Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Xanthine oxidase may contribute to oxygen free radical formation during reoxygenation after hypoxia, but in humans the enzyme is present in substantial amounts only in the liver and intestine. We developed a sensitive assay for xanthine oxidase using 14C-xanthine as substrate and investigated whether xanthine oxidase was released into the systemic circulation when 19 newborn pigs were resuscitated after severe hypoxemia. In five piglets plasma xanthine oxidase concentrations increased from undetectable levels to a median value of 8 (range 4-18) microU/ml after 30 min of reoxygenation. In these pigs serum aspartate aminotransferase increased from 45 to 148 U/l, while alanine aminotransferase was unchanged (28-31 U/l). The release of xanthine oxidase did not seem to correlate with the severity of the histological brain damage after 4 days. We conclude that only low levels of xanthine oxidase are released to the systemic circulation after severe hypoxemia in newborn pigs.
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PMID:Release of xanthine oxidase to the systemic circulation during resuscitation from severe hypoxemia in newborn pigs. 763 44

We report the usefulness of monitoring hepatic venous saturation (ShVO2) during open heart surgery for a patient with severe liver dysfunction. The patient was a 55-year-old man who had been suffering from acute aortic regurgitation due to bacterial endocarditis. Indocyanine green retention test at 15 min was 55%. Serum GOT, GPT and T bilirubin were 56 U.l-1, 35 U.l-1 and 1.5 mg.dl-1 respectively. Aortic valve replacement was scheduled in spite of severe liver dysfunction because amelioration of congestive heart failure after the operation was expected to improve liver dysfunction to the previous chronic state. Anesthesia was induced and maintained by intermittent administration of diazepam and low dose of fentanyl with 100% oxygen. After induction, we inserted a balloon tipped pulmonary catheter with ultra-red beam into hepatic vein by fluoroscopy guidance and monitored ShVO2 as an index of hepatic oxygen supply/demand balance. During re-insertion of a thoracic catheter, we could detect the continued decrease in hepatic vein saturation even after the improvement of systemic circulatory state. Postoperatively, liver function became slightly worse for a short period and improved thereafter. These results suggest that ShVO2 monitoring is clinically useful in detecting hepatic oxygen supply/demand imbalance which circulatory monitoring could not uncover during open heart surgery.
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PMID:[The usefulness of monitoring hepatic venous saturation during open heart surgery for a patient with severe liver dysfunction]. 763 78

Sixty gnotobiotic rats with 5 strains of bacteria in intestine were randomized to 4 groups: (1) Sham injury group (controls, n = 6). (2) Early fluid resuscitation (EFR) group (n = 24), receiving fluid resuscitation (Parkland formula) immediately after scald (40% TBSA, third degree). (3) Delayed fluid resuscitation (DFR) group (n = 24) receiving resuscitation 6 hours later after scald. (4) Treatment group (n = 12) receiving DFR and the therapy of VitC and VitE. At 8, 24, 48 and 72 hours after injury, the animals (n = 6, at each point) were sacrificed and the content of oxygen free radicals (OFR), SOD,GSHPx and MDA in the heart, liver, kidney and lung were determined. Morphological Changes of organs, PaO2, PaCO2 and the content of serum CPK, LDH, GPT, GOT, BUN and Cr were also examined. Both EFR and DFR groups demonstrated elevated content of OFR and MDA and reduced content of SOD and GSHPx in their organs. Morphological and serological changes were also observed. All these changes were more obvious in DFR group than in EFR group. After the treatment of VitC and VitE, the changes were ameliorated. Our results suggested that DFR induced the production of OFR, resulting in lipid peroxidation and that OFR injury might be one of the main factors in the pathogenesis of multiple organ injury after DFR.
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PMID:[Multiple organ injury after delayed fluid resuscitation in severely scalded rats: role of oxygen free radicals]. 764 95

Porfimer sodium (Photofrin II) is a photosensitizer which distributes selectively to tumor tissues, and causes tumor cell death by combination with light irradiation. Photodynamic therapy (PDT) by combination of porfimer sodium and laser was developed as a new cancer therapy. Tumor selectivity of porfimer sodium are based on the following reasons; 1) high affinity for lipoprotein, especially, low density lipoprotein (LDL), 2) elevation of LDL receptor activity in cancer tissue, and 3) lack or imcompleteness of lymphatic system in cancer tissue. Porfimer sodium is activated by laser irradiation at 630 nm, which can reacts with tissue oxygen to produce highly reactive excited siglet oxygen (1O2). This highly reactive molecule is subsequently capable of killing tumor cells through oxidation of cellular component like mitochondrial enzymes. In addition, this highly reactive intermediate causes destruction of the tumor capillaries, which accelerates tumor cell death. The growth suppression or lethal damage to tumor cells by PDT of porfimer sodium and excimer dye laser were observed in experimental tumor models. In human clinical trials, the rates of complete response (CR) for roentgenographically occult lung cancer, stage I lung cancer, superficial esophageal cancer, superficial gastric cancer and carcinoma in situ or dysplasia of the cervix were 84.8%, 50.0%, 90.0%, 87.5% and 94.4%, respectively. The major side effects were cutaneous symptoms e.g. photosensitivity, pigmentation, increasing GOT, GPT but these symptoms were not severe. PDT using porfimer sodium and excimer dye laser must be clinically useful for the treatment of inoperable early cancer or conservation of organ functions.
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PMID:[Porfimer sodium (Photofrin-II)]. 766 80

Bleomycin-induced 6-thioguanine-resistant mutants pretreated with or without TRIEN (triethylenetetramine), a superoxide dismutase (SOD) inhibitor, or TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl), an SOD mimic, were analyzed by polymerase chain reaction (PCR)-based deletion screening in a Chinese hamster ovary (CHO) clone K1-BH4 and its derivative AS52 cells. As we proposed earlier, TRIEN would decrease and TEMPOL would increase the intracellular level of hydroxyl radical leading to a higher and lower recovery of deletion mutants. We found that the proportion of the deletion mutants induced by bleomycin at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus in K1-BH4 cells was 45.5% (25/55). The proportion of deletion HPRT- mutants induced by bleomycin pretreated with TRIEN was 31.0% (9/29) and with TEMPOL was 50.0% (14/28). The proportion of deletion mutants induced by bleomycin on the xanthine-guanine phosphoribosyltransferase (gpt) gene in AS52 cells was 61.0% (36/59). The proportion of deletion GPT- mutants induced by bleomycin pretreated with TRIEN was 56.8% (21/37) and with TEMPOL was 61.4% (27/44). The trend of the change of the proportion of bleomycin-induced deletion mutants as affected by TRIEN and by TEMPOL provides molecular evidence for the involvement of reactive oxygen species (ROS) in bleomycin mutagenesis in mammalian cells, in which deletion is a major type of induced mutation.
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PMID:Polymerase chain reaction-based deletion screening of bleomycin induced 6-thioguanine-resistant mutants in Chinese hamster ovary cells: the effects of an inhibitor and a mimic of superoxide dismutase. 769 Aug 90

I-compounds are indigenously appearing covalent DNA modifications that can be detected by 32P-postlabeling assay in tissues of normal animals without known exposure to any carcinogens or toxins. Although these compounds have not been structurally identified, indirect evidence from earlier work suggested the possibility of involvement of molecular fragments derived from lipid peroxides. Diquat is a herbicide that stimulates lipid peroxidation and massive intrahepatic oxidant stress through redox cycling-mediated generation of reactive oxygen species. In the present study, we examined the effects of diquat on hepatic I-compounds of male Fischer-344 rats. Two groups of rats, approximately 14 weeks and 8 weeks old, were given a hepatotoxic dose (0.1 mmol/kg) of diquat or equal volumes of saline, i.p. Two and 6 h later plasma alanine aminotransferase (ALT) activities were measured and hepatic DNA I-compound levels were examined by nuclease P1-enhanced 32P-postlabeling. Elevated ALT activities were observed in some animals in both groups, at both time points, but considerable inter-animal variation was seen. A total of 15-16 I-compound fractions were measured in control and in diquat-treated animals, but no extra spots indicative of treatment-induced adducts were detected. Despite the qualitative similarities, the quantities of individual I-compounds were markedly decreased at 2 h in diquat-treated animals of both age groups. In 14 week old rats the hepatic I-compound contents were decreased at 2 h by 22-59%, which was statistically significant (ANOVA, P < 0.05) for all of the 9 polar I-compound fractions and none of the non-polar fractions. Eleven I-spots from this group showed significant negative linear correlations (P < 0.05) with ALT values. In 8 week old rats treated with diquat a 22-43% depletion in I-compound contents was statistically significant for 4 of the 7 nonpolar and 2 of the 8 polar adduct fractions, but there was no significant correlation of I-compound contents with ALT values at the 2 h time point. By 6 h most of the I-spot levels had returned to normal or above normal values in both groups of animals. While most I-spots from 14 week old rats did not correlate with ALT levels at 6 h, two I-spots displayed positive correlations in the 8 week group. Overall, the susceptibility to diquat-associated DNA alterations appeared to differ with age.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Rapid decreases in indigenous covalent DNA modifications (I-compounds) of male Fischer-344 rat liver DNA by diquat treatment. 769 43

Halothane as an anaesthetic was evaluated in 12 adult camels, thiopentone being used as an induction agent. In six camels, clinical signs and haematological and blood biochemical changes were investigated while in other six haemodynamic, acid base and blood gas changes were monitored. The dose of thiopentone required to ensure intubation for halothane anaesthesia was 7.25 +/- 0.33 mg/kg. A modified technique of tracheal intubation was found to be safe and quick. During halothane administration all anaesthetic effects were predictable. Complete recovery occurred in 39.5 +/- 9.8 min after discontinuation of halothane administration. Halothane moderated the thiopentone-induced tachycardia. The mean arterial pressure decreased significantly. There was an increase in the arterial carbon dioxide and venous oxygen tension during halothane anaesthesia and development of hypoxaemia after its discontinuation. The alanine aminotransferase values increased during recovery, while plasma sodium, potassium and calcium decreased. Halothane appears to be safe for camels. However, to avoid hypoxaemia in the immediate post-anaesthetic period, oxygen administration should be continued.
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PMID:Evaluation of halothane as an anaesthetic in camels (Camelus dromedarius). 781 38

Platelet-activating factor (PAF) may play an important role in graft injury in liver transplantation. Livers excised from male Wistar rats were preserved in University of Wisconsin solution for 6 h and then perfused with Krebs-Henseleit solution containing vehicle (bovine serum albumin) or PAF. Impairment of parenchymal cells was assessed by reference to tissue adenosine triphosphate levels, oxygen consumption and alanine aminotransferase activity in the effluent. The effect on non-parenchymal cells was evaluated by measurement of purine nucleoside phosphorylase and alanine aminotransferase levels in the effluent. Administration of as little as 1.0 ng kg-1 PAF caused a significant decrease in adenosine 5'-triphosphate concentration and oxygen consumption (P < 0.05), although non-parenchymal cell injury was not affected. PAF can therefore cause liver graft dysfunction with hepatocytes as the main target, even in the absence of microcirculatory disturbance secondary to interaction between blood cells and endothelial cells.
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PMID:Effect of platelet-activating factor on cold-preserved liver grafts. 782 38

The potential beneficial effect of hepatocellular glutathione against inflammatory liver damage was investigated in a model of endotoxin-enhanced ischemia-reperfusion injury. Animals were subjected to 20 min of hepatic ischemia, followed by 4 hr of reperfusion. The injection of 0.5 mg/kg Salmonella enteritidis endotoxin potentiated liver injury and the postischemic oxidant stress, as indicated by increased plasma levels of glutathione disulfide. Depletion of hepatic glutathione levels by > 90% with phorone and inhibition of glutathione synthesis with buthionine sulfoximine further increased liver injury in this model, as indicated by enhancement of plasma alanine aminotransferase activities from 2,234 +/- 122 U/L to 4,024 +/- 282 U/L. Continuous infusion of a glutathione (GSH) solution in GSH-depleted animals (22 mumol/kg/hr) attenuated reperfusion injury by 55%. In vitro experiments demonstrated the capability of GSH to react rapidly with reactive oxygen species, such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). Only H2O2 oxidized GSH quantitatively to its disulfide; HOCl oxidized GSH to higher oxidation states. These data support the hypothesis that the enhanced release of hepatocellular GSH functions as a defense mechanism against reactive oxygen species generated by inflammatory cells during endotoxemia and reperfusion. This internal defense system of the liver may be of general importance in preventing, or at least limiting, liver damage by reactive oxygen generated in particular by Kupffer cells during their physiological function to remove gut-derived endotoxin and bacteria.
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PMID:Beneficial effects of extracellular glutathione against endotoxin-induced liver injury during ischemia and reperfusion. 783 22

In previous studies using isolated perfused rat livers, we have shown that reactive oxygen species are involved in hypoxic and ischaemic liver damage. Since albumin was shown to possess strong antioxidant properties we now investigated the capacity of albumin to prevent ischaemic and hypoxic damage in isolated perfused rat livers. Both, partial ischaemia and hypoxia/reoxygenation, resulted in marked hepatic injury as evidenced by an increased release of hepatic enzymes (GPT, LDH), by a strong decline of bile flow and by a decrease in hepatic GSH levels. With partial ischaemia, hepatic ATP depletion and calcium accumulation were also observed. Bovine serum albumin, added to the perfusate at concentrations of 0.1 or 1%, provided nearly complete protection against both types of liver injury. The same level of protection was also afforded by sulfhydryl-blocked and fatty acid-free bovine albumin preparations and by human albumin. In conclusion, the protective effect of albumin in our models of oxidative liver injury is neither due to the thiol moiety nor to the presence of oxidizable fatty acids in the albumin fraction. More likely, albumin provides protection by an unspecific binding of redox-active transition metal ions capable of catalyzing reactions which yield hydroxyl or hydroxyl-like radicals. Besides, unspecific sacrifice reactions of albumin with highly reactive oxygen species or other endogenous compounds may also be implicated.
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PMID:Protection by albumin against ischaemia- and hypoxia-induced hepatic injury. 787 Jun 99


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