Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma, whole blood, and red blood cell selenium levels were determined by spectrofluorometry in 30 patients with chronic heavy ethanol ingestion (group I) and 20 normal controls (group II). Nutritional and general medical evaluations were also performed. The mean plasma selenium level was 0.065 microgram/ml +/- 0.012 (SD) for group I versus 0.100 +/- 0.016 for group II (p less than 0.0001). Whole blood levels were 0.076 microgram/ml +/- 0.011 versus 0.114 +/- 0.015 (p less than 0.0001), and red blood cell levels were 0.092 microgram/ml +/- 0.016 compared with 0.130 +/- 0.025 (p less than 0.0001), respectively. Mean triceps skin fold was 8.2 mm +/- 3.5 for group I males versus 12.3 mm +/- 5.0 (p less than 0.005) for group II males but was not well correlated with whole blood selenium status (r = 0.33). Nutritional parameters of percentage of ideal body weight, midarm muscle circumference, serum albumin, and total lymphocyte count revealed no differences. Mildly elevated serum aspartate aminotransferase and/or alkaline phosphatase values occurred in 53% of alcoholics, but selenium levels in these patients were no different from those with normal liver tests. We conclude that depressed blood selenium levels occur frequently in patients with chronic heavy ethanol ingestion even in the absence of overt malnutrition. Since selenium deficiency can produce a spectrum of organ injury which resembles that associated with chronic alcoholism, the relationship of selenium deficiency to alcohol-induced organ injury deserves further study.
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PMID:Diminished blood selenium levels in alcoholics. 639 3

From this comparison of 37 black children with hepatic schistosomiasis (HS) and 53 with intestinal Schistosoma mansoni (IS) living in an endemic area, we propose easily identifiable clinical features of mild HS. These patients were generally well nourished school-age children who seldom complained of dysentery but who had a firm hepatomegaly with predominant enlargement of the left lobe and a firm splenomegaly. They were also mildly anaemic (9.4 +/- 2.2 g/dl) and had low serum albumin (30 +/- 7 g/l), raised aspartate transaminase (36 +/- 31 u/l) and high globulins (53 +/- 15 g/l). The implications of the absence of severe hepatosplenic schistosomiasis in many of these children are discussed.
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PMID:Clinical recognition of mild hepatic schistosomiasis in an endemic area. 671 May 66

Liver morphology and biochemistry were investigated in 61 morbidly obese subjects selected by defined criteria. Median overweight was 82 per cent (range 61 to 170 per cent), and median duration of overweight was 20 years (range two to 45 years). No patient had more than a moderate alcohol consumption and only one was diabetic. Four biopsies (7 per cent) showed normal liver tissue, while fatty change was the main diagnosis in most cases (85 per cent). Increasing degrees of fatty change was significantly (P less than 0.02) associated with presence of lipogranulomas (found in 54 per cent of the biopsies), focal necroses (found in 28 per cent), slight parenchymal inflammation (found in 33 per cent), and Kupffer cell proliferation (found in 49 per cent). Slight portal inflammation was seen in 23 per cent but portal fibrosis in only 2 per cent of the biopsies. No case of cirrhosis was registered. Patients with moderate or severe fatty change, lipogranulomas , focal necroses or with parenchymal inflammation were significantly more obese than patients without these changes (P less than 0.05). Even in absence of fatty change, obese subjects showed a markedly decreased serum albumin concentration and an elevated serum alkaline phosphatase activity (P less than 0.0001) compared with non-obese controls. Serum lactate dehydrogenase and aspartate aminotransferase were significantly raised only in patients with fatty change. With respect to serum bilirubin and plasma cholesterol concentrations no significant differences were detected between patient subgroups and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The liver in consecutive patients with morbid obesity: a clinical, morphological, and biochemical study. 672 92

The nutritional properties of protein bound epsilon-pyridoxyllysine residues in a phosphopyridoxyl bovine serum albumin (PP-BSA) preparation were examined by rat bioassay employing various levels of PP-BSA and pyridoxine (PN) fortification in the diets. Previous studies have shown that vitamin B-6 aldehydes can reductively bind to food proteins as epsilon-pyridoxyllysine complexes during processing and storage. The bound pyridoxyllysine was found to possess 50% molar vitamin B-6 activity, as indicated by slope ratios for rat growth, feed efficiency and liver pyridoxal 5'-phosphate concentration. The response curves indicated that high dosages of epsilon-pyridoxyllysine would fully satisfy the vitamin B-6 requirement. Direct antivitamin B-6 activity of epsilon-pyridoxyllysine was observed in diets containing low levels of PP-BSA. Classical rat acrodynia symptoms, depression of erythrocyte aspartate aminotransferase (AspAT) activity and elevation of in vitro coenzyme stimulation of AspAT were observed to be inversely related to PP-BSA concentration in the diet. The antivitamin B-6 effects were readily prevented by the presence of added 0.5--1.0 micrograms pyridoxing/g diet. In contrast to the previous study, the presence of PP-BSA in the diet did not inhibit the utilization of added PN. This difference was postulated to be due to a difference in vitamin B-6 concentration of the basal diets. The results of this study indicate that protein bound epsilon-pyridoxyllysine is nutritionally significant, presumably by its participation in the normal metabolism of vitamin B-6. The metabolic implications are discussed.
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PMID:Effects of epsilon-pyridoxyllysine bound to dietary protein on the vitamin B-6 status of rats. 676 60

A study of 16 haematological and 24 biochemical parameters in healthy, adult, male, volunteer Saudi blood donors was made, and enabled a preliminary determination of the reference values for these parameters to be made for Saudi Arabia. Statistically significant low means were observed for all the haematological parameters except the mean corpuscular haemoglobin concentration which was raised above Western levels and the mean corpuscular haemoglobin which was normal. A low total leucocyte count was seen to be due largely to a low neutrophil count, but accompanied by a raised lymphocyte count. The main biochemical differences were raised concentrations of serum albumin, alkaline phosphatase, conjugated bilirubin, aspartate aminotransferase, "liver" lactate dehydrogenase and alanine aminotransferase. Decreased concentrations of serum globulin, unconjugated bilirubin and calcium were also found. These changes are discussed in relation to putative endemic disease, ethnic origins and environmental factors.
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PMID:A pilot study of the reference values for the commoner haematological and biochemical parameters in Saudi nationals. 706 20

Venous blood values were determined on 19 Southdown sheep (9 adult ewes and 10 wether lambs). Principal sheep were given 12.5 ml of 3.3M urea solution/kg of body weight, which produced acute ammonia toxicosis. Whole blood ammonium-nitrogen was determined by ion exchange; venous blood gases and pH were measured with a pH blood gas analyzer; and 23 serum chemical analyses were obtained with a sequential multiple autoanalyzer computer. Analysis of variance for the data revealed significant changes for 20 values. The values are presented and discussed with regard to those that changed beyond acceptable limits (whole blood ammonium-nitrogen, venous blood pH, serum glucose, serum lactate dehydrogenase, serum alkaline phosphatase, serum creatine kinase, serum urea nitrogen, serum inorganic phosphorus, serum sodium, and serum potassium), those that changed within acceptable limits (PVo2, PVco2, serum triglycerides, serum free fatty acids, plasma volatile fatty acids, serum aspartate aminotransferase, serum total protein, serum albumin, serum creatinine, urea nitrogen-creatinine ratio, serum uric acid, serum cholesterol, serum low-density lipoproteins, serum calcium, serum iron and serum chloride), and those with no change (total and direct serum bilirubin and albumin-globulin ratio). Metabolic consequences of ammonia toxicosis are considered with regard to energy, lipid , protein, and acid-base and electrolyte balances. Blood values having possible laboratory diagnosis value and considerations for therapeutic adjustment are discussed.
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PMID:Ovine blood chemistry values measured during ammonia toxicosis. 710 77

Serum glycocholic acid (SGC) was measured by radioimmunoassay in 277 samples from 122 children with hepatobiliary disorders and from 23 healthy age-matched controls. In patients with hepatobiliary disease the SGC was more frequently abnormal (83%) than values for serum albumin (7%), prothrombin time (17%), bilirubin (22%), alkaline phosphatase (45%), aspartate transaminase (57%) and gammaglutamyl transpeptidase (63%). The cumulative frequency of abnormality of these six tests was equal to that of SGC alone. Serum glycocholic acid concentrations were raised in 13 patients in whom all other tests of liver function were normal. Two of these had clinical and histological evidence of liver disease, while four had biopsy-proven hepatic fibrosis or cirrhosis, and two of three with chronic active hepatitis in remission subsequently relapsed. Four patients have as yet, no other clinical or biochemical evidence of continuing liver disease. Serum glycocholic acid was normal in seven children with abnormal aspartate transaminase or gammaglutamyl transpeptidase in whom there is strong suspicion of significant hepatic disease. A wide range of values of SGC was found with marked overlap between the values found in the different disease entities studied. The SGC value was related to the serum concentration of aspartate transaminase and gammaglutamyl transpeptidase but not to other tests of liver function. Serum glycocholic acid concentration was considered in relation to the severity of histological abnormality in 25 percutaneous liver biopsies. The extent of the rise in SGC was related to the presence or degree of histological severity of oedema in the portal tracts, disruption of the limiting plate, parenchymal fibrosis and hepatocellular necrosis but not to other histological features. The very high incidence of abnormal SGC values found in this study does suggest that in an ordinary inpatient and outpatient service SGC determination is a practical and sensitive indicator of the presence of significant liver disease but for its comprehensive identification aspartate transaminase and gammaglutamyl transpeptidase must also be determined.
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PMID:Radioimmunoassay of serum glycocholic acid, standard laboratory tests of liver function and liver biopsy findings: comparative study of children with liver disease. 711 20

Renal and hepatic function was investigated in groups of 7 rats for 14 days after a single i.p. injection of 125 mg/kg purified kappa (kappa), lambda (lambda) or iota (iota) carrageenan. Kappa carrageenan was clearly nephrotoxic, as evidenced by a progressive, marked increase in serum creatinine and urea levels and in urinary N-acetyl-beta-D-glucosaminidase (NAG) activity. It also caused significant elevation in serum aspartate aminotransferase (AAT) activity from Day 2 to Day 7, and a progressive decrease in circulating albumin concentrations. Lambda carrageenan had no significant effect on serum creatinine or urea levels and caused only a transient increase in urinary NAG which was maximal on Day 2. Serum AAT levels were also significantly raised on Day 2. Iota carrageenan injection resulted in the deaths of 2/7 animals. Significant increases in serum creatinine levels were observed on Day 4: in 2 rats these increase were very pronounced as were those in urea levels, but no significant alterations in serum urea or urinary NAG levels were observed. No significant elevation in serum AAT was found, except for minor changes on Days 7 and 14. Whereas lambda carrageenan decreased serum albumin throughout the 14-day course of the experiment, albumin levels in lambda carrageenan-injected rats, whilst depressed during the first week, returned to normal by Day 14.
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PMID:A comparative study of renal and hepatic function in Sprague-Dawley rats following systemic injection of purified carrageenans (kappa, lambda and iota). 723 1

In primary biliary cirrhosis (PBC) liver copper retention occurs as a complication of cholestasis. By analogy with Wilson's disease, it has been suggested that copper retention is hepatotoxic in PBC, and this has been the rationale for the use of D-penicillamine in this disease. The hypothesis that copper is hepatotoxic in PBC has not been tested and in this study we have evaluated the role of liver copper retention in the pathogenesis of PBC. Sixty-four patients with PBC have been studied. Fifty-four had increased liver copper concentrations. Liver cell synthetic function was well preserved. All the patients had normal prothrombin times, and only two had subnormal serum albumin concentrations. There was no correlation between liver copper concentrations and the degree of liver cell damage assessed biochemically (aspartate transaminase), and histologically. Electron microscopy was performed on liver biopsies from five patients with markedly increased liver copper concentrations. The liver cell ultrastructure was compatible with cholestasis. Liver cells contained electron dense lysosomes, which were shown to contain copper and sulphur by x-ray probe microanalysis. The characteristic organelle changes associated with copper toxicity in Wilson's disease were not observed. The biochemical, histological, and histochemical differences between PBC complicated by liver copper retention, and Wilson's disease, indicates that there are differences in the handling of copper in these disease. In this study we could find no evidence to suggest that copper plays an important role in the pathogenesis of liver dysfunction in PBC.
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PMID:Is copper hepatotoxic in primary biliary cirrhosis? 730 88

The liver is thought to be the major source of circulating insulin-like growth factor (IGF-I) and IGF-binding protein-1 (IGFBP-1), whereas the primary production site of circulating IGFBP-3 remains unknown. As other tissues may contribute to the circulating pool of IGF-I and IGFBP, the aim of the present study was to assess the hepatic and renal arterio-venous difference and production rates of IGF-I, IGFBP-1, IGFBP-3, and GH in cirrhotic patients (n = 22) and matched control subjects (n = 27). IGFBP-1 and -3, IGF-I, and GH levels were measured by RIA in hepatic, renal, and peripheral veins and in the femoral artery. Levels of IGFBP-1 to -4 were additionally determined by Western ligand blotting. Hepatic venous IGFBP-1 was significantly increased in the cirrhotic patients (mean +/- SEM, 33.6 +/- 9.1 vs. 10.4 +/- 1.9 micrograms/L; P < 0.001), and arterio-renal-venous extraction was significant in both patients (6 +/- 2%; P < 0.01) and controls (11 +/- 1%; P < 0.001). Conversely, IGFBP-3 was decreased in the cirrhotic patients (1265 +/- 149 vs. 2712 +/- 137 micrograms/L; P < 0.001). IGFBP-3 correlated significantly with the wedged hepatic venous pressure (r = -0.49; P < 0.05), serum aspartate aminotransferase (r = -0.66; P < 0.01), serum bilirubin (r = -0.65; P < 0.01), serum albumin (r = 0.64; P < 0.01), and the Child score (r = -0.57; P < 0.01). IGF-I was significantly lower in the cirrhotics (57 +/- 10 vs. 143 +/- 11 micrograms/L; P < 0.001). No significant IGFBP-3 proteolysis was demonstrated in cirrhotics or controls. No significant differences were found in the values obtained simultaneously from hepatic, renal, and brachial veins or femoral artery, which suggests that no major net production or release of IGFBP-3 or IGF-I occurs in these tissues. No differences in IGFBP-2 or IGFBP-4 determined by Western ligan blot were found between patients and controls. The IGF-I concentrations correlated significantly with parameters of biochemical liver function. Basal GH concentrations were significantly higher in the cirrhotics (1.19 +/- 0.13 vs. 0.58 +/- 0.08 micrograms/L; P < 0.001). A significant hepatic disposal of GH was found in the patients (P < 0.05) and controls (P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Concentrations, release, and disposal of insulin-like growth factor (IGF)-binding proteins (IGFBP), IGF-I, and growth hormone in different vascular beds in patients with cirrhosis. 753


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