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)

One hundred and four workers ingested excessive levels of arsenic in an accident caused by leakage of pipeline in a copper-smelting factory. Clinical examinations were performed by physicians in a local hospital. Excreted urinary arsenic species were determined by cold trap hydride generation atomic absorption spectrometry. In the initial toxic phase, gastrointestinal symptoms were predominant (83 people, 79.8%). Most patients showed leucopenia (72 people, 69.2%), and increased serum alanine aminotransferase (84 people, 80.8%) and aspartate aminotransferase (58 people, 55.8%). Thirty-five patients (33.6%) had elevated red blood cells in urine. After 17 days of admission, many subjects (45 people, 43.3%) developed peripheral neuropathy and 25 of these 45 patients (24.0%) showed a decrease in motor and sensory nerve conduction velocity. In the comparison of urinary arsenic metabolites among subacute arsenic-poisoned, chronic high arsenic-exposed and control subjects, we found that subacute arsenic-poisoned patients had significantly elevated proportions of urinary inorganic arsenic (iAs) and methylarsonic acid (MMA) but reduced proportion of urinary dimethylarsinic acid (DMA) compared with chronic high arsenic-exposed and control subjects. Chronic exposed subjects excreted higher proportions of iAs and MMA but lower proportions of DMA in urine compared with control subjects. These results suggest that gastrointestinal symptoms, leucopenia, and hepatic and urinary injury are predominant in the initial phase of subacute arsenic poisoning. Peripheral neuropathy is the most frequent manifestation after the initial phase. The biomethylation of arsenic decreases in a dose rate-dependent manner.
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PMID:Clinical manifestations and arsenic methylation after a rare subacute arsenic poisoning accident. 1830

Danshen (DS) is used for treatment of various ischemic events in the traditional Chinese medicine. Hence, this study was designed to investigate its effect on ischemia/reperfusion injury (IRI) after experimental kidney transplantation (eKTx). Nephrectomized Sprague-Dawley rats underwent eKTx. Some animals were infused with 1.5 ml DS 10 min before surgery. Kidney grafts were transplanted after cold storage for 20 h in Histidine-Tryptophane-Ketoglutarate solution. After reperfusion blood samples were collected for blood urinary nitrogen (BUN), creatinine, lactate dehydrogenase (LDH), and alanine transaminase. Further, tissue was assessed for morphologic and pathophysiologic changes. Donor preconditioning with DS (DS-d) significantly decreased BUN, creatinine, LDH, and aspartate aminotransferase to 65-97% of controls while preconditioning of the recipient (DS-r) decreased values to 58-82% (P < 0.05). Tubular damage and caspase-3 decreased significantly in both DS-d and DS-r (DS-d: 96% and 67%, DS-r: 83% and 75% of controls) while heat shock protein 72 and superoxide dismutase increased significantly (DS-d: 143% and 173%, DS-r: 166% and 194% of controls). Further, inducible nitric oxide synthase and tumor necrosis factor-alpha decreased (DS-d: 84% and 61%, DS-r: 79% and 67% of controls) after DS. Preconditioning of both donors and recipients with DS significantly reduces IRI and thus improves graft function after eKTx.
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PMID:Danshen protects kidney grafts from ischemia/reperfusion injury after experimental transplantation. 1895 74

The factors that influence the long-term histological outcome of transplanted liver allografts in children are not yet fully understood, and the role of surveillance biopsies in patients with normal graft function remains controversial. The aims of this study were to describe the long-term graft histology of pediatric liver transplant recipients surviving at least 3 years and to analyze factors correlating with long-term histological outcome. Histological slides of 63 long-term liver transplant recipients were assessed for inflammation and fibrosis. The histological findings were correlated with clinical, biochemical, serological, and radiological findings. A significant proportion of biopsies from these patients showed some type of histological abnormalities, with fibrosis being observed in 61 (97%) patients. Duration of transplantation of >6 years and > or =grade 2 inflammation were significantly associated with advanced fibrosis. We could not identify any correlation between > or =stage 3 fibrosis and donor age, cold and warm ischemia time, history of de novo autoimmune hepatitis, hepatic artery thrombosis, chronic rejection, or alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase values. In conclusion, liver fibrosis appears to be a common finding in long-term pediatric liver transplant survivors. The cause of this fibrosis is uncertain, and normal alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase levels do not exclude the presence of significant fibrosis.
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PMID:Graft histology characteristics in long-term survivors of pediatric liver transplantation. 1897 86

An experiment with 250 one-day-old male broilers (Ross 308) was conducted to investigate the differences of some blood parameters of cold-induced ascitic and healthy broiler chicks in a 6-wk period. The chickens were divided into 2 groups of 5 replicates each. One group of these chickens was raised in normal temperature (NT) treatment and the other in cold temperature (CT) treatment to induce ascites. Mortality was necropsied daily to determine cause of death. At the end of the experiment (wk 6), 5 chickens from each replicate were randomly selected and slaughtered. The heart was removed; the right ventricle was dissected away from the left ventricle and septum. Weights of right and left ventricles were determined separately. Average BW gain and average feed intake were measured weekly, and weekly average feed conversion ratio was calculated. Serum glucose, total protein, cholesterol, triglyceride, activity of lactate dehydrogenase, as-partate aminotransferase, and alanine aminotransferase were determined. Throughout the study, the right ventricle-to-total ventricle ratio and total mortality percentage due to ascites of CT-treated birds at the end of experiment was greater (P < or = 0.05) than those of NT-treated ones. Fasting blood sugar of CT-treated birds in wk 4 and 6 was greater (P < or = 0.05) than NT-treated birds. Total blood protein of CT treatment was lower than NT-treated birds in every week and whole period, but this difference was only significant (P < or = 0.05) in wk 6. There was not a significant difference between 2 treatments for triglyceride and cholesterol, lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase. It was concluded that cold-induced ascites could affect serum protein and fasting blood sugar of broiler chickens.
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PMID:Changes of biochemical parameters and enzyme activities in broiler chickens with cold-induced ascites. 1909 64

Reperfusion injury causes liver dysfunction after warm or cold ischemia. Emerging data suggest a role of T cells as mediators in this ischemia/reperfusion (I/R) injury. In the T cells, a part of CD4(+)CD25(+)FoxP3(+) T regulatory cells (Tregs) were reported to facilitate recovery from I/R injury. These Tregs can be induced by TGF-beta in vitro. Interestingly, rapamycin was reported to selectively expand these Tregs in vitro. In the present study, addition of rapamycin to cultures containing TGF-beta further increased the frequency and absolute number of functional CD4(+) Tregs. Using a partial (70%) hepatic warm ischemia model, we investigated the effects of liver function recovery under the treatment of Tregs induced by rapamycin and TGF-beta. The treatment of Tregs significantly reduced serum alanine aminotransferase and aspartate aminotransferase compared to I/R control animals at 24 h after reperfusion (P<0.05). They also significantly attenuated the up-regulation of IFN-gamma and IL-17 compared to the I/R control animals (P<0.05). In conclusion, Tregs ameliorate the biochemical of hepatic I/R injury by preventing proinflammatory cytokines following a warm I/R insult. These data may pave the way to use Tregs as cell therapy to prevent hepatic I/R injury.
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PMID:In vitro induced CD4(+)CD25(+)Foxp3(+) Tregs attenuate hepatic ischemia-reperfusion injury. 1953 64

Arcobacter cryaerophilus was isolated from naturally infected rainbow trout ( Oncorhynchus mykiss Walbaum), and its pathogenicity was tested by intramuscular injection using healthy 1-year-old rainbow trout under cold-water conditions (at 5 degrees C). The lethal dosage of 50% end point (LD 50 ) for A. cryaerophilus was calculated as 7.79 x 10 5 viable cells. Experimental infection caused gross clinical abnormalities such as fallen scales, exophthalmia, oedema in injection region and at the base of fins, pale gills, kidney necrosis, hyperaemic areas in pale liver, haemorrhagic spots in heart, elongated spleen and swollen gallbladder. Activities of aspartate aminotransferase and alkaline phosphatase, and concentrations of glucose, total protein, albumin, cholesterol, triglyceride and calcium in the serum of the experimentally infected rainbow trout were significantly decreased compared with the healthy fish. Positive correlations were observed among blood parameters. Total lipid weights increased in the brain, muscle and liver tissues of infected fish and dropped in the gill and spleen tissues. Lipid peroxide contents in the brain, liver, kidney, spleen, muscle and gill tissues of infected rainbow trout were significantly higher than in healthy animals. The present work shows that A. cryaerophilus can be moderately virulent for rainbow trout at low water temperature, and changes in lipid and lipid peroxide contents of tissues and blood indices can highlight barely detectable effects of A. cryaerophilus infection in rainbow trout under laboratory conditions. However, the application of these indices in farm biomonitoring using rainbow trout will need more detailed studies and a careful consideration of the environmental parameters.
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PMID:Gross pathology, blood chemistry, lipid and peroxide contents in rainbow trout ( Oncorhynchus mykiss Walbaum) affected by experimental Arcobacter cryaerophilus infection at low water temperature. 1958 43

Legionella pneumophila is an aquatic bacterium that is also the agent of Legionnaires' disease pneumonia. Since L. pneumophila is transmitted directly from the environment to the lung, it is important to understand how legionellae survive at low temperatures. To identify genes that are needed for L. pneumophila growth at low temperature, we screened a population of mutagenized legionellae for strains that are specifically impaired for growth at 17 degrees C. From the 7,400 mutants tested, 11 displayed defects ranging from ca. 10-fold to a complete inability to grow at the low temperature. PCR and sequence analysis were then utilized to identify the genes whose loss had compromised growth. The proteins thereby implicated in low-temperature growth included components of the type II secretion system (LspE, LspG, LspH), a lipid A biosynthetic enzyme (LpxP), a ribonuclease (RNAse R), an RNA helicase (CsdA/DeaD), TCA cycle enzymes (citrate synthase), enzymes linked to fatty acid (FadB) or amino acid (aspartate aminotransferase) catabolism, and two putative membrane proteins that were, based upon their sequences, unlike previously characterized proteins. Given the magnitude of their mutant's defect, the aspartate aminotransferase, RNA helicase, and one of the putative membrane proteins were the factors most critical for L. pneumophila low-temperature growth. Thus, L. pneumophila not only employs some of the same processes and factors as other bacteria do in order to survive at low temperatures (e.g., LpxP, CsdA), but it also appears to possess novel modes of cold adaptation.
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PMID:Mediators of lipid A modification, RNA degradation, and central intermediary metabolism facilitate the growth of Legionella pneumophila at low temperatures. 1976 2

Many centers require a minimal graft to body weight ratio (GBWR) >or= 0.8 as an arbitrary threshold to proceed with right-lobe living donor liver transplantation (RL-LDLT), and there is often hesitancy about transplanting lower volume living donor (LD) liver grafts into sicker patients. The data supporting this dogma, based on the early experience with RL-LDLT at Asian centers, are weak. To determine the effect of LD liver volume in the modern era, we investigated the impact of GBWR on the outcome of RL-LDLT with a GBWR as low as 0.6 at the University of Toronto. Between April 2000 and September 2008, 271 adult-to-adult RL-LDLT procedures and 614 deceased donor liver transplants were performed. Twenty-two living donor liver transplantation (LDLT) cases with a GBWR of 0.59 to 0.79 (group A) were compared with 249 LDLT cases with a GBWR >or= 0.8 (group B) and with 66 full-graft deceased donor liver transplants (group C), who were matched 3:1 according to donor and recipient age, Model for End-Stage Liver Disease score, and presence of hepatitis C and hepatocellular carcinoma with the low-GBWR group. Portal vein shunts were not used. Markers of reperfusion injury [aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], graft function (international normalized ratio and bilirubin), complications graded by the Clavien score, and graft and patient survival were compared. As expected, LD recipients had a significantly shorter cold ischemia time (94 +/- 43 minutes for A, 96 +/- 57 minutes for B, and 453 +/- 152 minutes for C, P = 0.0001). However, the peak AST, peak ALT, absolute decrease in the international normalized ratio, day 7 bilirubin level, postoperative creatinine clearance, complication rate graded by the Clavien score, and median hospital stay were similar in all groups. The rate of biliary complications was higher with LD grafts than deceased donor grafts (19% for A versus 10% for B and 0% for C, P = 0.2). Patient survival was similar in all groups at 1, 3, and 5 years (91% for A versus 89% for B and 93% for C at 1 year, 87% for A versus 81% for B and 89% for C at 3 years, and 83% for A versus 81% for B and 87% for C at 5 years, P = 0.63). A Cox proportional regression analysis revealed only hepatitis C virus as a risk factor for poorer graft survival and not GBWR as a continuous or categorical variable. In conclusion, we found no evidence of inferior outcomes with smaller size grafts versus larger size LD grafts or full-size deceased donor grafts. Further studies are warranted to examine the factors affecting the function of smaller grafts for living liver donation and thereby define the safe lower limits for transplantation.
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PMID:A graft to body weight ratio less than 0.8 does not exclude adult-to-adult right-lobe living donor liver transplantation. 1993 39

The involvement of catecholamines in stress-induced heart injury is well documented. However, the contribution of adrenergic receptor types is less understood. Both the profile of plasma marker enzyme activities (lactate dehydrogenase-1 and aspartate transaminase) and the distribution and morphology of the lesions observed in tissue sections of adrenaline-injected mice resembled those of stressed (restraint and cold exposed) mice. Next, we compared the effect of isoproterenol (beta-adrenergic agonist) and phenylephrine (alpha1-adrenergic agonist) on both heart function and tissue injury. In Langendorff-perfused rat hearts, alpha1-adrenergic receptors made a minor contribution to the tonic effect of adrenaline, as indicated by the lack of effect on the heart rate and the delayed negative inotropic effect of phenylephrine. However, in whole mice, phenylephrine but not isoproterenol, induced an increase of both lactate dehydrogenase-1 and aspartate transaminase activities. Hearts of phenylephrine-injected mice showed necrotic lesions in subendocardial areas of the left ventricle. In addition a scattered focal leukocyte infiltration around single apoptotic-like myocytes was observed in the ventricle wall. Hearts of isoproterenol-injected mice showed a similar number of apoptotic-like myocytes, but a much lower number of necrotic areas, than phenylephrine-injected animals. Our results suggest that the cardiotonic effect of catecholamines involves mainly the beta-adrenergic receptors. However, the acute catecholamine-induced heart injury involves mainly alpha1-adrenergic receptors.
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PMID:Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine. 2023 97

CSM2, a cold-sensitive mutant of psychrophilic Pseudomonas syringae, grows like wild-type cells when cultured at 22 and 28 degrees C; but at 4 degrees C, the growth is retarded. In CSM2, AAT (coding for aspartate aminotransferase) is identified as the mutated gene. The expression of AAT in Pseudomonas syringae was transiently enhanced when cells were shifted from 22 to 4 degrees C indicating that AAT is cold-inducible. Complementation of the mutated AAT transformed CSM2 from a cold-sensitive phenotype to a cold-resistant phenotype like the wild-type cells, thus providing evidence for the first time that AAT is required for low-temperature growth.
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PMID:Aspartate aminotransferase is involved in cold adaptation in psychrophilic Pseudomonas syringae. 2055 70


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