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)

The continuous intragastric in vivo enteral feeding model in the rat developed by Tsukamoto and French has been very useful; however, it requires surgical expertise. Recently, we found that Kupffer cells isolated from rats treated only once with ethanol were sensitized to endotoxin 24 hours later. Accordingly, these experiments were designed to determine if a new, simple animal model of ethanol hepatotoxicity could be developed based on Kupffer cell sensitization. Female Wistar rats were given ethanol (5 g/kg body weight) once every 24 hours intragastrically. Livers were stained with hematoxylin-eosin to assess steatosis, inflammation, and necrosis, and tissue triglycerides, serum transaminases, and plasma endotoxin were measured. Kupffer cells were isolated 0 to 24 hours after one intragastric dose of ethanol daily, and intracellular Ca2+ ([Ca2+]i) was measured using fura-2, while tumor necrosis factor alpha (TNF-alpha) was measured by enzyme-linked immunosorbent assay. CD14 was evaluated by Western and Northern analysis. Ethanol caused steatosis, necrosis, and inflammation in only a few weeks, and after 8 weeks, serum aspartate transaminase (AST) levels were doubled. Values were similar to levels achieved in the enteral feeding model. Triglycerides were also increased significantly by ethanol as expected, and endotoxin levels were increased to 70 to 80 pg/mL. This latter increase was prevented (<20 pg/mL) by antibiotics implicating endotoxin. In isolated Kupffer cells from untreated control rats, [Ca2+]i increased to 82 +/- 7 nmol/L after addition of lipopolysaccharide (LPS) (100 ng/mL), and levels were elevated about twofold by ethanol given 24 hours earlier (174 +/- 15 nmol/L). In addition, TNF-alpha production by Kupffer cells was increased fourfold in cells isolated from rats treated with ethanol 24 hours earlier. Sterilization of the gut with antibiotics blocked all effects of ethanol on [Ca2+]i and TNF-alpha release completely. Moreover, 4 weeks after ethanol, CD14 in Kupffer cells was elevated about twofold. A new, simple chronic model of ethanol hepatotoxicity has been developed here based on sensitization of Kupffer cells to endotoxin.
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PMID:Development of a new, simple rat model of early alcohol-induced liver injury based on sensitization of Kupffer cells. 1034 8

This study determined whether free radical formation by the liver, tumor necrosis factor (TNF)-alpha production by isolated Kupffer cells, and plasma endotoxin are affected by dietary saturated fat. Rats were fed enteral ethanol and corn oil (E-CO) or medium-chain triglycerides (E-MCT) and control rats received corn oil (C-CO) or medium-chain triglycerides (C-MCT) for 2 wk. E-CO rats developed moderate fatty infiltration and slight inflammation; however, E-MCT prevented liver injury. Serum aspartate aminotransferase levels, gut permeability, and plasma endotoxin doubled with E-CO but were blunted approximately 50% with E-MCT. In Kupffer cells from E-CO rats, intracellular calcium was elevated by lipopolysaccharide (LPS) in a dose-dependent manner. In cells from E-MCT rats, increases were blunted by approximately 40-50% at all concentrations of LPS. The LPS-induced increase in TNF-alpha production by Kupffer cells was dose dependent and was blunted by 40% by MCT. E-CO increased radical adducts and was reduced approximately 50% by MCT. MCT prevent early alcohol-induced liver injury, in part, by inhibition of free radical formation and TNF-alpha production by inhibition of endotoxin-mediated activation of Kupffer cells.
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PMID:Medium-chain triglycerides inhibit free radical formation and TNF-alpha production in rats given enteral ethanol. 1071 67

Liver dysfunction is a well-recognized complication of intestinal failure in children. Advances in total parenteral nutrition (TPN) have allowed these children to survive while their intestinal tract gradually adapts. Unfortunately TPN may lead to cholestatic liver disease particularly in the young children. Progression of liver disease is associated with a poor prognosis and is an indication for small bowel transplantation. We report our experience of orthotopic liver transplantation in four children with short gut and sequential liver and small bowel transplantation in one child. All children had TPN-related liver failure. Causes of intestinal failure included necrotising enterocolitis (n=2), gastroschisis (n=1), intestinal atresia (n=1), and megacystic, microcolon syndrome (n=1). At the time of liver transplantation the children's mean age was 10.9 months (2.5-24) and weight 6.7 kg (4.8-10.1). The mean serum bilirubin was 522 micromol/liter (299-823), aspartate transaminase 423 IU/liter (49-1024) and international normalized ratio 2.8 (2-3.9). There were two deaths both from respiratory failure secondary to adenovirus pneumonia including the child who received a sequential small bowel transplant. Three children with isolated liver grafts are alive and off TPN at 20 months (mean) follow up (range 6-35). Isolated orthotopic liver transplantation has a role in selected children with intestinal failure, particularly those with short but normally functioning gut and progressing with satisfactory intestinal adaptation but developing liver disease. Those children with TPN-related liver disease and unadapted gut or irreversible intestinal disease need combined liver and small bowel transplantation. Sequential small bowel transplantation is feasible after orthotopic liver transplantation and may provide an option for the child with terminal liver and small bowel failure.
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PMID:Isolated liver transplant and sequential small bowel transplantation for intestinal failure and related liver disease in children. 1086 33

Activities of several metabolic enzymes show distinct patterns of zonation along the intestinal tract of tilapia (Oreochromis niloticus), rainbow trout (Oncorhynchus mykiss) and copper rockfish (Sebastes caurinus). Zonation is species and enzyme specific, with different metabolic activities concentrated in specific areas, and few generalizations can be made. The rockfish show the smallest degree of zonation, with highest activities in the third quarter of the intestine, and shallow gradients to either side, and a general upswing in activity towards the distal end. In the trout, mitochondrial enzyme activities (citrate synthase, glutamate dehydrogenase, malate dehydrogenase) are highest in the pyloric caeca and decrease along the length of the small intestine. This pattern is accentuated for malic enzyme and glucose 6-phosphate dehydrogenase. These enzymes drop precipitously in activity after the first few sections of the small intestine, while other NADP-linked dehydrogenases (isocitrate dehydrogenase, and 6-phosphogluconate dehydrogenase) show moderate activity in pyloric caeca and peak toward the distal section of the small intestine. In tilapia, glutamate dehydrogenase shows a similar decrease as in trout, but citrate synthase peaks towards the distal sections. NADP-dependent dehydrogenases reveal distinct patterns, peaking in different sections of the intestine-malic enzyme in the proximal midsection, glucose 6-phosphate dehydrogenase in the distal mid-section, and isocitrate dehydrogenase in the anal section. Enzyme activities in the stomach of trout and tilapia also show zonation, with the midsection generally displaying the highest activities. A 5-day treatment of tilapia with an intraperitoneal cortisol deposit (25 mg kg(-1) wet mass) drastically alters metabolic performance along the gut in enzyme specific patterns, generally increasing enzyme activities in site-specific arrangements. Cortisol treatment also leads to the expected increases in activities of phosphoenolpyruvate carboxykinase, pyruvate kinase and aspartate aminotransferase in liver, but not in kidney. Aspartate aminotransferase is the only enzyme in brain significantly increased by cortisol treatment. Short-term food deprivation changes enzyme patterns, often resembling those observed after cortisol administration. We conclude that brain, liver and intestinal amino acid metabolism is an important target for cortisol action in fish and that metabolic zonation is a key factor to be reckoned with when analyzing physiological phenomena in the fish intestine.
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PMID:Metabolic zonation in teleost gastrointestinal tract. Effects of fasting and cortisol in tilapia. 1278 63

The toxic effects of chronic oral administration (60 days) of aqueous crude extract (AE) of Plantago australis Lam. (Plantaginaceae) in rats at doses of 850 and 1700 mg/kg on biochemical (ALT, AST, creatinine, urea, glucose, alkaline phosphatase, total proteins and albumin), hematological (complete hemogram), and histopathological (heart, lung, liver, kidney, esophagus, stomach and gut) parameters were studied. All biochemical and hematological parameters were found to be in the normal range, but ALT in animals that received AE of 850 mg/kg was higher. Histopathological analysis of organs, especially the liver did not present alterations.
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PMID:Oral subchronic toxicity of aqueous crude extract of Plantago australis leaves. 1290 47

Using a polyclonal antiserum to Dippu-allatostatin 7 (Dippu-AST 7; formerly AST 1) of the cockroach Diploptera punctata, we have demonstrated the presence of AST-like immunoreactivity (ALI) in cells and processes throughout the nervous system, gut, and peripheral tissues of unfed fifth instar and adult Rhodnius prolixus. ALI in apparent neurosecretory cells of the brain, suboesophageal ganglion, and mesothoracic ganglionic mass, as well as in midgut endocrine cells, suggests that Rhodnius allatostatins may act as neurohormones/hormones. The presence of ALI in possible interneurons and areas of neuropile throughout the CNS also suggests roles as neuromodulators and/or neurotransmitters. Dippu-AST 7 inhibits spontaneous and leucokinin 1 (LK 1)-induced contractions of the Rhodnius hindgut in a dose-dependent manner. The low concentrations capable of inhibiting both spontaneous (10(-12)M) and LK 1-induced contractions (10(-10) to 10(-9)M) suggest that ASTs may be acting as neurohormones/hormones on the hindgut. We have also shown that Dippu-AST 7 influences the muscle activity of the Rhodnius dorsal vessel at concentrations as low as 10(-11)M.
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PMID:The distribution and effects of Dippu-allatostatin-like peptides in the blood-feeding bug, Rhodnius prolixus. 1470 34

The gene encoding the Spodoptera frugiperda allatostatin type-A peptide family (Y/FXFGL-amides) was isolated from S. frugiperda brain cDNA. The gene encodes a precursor of 231 amino acids containing nine (or ten) Y/FXFGL-a peptides that are tandemly arranged in three blocks. The comparison of the Spofr-AST A precursor with the respective precursor genes from two other lepidopteran species, Helicoverpa armigera and Bombyx mori, shows high homology in size, sequence (84 and 57%, respectively), and organisation of the allatostatins. One-step RT-PCR analysis using a Spofr-AST A-6 to A-9 probe shows that the gene is not only expressed as one transcript in the brain and midgut of larvae and adults in a time- and tissue-specific manner, but also in the reproductive tissues of adult S. frugiperda. Data confirm the nature of the allatostatin type-A peptides as brain/gut myoregulatory hormones, whereas their function(s) in ovaries, oviduct, and testes still have to be resolved. The cell-specific localization of the preprohormone expression, as demonstrated by whole mount in situ hybridization, confirms the overall distribution of the Spofr-AST A preprohormone as shown by RT-PCR and supports the pleiotropic functions of the peptides.
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PMID:Type-A allatostatins from the fall armyworm, Spodoptera frugiperda: molecular cloning, expression and tissue-specific localization. 1521 50

Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.
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PMID:Determination of the acute 50% lethal dose T-2 toxin in adult bobwhite quail: additional studies on the effect of T-2 mycotoxin on blood chemistry and the morphology of internal organs. 1528 27

Cricket- or B-type allatostatins [W(X(6))W-amides] inhibit the biosynthesis of juvenile hormones in vitro in crickets. Peptides of this family are present also in other insects where they may bare different functions. Here we report the identification of a partial sequence of the B-type preproallatostatin from Gryllus bimaculatus. By PCR screening of a random primer cDNA library and by RACE, a 535bp 3'cDNA sequence was obtained which encodes a putative translation product of 85 amino acids, containing three copies of Grybi-AST B1 and one copy each of Grybi-AST B2, Grybi-AST B3, and Grybi-AST B6. The last represents a novel member of this peptide family. By means of one-step RT-PCR, RNA dot blot, and RT in situ PCR analyses the mRNA expression of the gene in the central nervous system and the digestive tract of female adult crickets was demonstrated. The results confirm that the B-type allatostatins of G. bimaculatus are brain-gut peptides.
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PMID:Cloning and tissue-specific localization of cricket-type allatostatins from Gryllus bimaculatus. 1550 83

The crude extract of Achillea millefolium (Am.Cr) was studied for its possible hepatoprotective effect against d-galactosamine (d-GalN) and lipopolysaccharide (LPS) induced hepatitis in mice and antispasmodic effect in isolated gut preparations to rationalize some of the folklore uses. Co-administration of d-GalN (700 mg/kg) and LPS (25 microg/kg) produced 100% mortality in mice. Pre-treatment of animals with Am.Cr (300 mg/kg) reduced the mortality to 40%. Co-administration of d-GalN (700 mg/kg) and LPS (1 microg/kg) significantly raised the plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared with values in the control group (p < 0.05). Pre-treatment of mice with Am.Cr (150-600 mg/kg) significantly prevented the toxins induced rise in plasma ALT and AST (p < 0.05). The hepatoprotective effect of Am.Cr was further verified by histopathology of the liver, which showed improved architecture, absence of parenchymal congestion, decreased cellular swelling and apoptotic cells, compared with the toxin group of animals. In isolated rabbit jejunum preparations, Am.Cr caused a concentration-dependent (0.3-10 mg/mL) relaxation of both spontaneous and K(+)-induced contractions as well as shifting the Ca(++) concentration-response curves (CRCs) to the right, similar to that caused by verapamil. These results indicate that the crude extract of Achillea millefolium exhibits a hepatoprotective effect, which may be partly attributed to its observed calcium channel blocking activity.
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PMID:Studies on hepatoprotective, antispasmodic and calcium antagonist activities of the aqueous-methanol extract of Achillea millefolium. 1661 41


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