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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against oxidative organ damage distant from the original burn wound. Under brief ether anesthesia, the shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 seconds. EGb (50 mg/kg/day) or saline was administered intraperitoneally immediately and at 12 hours after the burn injury. Rats were decapitated 24 hours after burn injury and tissue samples from the liver and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by the chemiluminescence technique. Tissues also were examined microscopically. Blood urea nitrogen, creatinine, alanine aminotransferase, and aspartate aminotransferase levels and tumor necrosis factor- and lactate dehydrogenase activity were assayed in serum samples. Severe skin scald injury (30% TBSA) caused a significant decrease in GSH levels and significant increases in MDA levels, MPO activity, and collagen content of hepatic and renal tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum alanine aminotransferase, aspartate aminotransferase, and blood urea nitrogen levels, as well as lactate dehydrogenase and tumor necrosis factor-, were increased in the burn group as compared with the control group. However, treatment with EGb reversed all these biochemical indices, as well as histopathological alterations that were induced by thermal trauma. Our results show that thermal trauma-induced oxidative damage in hepatic and renal tissues is protected by the administration of EGb, with its antioxidant effects. Therefore, its therapeutic role as a "tissue injury-limiting agent" must be further elucidated in oxidant-induced tissue damage.
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PMID:Ginkgo biloba extract improves oxidative organ damage in a rat model of thermal trauma. 1627 67

Among the anesthetics influencing the nitric oxide (NO) pathway, ketamine is widely reported in the literature. We researched the variations in blood physiological parameters following ketamine/xylazine- or pentobarbital-induced anesthesia, with particular emphasis on plasmatic NO levels and oxidative stress-related factors. The effects of ketamine on hepatic blood flow during deep hypothermia were also examined. Adult male Sprague-Dawley rats were anesthetized intraperitoneally with ketamine/xylazine or with sodium pentobarbital. Animals underwent serial blood extraction to analyze acid-base balance and lactate levels in blood, as well as NO, MDA, SH groups, and AST levels in plasma samples. We demonstrated that ketamine leads to increased plasmatic NO levels, induces metabolic acidosis, and causes oxidative damage, though without reaching hepatic toxicity. When experimental hypothermia was induced, ketamine affected hepatic blood flow. Based on these results, we suggest that studies on physiological processes involving NO should exercise caution if anesthesia is induced by ketamine.
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PMID:Nitric oxide induced by ketamine/xylazine anesthesia maintains hepatic blood flow during hypothermia. 1638 21

In seven dogs weighing 17-25 kg, the terminal segment of the thoracic duct was isolated, under total pentobarbital anesthesia, so as to collect lymph continuously before, during and after infusion of a 20% fat emulsion Intralipid (Vitrum). Arterial blood and lymph were withdrawn simultaneously for analysis of total protein, amylase, cholesterol, triglycerides, urea and AST. The lymph flow rate was calculated in ml/min. Compared with the control period, during which a 5% glucose solution was administered, a two-hour infusion of the fat emulsion did not change the lymph flow rate nor the levels of biochemical parameters monitored in lymph. These results distinguish intravenous administration of a fat emulsion from a situation, in which fat is administered orally. The unchanged lymph amylase levels following fat administration suggest that no significant stimulation of external pancreatic secretion occurs after this route of fat administration.
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PMID:The effect of intravenous administration of fat emulsion on the flow rate and composition of thoracic duct lymph in the dog. 1683 69

Inflammatory reactions play an important role in ischemia/reperfusion injury in various organs. Since histamine is closely related to inflammatory reactions and immune responses, effects of postischemic administration of histaminergic ligands on ischemia-induced liver injury were examined in rats. Animals were subjected to warm ischemia for 30 min by occlusion of the left portal vein and hepatic artery under halothane anesthesia, and liver damage was evaluated by assessing plasma concentrations of transaminases after 24 h. Warm ischemia for 30 min provoked severe liver damage after 24 h, and the plasma concentrations of alanine transaminase (ALT) and aspartate transaminase (AST) were 8600 I.U./l and 13100 I.U./l, respectively. Subcutaneous injections of histamine twice, immediately and 6 h after reperfusion (20 mg/kg, each), alleviated liver damage. The plasma concentrations of ALT and AST in the histamine group were 35% and 24% of those in the control group, respectively. Neither mepyramine (3 mg/kg x 2), an H1 antagonist, nor cimetidine (15 mg/kg x 2), an H2 antagonist, affected the outcome in histamine-treated rats. However, thioperamide (5 mg/kg x 2), an H3/H4 antagonist, completely abolished the alleviation caused by histamine. Administration of dimaprit (1-10 mg/kg x 2), an H2/H4 agonist, mimicked the protective effect of histamine, and the effect of dimaprit is reversed by thioperamide, whereas neither H1 nor H2 antagonists altered the outcome caused by dimaprit. Clozapine (15 mg/kg x 2), an H4 agonist, also mimicked the protective effect of histamine. These findings indicate that stimulation of histamine H4 receptors after ischemic events prevents development of reperfusion injury in the liver.
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PMID:Suppression of ischemia/reperfusion liver injury by histamine H4 receptor stimulation in rats. 1686 Mar 12

The objective of this study was to investigate some metabolic and clinical effects of feed deprivation in horses that were submitted for orthopaedic surgery. The effects of preoperative feed restriction were investigated in 20 horses submitted for elective orthopaedic surgery. The patients were fasted from 12 hours before until 4 hours after surgery. Serum free amino acids, glucose,free fatty acids (FFA), white blood cell counts, creatine kinase (CK) and aspartate aminotransferase (AST) were determined 24 hours before surgery, 2 hours after the end of anaesthesia and 24 and 72 hours after surgery. Besides, abdominal sounds, appetite, faecal quality and body temperature were examined. Serum free amino acids did not react homogenously, concentrations were partly increasing or decreasing. Plasma glucose and FFA increased after surgery and returned to their preoperative levels 72 hours after surgery. A significant rise of the segmented granulocytes occurred 24 hours after surgery, all other parameters of the leukogram did not exceed the physiological range. AST reached its highest activity 24 hours after surgery, whereas CK activities were highest at 2 hours after surgery. Abdominal sounds were significantly reduced until 24 hours after surgery, however, appetite was not depressed. Faecal quality was physiological after surgery. Mean body temperature stayed within the physiological range. In conclusion, a relatively short perioperative fasting period had significant effects on the metabolic traits in horses, however the effects on physiological functions were minor. The consequences of major surgical procedures need to be addressed in future studies.
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PMID:Metabolic and clinical traits in horses undergoing feed deprivation for elective orthopaedic surgery. 1741 36

Severe burn induces the activation of an inflammatory cascade that contributes to the development of subsequent immunosuppression, increased susceptibility to sepsis, as well as generation of reactive oxygen radicals and lipid peroxidation, leading to multiple organ failure. In the present study, we investigated whether rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligand is protective against burn-induced remote organ injury. Under brief ether anaesthesia, shaved dorsum of the rats were exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10s. Rosiglitazone (4 mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn. Rats were decapitated 24h after injury and the tissue samples from lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, and creatinine, blood urea concentrations (BUN) were determined to assess liver and kidney function, respectively. Serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and lactate dehydrogenase (LDH) were also assayed. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, and significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum ALT, AST and BUN levels, as well as LDH, IL-1 beta and TNF-alpha were elevated in the burn group as compared to the control group. Rosiglitazone treatment reversed all these biochemical indices. According to the findings of the present study, rosiglitazone possesses a anti-inflammatory effect that prevents burn-induced damage in remote organs and protects against organ damage.
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PMID:Rosiglitazone, a PPAR-gamma ligand, protects against burn-induced oxidative injury of remote organs. 1746 12

Sepsis is the leading cause of death for intensive care patients. Lipopolysaccharide (LPS) administration to animals under anesthesia is a strategy for the study of uncontrolled release of proinflammatory cytokines. Anesthetics have been indicated that they can specially affect immune responses, such as the inflammatory response. Pentobarbital is an anesthetic used mainly in animal studies. Thus, the effect of pentobarbital on tumor necrosis factor-alpha (TNF-alpha) release was determined. The results revealed that pentobarbital suppressed the expression of TNF-alpha mRNA and its proteins, which may result from the decrease in the activities of nuclear factor-kappaB and activator protein 1 and the reduction of the expression of p38 mitogen-activated protein kinase by pentobarbital. After the inhibitory activity of the pentobarbital for TNF-alpha release was proven in vivo, the cytotoxic effects of LPS were examined in vivo with or without pentobarbital treatments. In vivo results indicated that plasma levels of alanine aminotransferase, aspartate aminotransferase, lactic dehydrogenase, creatine kinase, serum urea nitrogen, and amylase decreased dramatically in the anesthetic group with pentobarbital administration. Finally, the effect of pentobarbital on TNF-alpha-related cell death was monitored in vitro, and the results indicated the pentobarbital could directly enhance the viabilities of cells under the treatment of TNF-alpha and protected cells from apoptosis induced by deferoxamine mesylate-induced hypoxia. These results suggest that pentobarbital significantly influences the LPS-induced inflammatory response and protects cells from death directly and indirectly induced by TNF-alpha. The information provides a perspective to re-evaluate the results of the experiments in which animals were anesthetized with pentobarbital. The anti-inflammatory effects of the drugs may have been caused by the synergistic effect of pentobarbital.
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PMID:The reduction of tumor necrosis factor-alpha release and tissue damage by pentobarbital in the experimental endotoxemia model. 1754 46

The authors previously reported a case of decreased pseudocholinesterase activity in a patient with HELLP syndrome. It was assumed that the reduced pseudocholinesterase activity in HELLP syndrome is associated with impaired liver function. The present study assesses the prevalence of low pseudocholinesterase in patients with HELLP syndrome. Serum pseudocholinesterase activity was determined with spectrophotometer in 15 patients with HELLP syndrome. Two control groups matched for gestational age were recruited: 15 healthy women with uncomplicated pregnancy and 15 women with severe preeclampsia without HELLP. The prevalence of reduced pseudocholinesterase activity lower than normal limit was 60.0% (9/15) in patients with HELLP syndrome, 33.3% (5/15) in patients with severe preeclampsia, and 6.6% (1/15) in women with normal pregnancy, respectively (P =.009). The pseudocholinesterase activity was found to correlate with serum alanine aminotransferase levels (r = 0.417, P = .006) and with serum aspartate aminotransferase levels (r = 0.462, P = .002). Considering the increased prevalence of reduced pseudocholinesterase activity in patients with HELLP syndrome, the authors suggest that whenever general anesthesia is applied in these patients, the anesthesiologist should be aware that the patient may show slow metabolic degradation of choline-ester drugs.
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PMID:Reduced pseudocholinesterase activity in patients with HELLP syndrome. 1763 31

Twelve healthy two-month-old Landrace x Yorkshire pigs of both sexes were randomly assigned to receive either tiletamine and xylazine (zx) or zolazepam and xylazine followed 20 minutes later by yohimbine (zxy). The pigs' scores for immobilisation and analgesia, and their rectal temperature, heart rate, respiration rate, pO(2), pCO(2), alkaline phosphatase, aspartate aminotransferase, glucose and total plasma proteins were determined before and five, 25, 45, 65 and 85 minutes after the administration of the tiletamine/zolazepam and xylazine. The mean total scores for immobilisation and analgesia of the zxy pigs were significantly lower than those of the zx pigs after 85 minutes. The mean rectal temperatures of the zxy pigs were significantly lower than those of zx pigs after 25, 45 and 65 minutes. The mean respiratory rates of the zx pigs were significantly lower than those of zxy pigs after five minutes. The mean pCO(2) of the zxy pigs were significantly lower than those of zx pigs five minutes after the administration of yohimbine. The mean glucose concentration of the zxy pigs were significantly lower than those of zx pigs after 65 and 85 minutes. The mean concentration total protein of the zxy pigs were significantly lower than those of zx pigs throughout the period of anaesthesia. Both groups became laterally recumbent within three minutes. When recovering from anaesthesia, the pigs treated with yohimbine took significantly less time to achieve sternal recumbency (mean [sd] 52.2 [8.9] v 76.2 [20.6] minutes) and less time to be able to stand (mean [sd] 77.0 [9.8] v 98.7 [15.8] minutes), and walk (mean [sd] 81.3 [11.3] v 110.8 [18.6] minutes).
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PMID:Antagonistic effects of yohimbine in pigs anaesthetised with tiletamine/zolazepam and xylazine. 1798 41

To document the changes in serum serotonin, adrenocorticotrophic hormone (ACTH), corticosterone levels and select biochemical parameters in response to inhalant anaesthesia, 20 New Zealand White (NZW) rabbits were assigned to two treatment groups: halothane and isoflurane. Induction of anaesthesia was achieved using a face mask (3.5% halothane and 4.5% isoflurane in oxygen) followed by endotracheal intubation and maintenance of anaesthesia for 30 min (1.5% halothane and 2.5% isoflurane in oxygen). Blood samples were obtained before anaesthetic induction, and at 1, 10, 30, 60, 120 min and 24, 48 and 72 h after endotracheal intubation. Serum serotonin and corticosterone levels were measured by competitive enzyme immunoassay, ACTH by radioimmunoassay. Serum glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen (BUN) and creatinine levels were measured using an automated analyser. Significant increases in serum ACTH and corticosterone levels occurred after halothane administration while serum serotonin levels did not change. An increase in serum corticosterone and serotonin levels occurred in the isoflurane group but no changes in ACTH concentrations were detected. Administration of halothane significantly increased serum glucose, ALT, AST, BUN and creatinine levels. After isoflurane administration, there was a significant increase in serum glucose, AST, BUN and creatinine levels. Based on these results, halothane stimulates the hypothalamic-pituitary-adrenal axis to a greater extent than isoflurane, but isoflurane increases serum serotonin levels. Both anaesthetic agents alter select biochemical parameters. These results should be taken into account when blood samples are evaluated in treated isoflurane or halothane anaesthetized rabbits.
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PMID:Pituitary-adrenocortical axis, serum serotonin and biochemical response after halothane or isoflurane anaesthesia in rabbits. 1798 36


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