Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum, urine and tissue biochemical findings were studied in 21 cases of fulminant Wilson's disease with respect to the value of a recently described biochemical index based on serum alkaline phosphatase and total serum bilirubin levels, and these cases were compared with 193 other cases of fulminant liver failure. Serum bilirubin, alkaline phosphatase and AST levels found in fulminant Wilson's disease were significantly different from those found in other cases of fulminant liver failure, but differentiation from other causes of fulminant liver failure on the basis of these biochemical parameters was not possible. The alkaline phosphatase/bilirubin and aspartate AST/bilirubin ratios derived from the above parameters were also significantly lower in fulminant Wilson's disease than in other categories of fulminant liver failure, but distinction between diagnostic categories on this basis was not possible. When ratios that correctly identified all cases of fulminant Wilson's disease were selected, 59/190 (31%) and 84/190 (44%) cases of non-Wilsonian fulminant liver failure would erroneously be assigned a diagnosis of fulminant Wilson's disease, by alkaline phosphatase/bilirubin and AST/bilirubin ratios, respectively. A low alkaline phosphatase-to-bilirubin ratio (< 0.57) in any category of fulminant liver failure suggested a significantly worse prognosis than in cases with higher ratios (chi 2, Yates' corrected = 5.37, p = 0.02). In the Wilson's disease group, serum and hepatic copper and ceruloplasmin concentrations were normal in 4/21, 2/15 and 2/19, respectively, whereas urinary copper level was elevated in 18/18 and was the most valuable test in diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of simple biochemical indexes to reliably differentiate fulminant Wilson's disease from other causes of fulminant liver failure. 142 59

The possible aggravation of liver injury by impaired cellular antioxidant function was investigated. A vitamin E-deficient diet (0.5 mg/kg alpha-tocopherol; control 100 mg/kg) significantly reduced rat liver alpha-tocopherol concentrations after 4 weeks (1.8 +/- 1.7 micrograms/g; control 34.4 +/- 2.4 micrograms/g, p < 0.001). The effects of copper loading (Cu, 3 g/kg diet); galactosamine (GalN, 0.85 g/kg i.p.); or carbon tetrachloride (CCl4, 10 mmol/kg i.p.) were examined. Serum aspartate transaminase activity was elevated slightly by vitamin E deficiency but not by hepatic copper accumulation. In vitamin E-replete (E+) and vitamin E-deficient (E-) rats, GalN or CCl4 caused a large and comparable elevation in serum AST and OCT activity. This effect on AST was markedly reduced by copper loading in vitamin E replete (E+) rats, but in E(-) rats copper had significantly less protective effect. Copper also diminished the OCT response to GalN in E+, though not E-, rats. A significant rise in total hepatic alpha-tocopherol content followed administration of GalN or CCl4 in both normocupric and copper-laden E(-) rats. Thus alpha-tocopherol deficiency (a) was not hepatotoxic per se; (b) failed to potentiate the toxicity of copper, GalN or CCL4; but (c) partially abolished the protection by copper against toxin-induced liver injury. Retention of hepatic alpha-tocopherol after liver damage may partly explain low serum vitamin E levels seen in clinical liver disease.
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PMID:Alpha-tocopherol deficiency fails to aggravate toxic liver injury but liver injury causes alpha-tocopherol retention. 148 10

Three hundred and seventy-three female and 213 male nonalcoholic subjects, aged 60-100 y, who had participated in a nutritional status survey of elderly people in the Boston area were grouped according to usual alcohol intake: 0-4, 5-14, or 15+ g/d. The age- and sex-adjusted mean intake of calories, fat, protein, carbohydrate, and 10 micronutrients and the mean levels of 14 nutrient and 22 nonnutrient biochemical indices were compared for the three categories of alcohol intake. The mean micronutrient intakes were also adjusted for total caloric intake and the mean nutrient biochemical concentrations were also adjusted for the corresponding nutrient intakes. The results suggest that caloric intake and blood concentrations of retinol, iron, ferritin, HDL cholesterol, AST, and ALT increased with increasing alcohol intake whereas folate and phosphorus intakes and blood measures of riboflavin, copper, zinc, urea nitrogen, and creatinine decreased with increasing alcohol intake.
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PMID:Moderate alcohol intake and nutritional status in nonalcoholic elderly subjects. 280 94

Copper is believed to be hepatotoxic in Indian Childhood Cirrhosis and Wilson's disease. However, copper-loading causes only minimal hepatic damage in animal models. The hypothesis was therefore proposed that a second hepatic insult may precipitate or perpetuate liver injury in a copper-laden liver. In non-copper-dosed rats CCl4 (10 mmol/kg, i.p.) produced elevated serum AST (809 +/- 298 IU/l, normal 20 +/- 5) and ALT (295 +/- 157 IU/l, normal 6 +/- 1) and extensive liver cell necrosis, portal tract inflammation, fat deposition, and perilobular hepatocyte ballooning. In rats whose liver copper was elevated from 75 +/- 13 to 461 +/- 13 micrograms/g by oral copper supplementation, CCl4 produced much smaller increases in AST (492 +/- 80 IU/l) and ALT (172 +/- 57 IU/l) and mild focal liver cell necrosis. Fat deposition and perilobular vacuolation were not reduced. Prior copper-loading of rats unequivocally protected against the CCl4-induced liver injury. Triglyceride accumulation, however, was apparently unaffected. The possible interactions of copper with prostaglandin-mediated inflammation and with free-radical-induced liver damage are discussed.
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PMID:The effect of carbon tetrachloride on the copper-laden rat liver. 292 91

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

Three housed North Ronaldsay sheep were treated with copper in the form of cupric oxide "needles", two at the manufacturer's recommended dosage rate and the third at twice this level. Sheep of this breed are especially sensitive to high dietary intake of copper. Pre- and post-dosing blood samples were monitored for changes in packed cell volume and changes in content of plasma copper, bilirubin, AST and SDH. Weight changes were also recorded. The animal dosed at twice the recommended level died on day 19 post-dosing of acute copper poisoning. The two dosed at the standard rate remained healthy and put on weight steadily throughout the six months following treatment. Two Welsh Mountain sheep dosed at the standard rate and maintained and examined in the same way likewise showed no signs of copper toxicity.
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PMID:Susceptibility of North Ronaldsay sheep to copper from cupric oxide needles. 397 74

Several biochemical events accompany and mediate the development of chronic liver disease and its evolution into cancer. Low plasma zinc and high copper levels have been observed in various liver diseases, such as liver cirrhosis and viral hepatitis, while increased oestradiol levels have been documented in chronic liver damage and hepatocellular carcinoma. We administered CCL4 intragastrically to 10 female Sprague Dawley rats for 30 weeks. All animals developed cirrhosis and four also developed hepatocellular carcinoma. Plasma levels of zinc, copper and oestradiol were significantly higher in the latter group than in animals with simple cirrhosis. Progesterone, AST and bilirubin showed a trend toward significant differences whereas testosterone and ALP levels were unchanged. These findings add to the evidence that sex hormones and trace elements are involved in the process of the development of chronic liver damage and carcinogenesis.
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PMID:Sex hormones and trace elements in rat CCL4-induced cirrhosis and hepatocellular carcinoma. 835 89

1. Over an 8-year period, 19 biochemical parameters have been determined at various ages in the blood serum of 92 clinically healthy Lechwe waterbucks (Kobus leche), 33 males and 59 females. 2. Significant differences have been noted with age. In neonates, the lowest values of total proteins, glucose, creatinine, urea, AST, ALT and iron have been noted; the highest ones have been seen for cholesterol, alkaline phosphatase, calcium and phosphorus. 3. With regard to sex, raised values of glucose, urea, alkaline phosphatase and ALT, and lowered values of cholesterol, have been noted in juvenile females compared with males of the same age. 4. In adult females, higher levels of urea and cholesterol and lower levels of glucose, triglycerides and natrium have been recorded compared with males. 5. With sex and age, no significant changes have been found in the levels of GGT, magnesium, chlorides and copper. 6. Our findings are discussed with those abstracted from the literature for related species.
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PMID:Serum chemistry profiles for Lechwe waterbucks (Kobus leche): variations with age and sex. 840 53

Citrullus colocynthis seed was fed at 2% and 10% of the basal diet to 7-d-old Bovans-type chicks for 6 w. Average body weights and efficiency of feed utilization were markedly depressed in the chicks on 10% Citrullus feed, and the serum activities of LDH, AST and CK and concentrations of total lipid and zinc were significantly increased. The concentration of serum total iron binding capacity was particularly reduced in chicks on 2% Citrullus feed. The concentrations of other serum and blood constituents and of hepatic copper, manganese and zinc were not significantly changes. Lesions seen in the intestines, livers, kidneys and other tissues were fully reversed 4 w after removal from the experimental diet.
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PMID:An estimation of Citrullus colocynthis toxicity for chicks. 854 Feb 28

The objective of this study was to determine the concentration of Zinc (Zn), Copper (Cu) and Manganese (Mn) in hepatic tissue from extrahepatic biliary atresia (EHBA). Liver biopsy samples were obtained at time of portoenterostomy from 49 infants ages 1.1 to 20.7 months (median 2.1) with EHBA. Samples were dry ashed and analyzed by flame (Zn) or flameless (Cu and Mn) atomic absorption spectrophotometry. Hepatic Cu concentrations are physiologically elevated at birth and decline rapidly during the first 2 month of life, therefore only samples from 29 infants, ages greater than 8 weeks were considered for Cu. Concentrations (mg/kg dry weight, mean and range) were: Zn 142 (70-507), Cu 204 (19-570), Mn 9.1 (2.8-21.8) vs. literature controls in the same age range: Zn 262 (82-543), Cu 92, Mn 4.3 (3.3-11.5). No correlations were found between serum alkaline phosphatase, AST or total bilirubin and hepatic trace element concentrations, between trace element concentrations and age, or between Cu and Mn. Decreased bile flow with intrahepatic cholestasis may result in hepatic accumulation of Mn as well as Cu. The low hepatic Zn concentrations indicate the need for further study of Zn metabolism in this population.
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PMID:Hepatic concentrations of zinc, copper and manganese in infants with extrahepatic biliary atresia. 884 56


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