associated with an increase in alanine aminotransferase levels [40].

References