Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the diagnosis of chronic (as opposed to acute) liver diseases, combinations of indicators are needed to improve specificity. Alanine aminopeptidase (AAP; microsomal aminopeptidase, EC 3.4.11.2) activity in serum reportedly is a very sensitive indicator of intrahepatic cholestasis and biliary obstruction; it is also particularly useful in diagnosing chronic liver disease when combined with an indicator of hepatocyte damage such as aspartate aminotransferase or alanine aminotransferase. We optimized the assay of AAP in serum, automated the assay by using a centrifugal analyzer, then used this automated assay to determine activity in 202 individuals, ages one to 73 years. The preliminary results were analyzed in terms of the effects of age, sex, smoking, and alcohol consumption on AAP activity in serum. Striking sex-related differences were observed: AAP activity in males declined 2.5 times more rapidly with age than did that in females; indeed, activity in adult females remained essentially constant. Moreover, AAP values were higher in men who smoked than in those who did not, the difference being of borderline significance by analysis of covariance (p = 0.0865) but significant by partial correlations (p = 0.02). No similar differences were seen for women smokers and non-smokers. When the effects of other variables were held constant, alcohol consumption alone did not significantly correlate with AAP activity in men or women.
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PMID:Alanine aminopeptidase in serum: automated optimized assay, and effects of age, sex, smoking, and alcohol consumption in a selected population. 288 Jun 80

Experiments were undertaken to examine the ability of selenium to protect against acetaminophen-induced hepatotoxicity and to examine possible mechanisms for this protective effect. Pretreatment of male, Sprague-Dawley rats with sodium selenite (12.5 mumol Se/kg, ip) 24 hr prior to acetaminophen administration produced a significant protection against the hepatotoxic effects of acetaminophen as assessed by a decrease in the plasma appearance of alanine aminotransferase and aspartate aminotransferase activities following acetaminophen. This was accompanied by an increase in the hepatic glutathione levels in selenium-treated animals and an inhibition in the decrease in hepatic glutathione content observed in animals receiving hepatotoxic doses of acetaminophen. Selenium pretreatment decreased the in vivo covalent binding of acetaminophen metabolites to hepatic protein, but did not alter hepatic microsomal cytochrome P-450 content or NADPH cytochrome c reductase activity, suggesting that selenium does not significantly alter the metabolism of acetaminophen to reactive electrophilic metabolites by the cytochrome P-450-dependent mixed-function oxidase enzyme system. Selenium produced an increase in the activity of gamma-glutamylcysteine synthetase which may account for the increased glutathione availability in selenium-treated animals and increased the activities of glutathione S-transferase and glucose-6-phosphate dehydrogenase. Examination of the urinary metabolite profile in selenium-treated animals revealed that the urinary excretion of acetaminophen and its metabolites was significantly increased over a 72-hr period. The increase occurred in the AAP-glucuronide metabolite while parent AAP and AAP-sulfate were actually decreased in selenium-treated rats. No change in recovery was observed in the AAP-glutathione or AAP-mercapturate urinary metabolites. While the glutathione conjugating system is enhanced by selenium treatment, amelioration of acetaminophen toxicity is most likely the result of enhanced glucuronidation which effectively diverts the amount of acetaminophen to be converted by the cytochrome P-450 system to the toxic metabolite.
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PMID:Protective effects of selenium on acetaminophen-induced hepatotoxicity in the rat. 290 Nov 47

An adult female bottlenose dolphin (Tursiops truncatus) stranded alive and subsequently died several minutes later on the Mediterranean coast of Spain on 14 July 2010. Clinical examination revealed foam through the blowhole and rales upon lung auscultation. On venipuncture, the blood was abnormally dense and dark. Hematological and biochemical abnormalities included dehydration, leukocytosis (48 600 leukocytes microl(-1)) characterized by neutrophilia (48 200 neutrophils microl(-1)), and elevated bilirubin (4.38 mg dl(-1)), alanine aminotransferase (382.3 U l(-1)), aspartate aminotransferase (1449.3 U l(-1)), lactate dehydrogenase (1631.3 U l(-1)), and creatine kinase (404.7 U l(-1)). The most relevant findings of the gross examination were rhomboid-shaped skin lesions, stable froth in the trachea, pulmonary congestion, abnormally thick and rough pleura with adhesions, edematous and congestive superficial cervical and tracheobronchial lymph nodes, red-tinged urine, and severe brain congestion. Histopathology of the kidney, lung, skin, and brain revealed multisystemic intravascular bacterial emboli. Samples of skin, brain, and lung were cultured on Columbia blood agar under both aerobic and anaerobic conditions, and pure and heavy bacterial cultures were obtained from skin and brain samples. The microorganism isolated was Gram-positive, catalase-negative, facultatively anaerobic, and rod-shaped. The isolates were identified as Erysipelothrix rhusiopathiae by the API Coryne biochemical system. Based on the gross and microscopic findings, a diagnosis of acute E. rhusiopathiae septicemia was made. To the best of our knowledge, this is the first report of E. rhusiopathiae septicemia in a free-ranging bottlenose dolphin.
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PMID:First case of erysipelas in a free-ranging bottlenose dolphin (Tursiops truncatus) stranded in the Mediterranean Sea. 2230 33

This study aimed to investigate the effects of polysaccharide from Angelica and Astragalus (AAP) on carbon tetrachloride (CCl4) induced liver damage in mice. A total of 120 Kunming mice were randomly distributed among 6 groups comprising (i) the normal control mice, (ii) the CCl4 treatment group, (iii) the bifendate treatment group, (iv) the AAP treatment group, (v) the Angelica sinensis polysaccharide (ASP) treatment group, and (vi) the Astragalus membranaceus polysaccharide (AMP) treatment group. AAP, ASP and AMP were administered to mice treated with CCl4. The activities of alanine transaminase (ALT) and aspartate transaminase (AST) in the serum, and superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver tissues were quantified, as well as the liver index. Hepatic histological changes were observed by staining liver sections with hematoxylin and eosin. Our results show that bifendate, AAP, ASP, and AMP significantly decreased the activities of MDA, AST, and ALT, and enhanced the activity of SOD in CCl4-treated mice. Bifendate, AAP, ASP, and AMP consistently ameliorated the liver injuries induced with CCl4. Notably, the hepatoprotective effect of AAP was stronger than that of bifendate, ASP, or AMP. In addition, AAP alleviated liver inflammation and decreased the liver indexes of mice induced with CCl4. These effects were at least partly due to the antioxidant properties of AAP in scavenging free radicals to ameliorate oxidative stress and to inhibit lipid peroxidation.
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PMID:Polysaccharides from Angelica and Astragalus exert hepatoprotective effects against carbon-tetrachloride-induced intoxication in mice. 2541 37

Acetaminophen (N-acetyl-p-aminophenol, AAP) is an effective analgesic and antipyretic drug with minimal toxicity when used at therapeutic doses. However, AAP overdose is the most common cause of drug-induced acute liver failure and one of the main causes of morbidity and mortality. p-Coumaric acid (PCA) is the most abundant isomer of hydroxycinnamic acid in nature, and it can be widely found in fruits, vegetables, and plants products. PCA has strong antioxidant activity and exhibits protective effects in numerous disease models associated with reactive oxygen species (ROS) generation. In this study, we investigated the protective effects of PCA on AAP-induced hepatotoxicity and the underlying mechanisms using an in vivo model. We found that PCA ameliorates AAP-induced hepatotoxicity as well as the reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity. Furthermore, we observed that PCA suppressed hepatic apoptosis via ROS-mediated DNA damage responses and inflammation by modulating the mitogen-activated protein kinase (MAPK) signaling axis in an ROS-dependent manner. These findings indicate that the administration of PCA protects against AAP-induced hepatotoxicity, suggesting it could be a novel therapeutic strategy for AAP-induced liver injury.
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PMID:Protective effects of p-coumaric acid against acetaminophen-induced hepatotoxicity in mice. 3014 9