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)

After a chloroform intraperitoneal injection, lactate dehydrogenase, alanine aminotransferase and particularly aspartate aminotransferase serum activities are much more raised in deficient animals. Liver ornithine decarboxylase (ODC) activity normally decreases in rats between the 4th. and the 7th. month after the weaning. In vitamin A deficient animals, basal values of the enzyme activity are lower and the decrease is deeper. But even at month 7, liver sustains a partial capacity of ODC recovery if retinol is fed during 15 days. Chloroform administration strongly enhances liver ODC activity in normal rats. In the deficiency, stimulation is lower in absolute value but relatively higher if referred to basal level. After retinol refeeding, chloroform stimulates enzyme activity to nearly normal values. Vitamin A deficiency impairs obviously liver ODC activity and its response to chloroform stimulation in rats, but the stroke is at least partially reversible in our conditions. Moreover, deficient animals maintain a non negligible capacity of ODC response under chloroform stimulation.
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PMID:[Toxicity of chloroform and vitamin A status in the rat]. 145 50

Two hundred eighty-four female adults (aged 40-70 years) were longitudinally studied to investigate the relationship between dietary supplemental vitamin A and serum biochemical markers of vitamin A toxicity. Serum retinol, retinyl esters, and retinol-binding protein (RBP), alkaline phosphatase and aspartate aminotransferase activities and bile acids were measured at baseline, 1 and 2 years. Fasting serum retinol and retinyl ester concentrations were determined by high-performance liquid chromatography, and dietary and supplemental intake of vitamin A were assessed by 3-day food records. There was no difference in dietary vitamin A intake between supplement users and nonusers. In supplemental users, the mean +/- SEM supplemental vitamin A intake was 952 +/- 81 IU/day (range 250-5000 retinol equivalents/day). Serum retinol, retinyl esters, and RBP concentrations were not different between the two groups during the 2-year period. For each group, serum retinyl esters significantly increased over time (p < 0.03), but the magnitude of the increase was not different between the groups. Serum levels of retinol, retinyl esters, and RBP were not correlated with vitamin A intake or age in either group. Biochemical measures of liver damage (serum alkaline phosphatase and aspartate aminotransferase activities and serum bile acids) were not related to serum retinol, retinyl esters or RBP concentrations, nor were they different between nonusers and users of supplemental vitamin A. This study provides evidence that long-term supplemental vitamin A in doses commonly found in multivitamin supplements does not present a risk for hypervitaminosis A.
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PMID:Lack of an effect of multivitamins containing vitamin A on serum retinyl esters and liver function tests in healthy women. 146 Jan 82

The inability of the 'ethanol/high vitamin A Lieber-DeCarli diet' to induce liver fibrosis in two different rat strains was further evaluated by determining changes in parameters of liver cell damage and of retinoid and lipid metabolism. In the ethanol/vitamin A-treated group, slight but constant hepatic cell damage, as indicated by elevated alanine aminotransferase, aspartate aminotransferase and glutamate dehydrogenase activities in blood, was already observed at 6 months and maintained until the time of death at 16 months. Serum gamma-glutamyl transaminase activities were not raised. Moderate parenchymal liver cell damage was not accompanied by fibrosis. Hypertriglyceridemia or hypercholesterolemia were observed at 6-16 months of chronic alcohol administration. This response was strain dependent. In ethanol-treated rats of both strains, total liver retinoids and serum retinol concentrations were not altered. Therefore, the hypothesis that interaction between alcohol and retinoids is a major factor in the pathogenesis of alcoholic liver disease, needs to be reconsidered.
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PMID:Chronic administration of ethanol with high vitamin A supplementation in a liquid diet to rats does not cause liver fibrosis. 2. Biochemical observations. 174 28

This study examined the association between dietary supplementation with vitamin A and biochemical symptoms of toxicity in 116 healthy elderly volunteers (47 male, 69 female), aged 64-88 y. Plasma retinol and retinyl ester concentrations, seven liver-function tests, and dietary and supplemental vitamin A intakes were measured annually for 5 y. Supplemental intake range was 0-47,000 IU/d; dietary intake range was 2528-23,032 IU/d. Fasting retinol and retinyl ester concentrations were determined by HPLC and dietary intake was assessed by a 3-d food record. Supplemental vitamin A intake was highly correlated with retinyl ester concentrations (r = 0.74, P = 0.0001). Retinyl esters ranges from 3.4% to 10.2% of retinol concentrations. Retinyl ester concentrations did not increase over time, regardless of supplement amount. The association of retinyl esters and liver-function tests was significant only for aspartate aminotransferase activity in females (r = 0.47, P = 0.0001). The supplementation amount in this study was not associated with vitamin A toxicity.
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PMID:A longitudinal study of the relationship between vitamin A supplementation and plasma retinol, retinyl esters, and liver enzyme activities in a healthy elderly population. 195 Nov 60

A prospective study was performed in the Dutch flower bulb culture to investigate the possible effects of subchronic exposure to the soil fumigant 1,3-dichloropropene (DCP) on liver and kidney function and on glutathione conjugation capacity in blood. Urine spot samples and venous blood samples from 14 workers applying DCP (applicators) were taken at the start of the season in July, and after the season in October. The parameters of liver function measured were: alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyltranspeptidase, and total bilirubin (conjugated and unconjugated). Total bilirubin was significantly decreased from 9.5 before to 7.0 mumol/l after the season. In combination with an increase in serum gamma-glutamyltranspeptidase activity from 12.5 to 19.5 U/l this indicates moderate hepatic enzyme induction. To study renal function, creatinine and beta 2-microglobulin in serum, and beta 2-microglobulin, albumin, alanine aminopeptidase, beta-galactosidase, and retinol binding protein in urine were measured. The glomerular function parameters albumin in urine and creatinine in serum changed significantly during the season: albumin concentration increased from 5.2 to 7.6 mg/l, whereas creatinine concentration [corrected] decreased from 93.0 to 87.5 mumol/l. The tubular function parameter retinol binding protein also increased in concentration from 20.0 to 26.9 micrograms/l. Therefore, a subclinical nephrotoxic effect of subchronic exposure to DCP cannot be excluded. Effects on glutathione conjugation capacity were studied by measuring erythrocyte glutathione S-transferase activity and blood glutathione concentrations. The activity of glutathione S-transferase in erythrocytes was significantly decreased from 4.7 before to 3.3 U/g haemoglobin after the season. The same was true for the blood glutathione concentrations, which decreased from 0.93 to 0.82 mM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biological effect monitoring of occupational exposure to 1,3-dichloropropene: effects on liver and renal function and on glutathione conjugation. 191 9

The effect of vitamin A on experimental hepatic fibrosis in rats induced by administration of carbon tetrachloride (CCl4) and pig serum was studied. Vitamin A content in the CCl4-induced cirrhotic liver decreased significantly. Administration of pig serum caused hepatic fibrosis without hepatocytic damage. Vitamin A suppressed induction of experimental hepatic fibrosis by CCl4 and pig serum. Neither hepatocytic injury nor increased activities of serum aspartate aminotransferase and glutamic pyruvic transaminase induced by CCl4 was diminished by vitamin A. These data provide evidence that vitamin A inhibits hepatic fibrogenesis and that this effect may be mediated by an action on stellate cells rather than hepatocytes.
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PMID:Suppression of experimental hepatic fibrosis by administration of vitamin A. 257 84

Two milk feeding systems were investigated as influencing the health and development of calves. After the termination of colostrum feeding, the ten animals of the experimental group were given whole milk whereas the control group (also ten calves) was given the Laktosan milk replacer. By the age of three months, blood was collected from the calves for biochemical examination in weekly intervals, later once a month. The content of urea, determined in the blood plasma of the calves of the experimental group was significantly lower in the fourth to seventh week. The plasma levels of nitrogen, potassium, calcium and magnesium were about the same in the experimental and control groups, being within the limits of the reference values. At the age of six to nine weeks, the content of inorganic phosphorus in the blood plasma of the tested animals was statistically significantly higher. Vitamin A concentration in the blood plasma was about the same in both groups. The content of vitamin E in the blood plasma of the calves of the experimental group was statistically significantly higher in the fourth to eight week of age. No significant differences between the two groups were observed in the plasmatic activities of aspartate aminotransferase (AST) and gamma-glutamyl transferase (GMT). The activities of alkaline phosphatase (ALP) were significantly higher in the third to fifth week of life. From the fifth to eighteenth week of age, the average daily weight gains were significantly higher in the calves given whole milk.
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PMID:[The effect of the use of milk-based feed mixtures and whole milk on the development of selected indicators in the blood plasma in calves]. 308 69

Serial nutritional assessments using arm anthropometry, computed tomography of the thigh, and serum biochemical indexes during an eight-month period were performed on nine children with short-bowel syndrome receiving home parenteral nutrition. The mean patient age at the beginning of the study was 3.0 years. In anthropometric measurements, the mean body weight of our test population did not deviate from that of the normal population. Most patients were below the normal median for height. The mean midarm muscle area was 114% of the normal median, and the mean midarm fat area was 98% of the normal median. The mean weight and height velocities were 148% and 122% of the standard, respectively. Retinol-binding protein values, albumin levels, and total lymphocyte counts of the patients were low, while levels of aspartate aminotransferase and alanine aminotransferase were slightly elevated. Midarm muscle and fat compartment sizes were highly correlated with thigh muscle and fat compartment sizes, as demonstrated by computed tomography. Our results demonstrate that children with short-bowel syndrome receiving home parenteral nutrition can maintain normal growth characteristics and extremity compartment sizes.
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PMID:Nutritional assessment of children with short-bowel syndrome receiving home parenteral nutrition. 311 87

This study was conducted in order to assess the nutritional status of thiamin, riboflavin, pyridoxine, carotene, retinol, ascorbic acid, plasma iron, hemoglobin and plasma albumin of the elderly living in two cooperative farms (Kibbutzim), in Israel. Blood samples from elderly subjects aged 60 to 85 (33 women, 26 men), were collected for analysis. Thiamin, riboflavin and pyridoxine status were assessed by using enzymatic activation coefficient. Transketolase was used for determining thiamin status, glutathione reductase for determining riboflavin status and glutamate oxaloacetate transaminase for pyridoxine status. Transketolase activation coefficient ranged from 1.05-1.59 with a mean 1.18 and SEM 0.02, glutathione reductase coefficient ranged from 1.08-1.50 with a mean 1.25 and SEM 0.07 and glutamate oxaloacetate transaminase activation coefficient ranged from 1.71-2.15 with a mean 1.83 and SEM 0.06. Deficient levels were found in the following: Leucocyte ascorbic acid 5% of the population, hemoglobin 18%, plasma iron 20%, carotene 32% and plasma retinol 20%, thiamin 14% and riboflavin 32%. No deficient state was found in pyridoxine.
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PMID:Nutritional status in elderly population in kibbutzim. 407 7

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88


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