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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report on occurrence, causes and diagnostics of liver affections observed in fattening bulls in Ukrainia between 1982 and 1988. For this purpose, 2747 bulls in 10 fattening plants had been controlled clinically once during the last month of their final fattening period (lasting, according to the feeding schedule, from the 4th until the 12th, or from the 6th until the 18th month of life), and 1318 of them were controlled for eventual hepatic lesions at slaughter. The authors found an increase in liver affections during the final fattening period. The type of lesion found preferentially in the different fattening plants showed a certain correlation with feeding used in these: The prevalence of liver lesions (i.e. in 87.2% of the animals controlled) were found in fattening bulls fed cereal branstraw-pellets; among these, liver abscesses were most frequent (i.e. 55.2% of all lesions observed in this group). Steatosis of the liver was prevalent in fattening bulls receiving eating offalls (i.e. 82.7% of all lesions found in that group), whereas liver cirrhosis was prevalent in fattening bulls fed with sugar beet chips-silage. In Holstein-bulls, liver lesions were about double as frequent as in Fleckvieh-bulls (i.e. 37.3 and 16.7% of the livers controlled were found involved, respectively). Diagnostical value of several clinical parameters controlled is discussed (i.e. size and sensitivity of liver percussion field, activity of SDH, LDH, AST and ALT in serum, serum concentration of vitamin A, D3-25 and E, concentration of Vitamin A in liver, and concentration of cholic acids and of their glucoconjugates in bile).
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PMID:[Liver diseases of fattening bulls]. 150 64

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

Large doses of retinol (vitamin A) have been shown to potentiate the hepatotoxicity of several chemicals in rats. The objective of this study was to determine how retinol would affect the pulmonary and hepatic toxicity caused by 1-nitronaphthalene (1-NN). All-trans-retinol (75 mg/kg/day, po) was administered for 7 days to male Sprague-Dawley rats. One day after the last dose of retinol, animals were given a single injection of 1-NN (100 mg/kg, ip). At 24 hr, animals receiving retinol vehicle and 1-NN exhibited respiratory distress syndrome and chromodacryorrhea. Pulmonary morphological changes included necrosis and exfoliation of the bronchiolar epithelium, as well as infiltration of inflammatory cells into the interstitial areas around affected bronchioles. The bronchioalveolar lavage fluid from these animals exhibited significant increases in the activities of gamma-glutamyl transpeptidase (GGT), lactate dehydrogenase (LDH), as well as protein and inflammatory cell content. Following pretreatment with retinol, none of the animals treated with 1-NN exhibited outward signs of toxicity. In addition, the lavage fluid of these rats revealed significant reductions in inflammatory cells, protein, and LDH activity. However, lavage fluid GGT activity was significantly increased. Morphological evaluation of the lungs revealed nonciliated bronchiolar epithelial (Clara) cell damage with no associated inflammation. Retinol pretreatment resulted in potentiated hepatotoxicity as indicated by increases in plasma alanine aminotransferase and GGT activities, as well as plasma total bilirubin. The altered plasma enzyme activities correlated with increased hepatocyte and bile duct epithelial necrosis, as well as an increased infiltration of neutrophils into the areas around bile ducts. Retinol potentiation of 1-NN-induced hepatocyte necrosis was significantly reduced following pretreatment with gadolinium chloride (GdCl3). From these experiments, we conclude that in the lung pretreatment with retinol decreased the severity of 1-NN-induced toxicity apparently by an anti-inflammatory mechanism. In the liver, retinol potentiated 1-NN-induced liver injury apparently through a proinflammatory mechanism by activating Kupffer cells and increasing the infiltration of neutrophils into the periportal regions adjacent to bile ducts.
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PMID:All-trans-retinol alteration of 1-nitronaphthalene-induced pulmonary and hepatic injury by modulation of associated inflammatory responses in the male Sprague-Dawley rat. 759 3

The interactive effects between retinol and various hepatotoxicants (allyl alcohol, acetaminophen, carbon tetrachloride, D-galactosamine, and phalloidin) were studied in the male Swiss Webster mouse. The mice were administered retinol at 75 mg/kg/day (or the vehicle of retinol) by oral gavage for 7 days. Hepatoxicity produced by the chemicals was determined by plasma alanine aminotransferase (ALT) activity and histopathology. After 7 days of retinol pretreatment, the hepatotoxicities of allyl alcohol, acetaminophen, and galactosamine were potentiated. Interestingly, the hepatotoxicity of carbon tetrachloride and phalloidin was protected by identical retinol pretreatment. Microscopic examination of histologic liver sections demonstrated the specific hepatic necrosis associated with each individual chemical and confirmed the ALT values obtained. Once an interaction between retinol and the five hepatotoxicants was established, the duration of retinol pretreatment necessary to elicit an interaction was determined for each hepatotoxicant. Results demonstrated that the duration of retinol pretreatment was specific for each hepatotoxicant. The accumulation of retinoids in the liver during retinol pretreatment was determined using high-performance liquid chromatography analysis. Significant increases in the basal liver levels of retinol and retinyl palmitate were seen within 1 to 3 days of retinol treatment compared to control. Retinol pretreatment resulted in potentiation or protection of specific hepatotoxicant-induced liver damage. Currently, studies are being conducted which probe into the mechanisms of these interactions.
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PMID:The interactions between retinol and five different hepatotoxicants in the Swiss Webster mouse. 766 12

Evidence suggests that 7 days of retinol pretreatment potentiates chemical-induced liver injury by a mechanism that involves activation of Kupffer cells (KC). These studies were designed to determine if shorter dosing regimens of retinol potentiate carbon tetrachloride (CCl4). Initially, a single dose of retinol was shown to potentiate the hepatotoxicity of CCl4. Male Sprague-Dawley rats were pretreated with all-trans-retinol (75 mg/kg p.o.) 24 hr prior to KC isolation or administration of CCl4 (0.2 ml/kg i.p.). KC isolated at 24 hr after retinol released increased amounts of superoxide anion when stimulated with zymosan or phorbol myristate acetate. At 24 hr after CCl4, plasma ALT activities and histological sections of liver were examined. Retinol-pretreated rats showed a significant elevation in both enzyme leakage and centrilobular to midzonal necrosis compared to retinol vehicle controls following CCl4. Although complete protection was not seen, depletion of KC or neutrophils (PMNs) (by gadolinium chloride (GdCl3) or a PMN-depleting antibody, respectively) significantly reduced the hepatotoxicity of 1 day retinol/CCl4 liver injury. Immunohistochemical analysis of livers showed significant elevations in positive staining for ED2, ED1, and HIS48 in retinol-pretreated rats given CCl4. GdCl3 effectively reduced ED2 staining but did not greatly affect HIS48 staining. Additional studies were performed to estimate the effect of retinol on noninflammatory processes. While total cytochrome P450 was not increased, the activity and concentration of CYP2E1 were both significantly elevated after a single dose of retinol. Hepatocytes isolated from 1-day retinol-treated rats were also more susceptible to CCl4 injury, a consequence that is most likely related to elevated CYP2E1 activity. These findings suggest that a single pretreatment with retinol may potentiate CCl4 hepatotoxicity by multiple mechanisms which involve increased biotransformation and inflammatory cell activities.
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PMID:The role of inflammatory cells and cytochrome P450 in the potentiation of CCl4-induced liver injury by a single dose of retinol. 897 75

In the mouse, retinol administration attenuates carbon tetrachloride (CCl4)-induced hepatic injury. We have investigated the role of cytochrome P4502E1 (CYP2E1) in this interaction. Male Swiss Webster mice were administered retinol (75 mg/kg/d) or vehicle for 3 days prior to CCl4 (30 microl/kg, ip). Hepatotoxicity produced by CCl4 was assessed by plasma alanine aminotransferase (ALT) activity and light microscopy (ALT activity of 1391+/-430 vs. 274+/-92 IU/L for vehicle + CCl4 and retinol + CCl4 treatments respectively, p < 0.05). Retinol's attenuation of liver injury was maintained when CCl4 was administered 48 h after the conclusion of the retinol pretreatment. Aniline hydroxylation activity, an indicator of CYP2E1 catalytic activity, determined on day 4 was 33.8% of untreated control in vehicle + CCl4 treatments while the retinol + CCl4 treatment group was 94.2% of untreated control. Additionally, CYP2E1 immunoreactive protein was 78% lower in vehicle + CCl4 vs. retinol + CCl4 treatment groups. Attenuation of potentiated hepatotoxicity was also observed when CYP2E1 was induced by acetone (ALT activity of 3119+/-1066 vs. 247+/-77 IU/L for vehicle and retinol treatments respectively, p < 0.05). In the mouse, retinol itself does not alter constitutive or inducible CYP2E1 expression. However, in combination with CCl4 retinol does reduce the amount of CCl4 bioactivated to its toxic metabolite. We conclude that retinol attenuates CCl4-induced hepatotoxicity by causing a decrease in CCl4 bioactivation but does not cause a decrease in CYP2E1 expression.
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PMID:Role of cytochrome P4502E1 in retinol's attenuation of carbon tetrachloride-induced hepatotoxicity in the Swiss Webster mouse. 1056 6

Retinol pretreatment (75 mg/kg/day, 4 days) potentiated paracetamol-induced hepatotoxicity in BALB/c mice (alanine aminotransferase (ALT) activity; 2510+/-602 vs 1155+/-282 IU/l; retinol+paracetamol vs corn oil+paracetamol, respectively, P<0.05); however, this potentiation did not occur in the kidney, indicating an organ-specific response. Retinol treatment alone was not toxic in either organ, as indicated by ALT activity, blood urea nitrogen and creatinine. The potentiation effect could be mediated by retinol's induction of CYP450 isoforms relevant to paracetamol metabolism or through depletion of glutathione. Therefore, these parameters were investigated in both organs. Following retinol treatment, renal CYP2E1 and hepatic CYP1A2 and CYP2E1 catalytic activities and polypeptide levels were unchanged. However, retinol significantly decreased both the catalytic activity (0.23+/-0.03 vs 0.53+/-0.06 nmol/mg/min; retinol vs untreated, respectively, P<0.05) and polypeptide levels (58+/-0.6% of control) of hepatic CYP3A. Inhibition of renal CYP3A did not occur as catalytic activity and polypeptide levels were unchanged from control. Following retinol treatment, total reduced glutathione levels, in both organs, were not significantly different from control. Therefore, the potentiation of paracetamol-induced hepatotoxicity is independent of CYP450 and glutathione.
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PMID:The effect of retinol on hepatic and renal drug-metabolising enzymes. 1125 46

The protective effects of betaine in ethanol hepatotoxicity were investigated in 24 female wistar albino rats. Animals were divided into three groups: control, ethanol and ethanol + betaine group. Animals were fed liquid diets and consumed approximately 60 diet per day. Rats were fed ethanol 8 kg(- 1) day(- 1). The ethanol + betaine group were fed ethanol plus betaine (0.5% w/v). All animal were fed for 2 months. Reduced glutathione, malondialdehyde and vitamin A were determined in the liver tissue. Alanine aminotransferase activities were also measured on intracardiac blood samples. GSH levels in the ethanol group were significantly lower than these in the control group (p < 0.001). GSH was elevated in the betaine group as compared to the ethanol group (p < 0.001). MDA in the ethanol group was significantly higher than that in the control group (p < 0.05). MDA was decreased in the betaine group as compared to the ethanol group (p < 0.05). Vitamin A in the ethanol group was significantly lower than that in the control group (p < 0.01), but, in the ethanol + betaine group it was high compared with the ethanol group (p < 0.01). ALT in the ethanol group was higher than that in the control group (p < 0.05). Oxidative stress may play a major role in the ethanol-mediated hepatotoxicity. Betaine may protect liver against injury and it may prevent vitamin A depletion. Therefore, it may be a useful nutritional agent in the prevention of clinical problems dependent on ethanol-induced vitamin A depletion and peroxidative injury in liver.
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PMID:Ethanol-induced hepatotoxicity and protective effect of betaine. 1174 10

Retinol binding protein (RBP) in the plasma of rats treated with D-galactosamine was monitored to establish whether its level can be used to evaluate drug-induced hepatotoxicity. Blood was withdrawn by heart puncture at 0 hours and 12 hours after the administration of D-galactosamine (400 mg/kg body weight i.p.) to rats. Lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) in the plasma at 12 hours after the D-galactosamine administration significantly increased, while RBP in the plasma at that time significantly decreased. On the other hand, the albumin in the plasma was unaffected at 12 hours after the D-galactosamine administration. Thus RBP seems to monitor different aspects of drug-induced hepatotoxicity than LDH and ALT and to detect the drug-induced hepatotoxicity more sensitively than albumin level under the present conditions.
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PMID:Evaluation of drug-induced hepatotoxicity by plasma retinol binding protein. 1198 Mar 63

Retinol binding protein (RBP) in plasma of rats treated with carbon tetrachloride (CCl4) was monitored to clarify if RBP is available for the evaluation of the drug-induced hepatotoxicity. Blood was withdrawn by heart puncture at 0 hr and 12 hr after i.p. administration of CCl4 (0.2 ml/kg) to rats. Lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) in plasma significantly increased at 12 hr after CCl4 administration, compared with the control, while RBP in plasma significantly decreased. On the other hand, albumin in plasma was unaffected at 12 hr after CCl4 administration. Thus RBP seems to monitor the different aspects in the drug-induced hepatotoxicity from LDH and ALT, and from the viewpoint of protein synthesis in the liver, to be more sensitively affected by the drug-induced hepatotoxicity than albumin.
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PMID:Retinol binding protein in plasma to evaluate the hepatotoxicity of rats treated with CCl4. 1288 22


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