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)

A 55-year-old female was admitted to our hospital because of high fever, nonproductive cough and dyspnea. Initially she had been treated with cephem antibiotics by a local doctor. However, acute respiratory failure due to severe pneumonia developed. The partial pressure of oxygen in arterial blood was 55.5 Torr. Her chest X-ray revealed wide-spread infiltrates with air bronchograms throughout the entire left lung, and pleural effusions were also present in the chest CT scan. Because the patient had a history of the contact with birds, we suspected psittacosis and administered Minocycline immediately. As a result, her clinical condition improved and the abnormal shadow on the chest X-ray film improved markedly in three days. Because the serum titer of a complement fixation test against Chlamydia rose to 1:512, we made the diagnosis of psittacosis. In addition, femoral muscle pain, and a high level of serum GOT, GPT, CK, Aldolase and Myoglobin indicated hepatitis and myositis. In the lung tissue specimens obtained by TBLB performed on the 10th hospital day, slight interstitial pneumonia and intracellular inclusion bodies were found by light microscopy and Chlamydial agents were found electron microscopically.
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PMID:[A case of fulminant psittacosis showing Chlamydia in TBLB specimens]. 204 Dec 51

The objective of this study was to test the hypothesis that the extracellular oxidation of glutathione (GSH) may represent an important mechanism to limit hepatic ischemia/reperfusion injury in male Fischer rats in vivo. Basal plasma levels of glutathione disulfide (GSSG: 1.5 +/- 0.2 microM GSH-equivalents), glutathione (GSH: 6.2 +/- 0.4 microM) and alanine aminotransferase activities (ALT: 12 +/- 2 U/l) were significantly increased during the 1 h reperfusion period following 1 h of partial hepatic no-flow ischemia (GSSG: 19.7 +/- 2.2 microM; GSH 36.9 +/- 7.4 microM; ALT: 2260 +/- 355 U/l). Pretreatment with 1,3-bis-(2-chloroethyl)-1-nitrosourea (40 mg BCNU/kg), which inhibited glutathione reductase activity in the liver by 60%, did not affect any of these parameters. Biliary GSSG and GSH efflux rates were reduced and the GSSG-to-GSH ratio was not altered in controls and BCNU-treated rats at any time during ischemia and reperfusion. A 90% depletion of the hepatic glutathione content by phorone treatment (300 mg/kg) reduced the increase of plasma GSSG levels by 54%, totally suppressed the rise of plasma GSH concentrations and increased plasma ALT to 4290 +/- 755 U/l during reperfusion. The data suggest that hepatic glutathione serves to limit ischemia/reperfusion injury as a source of extracellular glutathione, not as a cofactor for the intracellular enzymatic detoxification of reactive oxygen species.
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PMID:Vascular oxidant stress and hepatic ischemia/reperfusion injury. 206 Aug 45

In order to determine the behavior of glutamic oxalacetic (GOT), glutamic-pyruvic (GPT) and lactic dehydrogenase (LDH) transaminases after a period of asphyxia, a study was conducted in 120 newborn children which were placed into two groups: group 1 of the asphyxiated children who were given oxygen at intermittent positive pressure for more than a minute and group 2 of healthy children with an Apgar greater than 7 after the first and five minutes and without any apparent pathology. The results showed a real increase in the quantities of all three transaminases among those in the group of asphyxiated children, which on the other hand did not occur in the healthy group of children where levels remained normal. There was statistical differences (P less than 0.001) by which we can conclude that the quantification of these enzymes can be useful as a diagnostic tool in cases of perinatal asphyxia.
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PMID:[Increase in glutamic-oxaloacetic and glutamic-pyruvic transaminases and lactic dehydrogenase as a diagnostic aid in perinatal asphyxia]. 222 19

In vivo covalent binding of halothane biotransformation-reactive intermediates to hepatic protein and lipid was examined in association with the subsequent development of hepatic necrosis in the guinea pig. Oxidative halothane biotransformation was inhibited by the use of deuterated halothane, whereas reductive metabolism was enhanced by low inspired oxygen concentrations. Male outbred Hartley guinea pigs (n = 8) were exposed to either 1% (v/v) halothane or deuterated halothane--with a fractional inspired O2 concentration (FIO2) of 0.40 or 0.10--for 4 h. Livers removed from half of the animals immediately after anesthesia were evaluated for organic fluorine bound to protein and lipid. The remaining animals were evaluated for a hepatotoxic response up to 96 h after exposure. Only guinea pigs that received 1% halothane at an FIO2 of 0.40 had centrilobular necrosis develop with significantly increased plasma alanine aminotransferase activities. All other treatment conditions significantly reduced oxidative halothane biotransformation, as indicated by decreased plasma trifluoroacetic acid concentrations. These reductions were associated with a significant decrease in organic fluorine bound to hepatic proteins. An FIO2 of 0.10 during halothane anesthesia significantly enhanced reductive biotransformation, as indicated by plasma fluoride ion concentrations. This was associated with a significant increase in organic fluoride bound to hepatic lipids. Centrilobular necrosis did not develop under these conditions. Thus, covalent binding to subcellular proteins by the trifluoroacetyl acid chloride intermediate generated by oxidative halothane biotransformation is implicated as a mechanism of centrilobular necrosis in guinea pigs. Binding to lipids by reductive pathway generated free radicals does not appear to be involved in production of the lesion.
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PMID:Covalent binding of oxidative biotransformation intermediates is associated with halothane hepatotoxicity in guinea pigs. 224 97

The role of superoxide and lipid peroxidation in liver injury induced by ischemia-reperfusion was investigated in rats. Ischemic condition of the liver was created by applying small clamps to the right branch of portal vein and the right hepatic artery for 15 min. Clamping of hepatic artery and portal vein could decrease the hepatic blood flow to about 30% of that measured before the clamping. Levels of serum GPT and thiobarbituric acid (TBA) reactive substances in the liver tissue were significantly increased 30 min after the reperfusion following 15 min of ischemia. The increase in serum GPT and TBA reactants in the liver tissue was significantly inhibited by the treatment with superoxide dismutase combined with catalase. The treatment with allopurinol significantly inhibited the elevation of serum GPT levels and showed a tendency to inhibit the increase in TBA reactants in liver tissue. These results suggest that active oxygen species and lipid peroxidation may play an important role in the pathogenesis of ischemia-reperfusion injury in the liver, and hypoxanthine-xanthine oxidase system may be one of the main sources of active oxygen species.
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PMID:[Role of active oxygen species and lipid peroxidation in liver injury induced by ischemia-reperfusion]. 232 99

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.
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PMID:Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs. 236 Jun 37

The purpose of this study is to examine effects of hyperoxic gas mixtures on changes of blood indices during bicycle exercise of human. Oxygen-enriched gases (30% O2) were inspired during the ramp load exercise of 25 watt/min. Changes of blood indices were analyzed with Sequential Multiple Analyzer with the computer (SMAC). The improvement of exercise performance were discussed about relationship between function of hyperoxic gas and physiological mechanism. Three experimental conditions were set as follows (I) 30% O2 +N2 gases balance, (II) air (21% O2), and (III) 30% O2 +2% CO2 +N2 gases balance. Arterial blood were sampled from the radial artery of the forearm in order to analyze following items; 1) pH level, PaO2, PaCO2, and HCO3 of these blood gases, 2) Blood sugar, TG, and F-CH of the blood contents, 3) red blood corpuscle, white blood corpuscle, Hb, and Ht values, 4) LDH, CK, GOT, and GPT of the blood enzymes, 5) TP, ALB, Na, K, Ca and Cl of the electric ions. In the case of inspiring hyperoxic gases, the recovery rate of blood indices increased after this ramp load exercise remarkably, and the whole exercise metabolism were removed from acidosis tendency to alkalosis value of the resting condition significantly. At hyperoxic experimental conditions, the blood sugar and oxygen consumption were much more decreased than these at normal oxygen content one during both states of exercise and recovery times. These data of the blood indices would support strongly to the hypothesis that improvement of oxygen delivery should be depended upon the enhanced performance with the hyperoxic gases. There might be effects of the hyperoxia on the cellular metabolism and on function of the vascular muscle during those aerobic exercise.
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PMID:[Effects of breathing high concentrations of oxygen on changes in blood indices during bicycle exercise]. 238 13

Prostaglandin E1 was administered to 19 patients to induce hypotension during intracranial surgery. Urine volume during the operation and after the first day was well maintained, and serum BUN and creatinine were within normal ranges after the surgery. Serum GOT and GPT increased significantly on the 7th and 14th day after the operation compared with the control, but this did not seem to be the results of PGE1 administration. LDH and ALP showed no significant change. Thirty minutes and two hours after the administration of PGE1, arterial blood oxygen tension decreased significantly. These results suggest that PGE1 does not adversely affect the liver and kidneys, and it can be used safely and is useful to control blood pressure during intracranial operation.
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PMID:[Clinical use of prostaglandin E1 during intracranial surgery]. 238 55

Various parameters were investigated to know whether a viability assay before liver transplantation was possible. Two series of experiment were performed. The first consisted of 2 groups of ischemically injured canine livers which had definitely different viability. GPT, bilirubin, lactate pyruvate ratio, ketone body ratio ammonium in the perfusate, hepatic tissue flow, and hepatic tissue oxygen consumption were measured during hypothermic machine perfusion at 6 degree C. As a result, tissue flow and tissue oxygen consumption were found to be good parameters because they indicated the viabilities of the isolated liver grafts accurately and instantly in the both groups. In the second series, 9 ischemically injured canine livers were hypothermically perfused to assay their viability and orthotopically transplanted. In the cases that the oxygen consumption was below 3.0 mumol/min./100g, no grafts sustained the lives of the recipients. We concluded that if we measure the oxygen consumption of hypothermically perfused livers, we can eliminate the low viability livers before transplantation and avoid primary graft non-function.
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PMID:[Viability assay for liver transplantation]. 259 4

Four groups of isolated rat livers underwent perfusion at 37 degrees C for 1 h, at 37, 40, 43 or 45 degrees C, respectively, during the 2nd hour and then at 37 degrees C again for the 3rd hour. Vascular resistance slightly decreased during hyperthermia and then significantly increased after restarting normothermic perfusion. At 40 degrees C bile production, oxygen consumption, glucose and lactate release did not significantly differ from those found in the 37 degrees C group. At 43 and 45 degrees C all these parameters were significantly impaired when compared to the 37 and 40 degrees C groups and did not recover after normothermic perfusion was restored. GOT and GPT release increased in proportion to the temperature. Microscopic examination revealed normal histologic features in 37 and 40 degrees C specimens while alterations such as vacuolization and focal necrosis were found in the 43 and 45 degrees C groups. These data indicate that the highest temperature that is well tolerated by isolated rat livers for 1 h is located between 40 and 43 degrees C.
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PMID:Effect of hyperthermia on isolated perfused rat liver. 262 78


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