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 effect of LC50 (1.8 mg/l) and a sublethal (0.3 mg/l) concentration of mercuric chloride on the blood of a teleost fish, Ophiocephalus (Channa) punctatus (the freshwater murrel-soley) was observed at 96 h and 15 and 30 days. Haemoglobin and haematocrit decreased after exposure, but no marked alteration was observed in total plasma protein. Glucose, cholesterol, urea, sodium, chloride, calcium and phosphate increased after acute and chronic exposures. Glutamic-oxalacetic transaminase, glutamic-pyruvic transaminase and amylase activities increased after exposure to LC50 for 96 h and to the sublethal concentration for 15 and 30 days. No marked alteration was observed in acid phosphatase activity. Alkaline phosphatase activity decreased in acute exposure, and increased in chronic exposure. Cholinesterase activity decreased after both acute and chronic exposures.
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PMID:Mercury induced haematological and biochemical anomalies in Ophiocephalus (Channa) punctatus. 746 53

Previous reports have suggested the use of supraceliac aortic clamping in the surgical treatment of abdominal aortic aneurysm of difficult approach. The objective of the present report was to study the hepatic and renal metabolic changes of three groups of dogs submitted to temporary clamping (30 minutes) of the abdominal aorta at three different levels: below the renal arteries, infrarenal group (8 dogs); above the renal arteries, suprarenal group (9 dogs); above the celiac artery, supraceliac group (9 dogs). Blood bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen, and creatinine levels were measured before clamping and 5 minutes and 24 hours after reperfusion of the aorta. Bilirubin levels remained unchanged 5 minutes and 24 hours after reperfusion in all three groups. Alkaline phosphatase levels were significantly increased in all three groups 24 hours after reperfusion. ALT levels increased significantly in the supraceliac group and AST levels increased significantly in the infrarenal and supraceliac groups 24 hours after reperfusion of the aorta. However, despite these significant increases after reperfusion, the levels of these hepatic enzymes were still within the normal range for dogs. Urea nitrogen and creatinine levels showed that renal function did not change in any of the three groups. We conclude that supraceliac, infrarenal or suprarenal aortic clamping for 30 minutes do not promote any important changes in the hepatic or renal function of dogs.
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PMID:Supraceliac clamping in the surgical treatment of abdominal aortic aneurysm. An experimental study in dogs. 761 Mar 26

Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.
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PMID:Cimetidine prevents and partially reverses CCl4-induced liver cirrhosis. 791 3

Rats were fed on diets containing rapeseed oil, either containing low or high erucic acid content as well as the hydrogenated ones for 6 weeks. Body weight gain, biochemical and pathological parameters were investigated. The data showed high body weight gain for rats fed diets containing low erucic rape oil (LERo) compared with those fed either the high erucic rape oil (HERo), the hydrogenated or the partially hydrogenated oil diets. All rats showed non significant changes for total lipids, total cholesterol, GPT and GOT, except the partially hydrogenated rape oil diet which showed significant decrease for total cholesterol. Alkaline phosphatase however showed a significant decrease, while plasma phospholipids showed significant increase in rats fed on the hydrogenated oil diet. Triglycerides indicated non significant increase except in the group that received low erucic rape oil diet. Histopathological study showed changes in all tissues examined (liver and kidney).
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PMID:Biochemical and toxicological studies on the effect of high and low erucic acid rapeseed oil on rats. 793 43

Cholestasis is the predominant complication in patients with total parenteral nutrition-related liver disease. Ursodeoxycholic acid has been reported to be beneficial for patients with various chronic cholestatic liver diseases. The aim of this prospective study was to determine the effects of short-term administration of ursodeoxycholic acid in nine patients (mean age 54 years) treated with home total parenteral nutrition (31 +/- 2 (mean +/- SEM) kcal/kg per day) for 13.9 +/- 5.2 months for short bowel syndrome; all presented biological evidence of hepatic cholestasis (mean alkaline phosphatase activity 5.2 times the upper limit of the normal) which appeared during nutrition; there was no cause of hepatic dysfunction other than total parenteral nutrition. Patients received 11.2 +/- 0.8 mg/kg per day of ursodeoxycholic acid orally for 1 (n = 9) or 2 (n = 5) 2-month periods, each of which was followed by a 2-month wash-out period. Liver function tests were performed before and at the end of each period. Compared with non-treatment periods, the two periods of ursodeoxycholic acid administration induced a significant reduction in gamma-glutamyl transpeptidase (27.1% and 20.4% respectively; p = 0.001) and alanine aminotransferase serum activities (7.0% and 34.8% respectively; p = 0.01) from baseline values. Alkaline phosphatase activity (p = 0.09), aspartate aminotransferase (p = 0.11) and bilirubin (p = 0.75) serum activities underwent no significant change during the study. These preliminary results strongly suggest that short-term ursodeoxycholic acid administration leads to biochemical improvement in liver function tests in patients with total parenteral nutrition-related liver disease.
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PMID:Is ursodeoxycholic acid an effective therapy for total parenteral nutrition-related liver disease? 800 5

In order to assess the liver protective activity and the antioxidant properties of a new silybin complex (IdB1016), we carried out a short-term pilot study on 20 patients with chronic active hepatitis (CAH), randomly assigned to 240 mg of silybin b.i.d. (10 patients, 4 m/6 f, mean age: 50 years) or placebo (10 patients, 2 m/8 f, mean age: 55 years). Blood samples were collected before and after 7 days of treatment for liver function tests (LFTs), malonaldehyde (MDA) as an index of lipid peroxidation, and copper (Cu) and zinc (Zn), two trace elements involved in protecting cells against free radical-mediated lipid peroxidation. In the treated group, there was a statistically significant reduction of mean (+/- SEM) serum concentrations of aspartate aminotransferase (AST) from 88.0 (+/- 13.3) to 65.9 (+/- 7.5) u/l, (p < 0.01), of alanine aminotransferase (ALT) from 115.9 (+/- 12.9) to 82.5 (+/- 10.6) u/l (p < 0.01), of gamma-glutamyltranspeptidase (gamma-GT) from 51.4 (+/- 9.3) to 41.3 (+/- 4.2) u/l (p < 0.02) and of total bilirubin (TB) from 0.76 (+/- 0.08) to 0.53 (+/- 0.04) mg/dl (p < 0.05). Alkaline phosphatase (AP) fell slightly from 143.4 (+/- 6.4) to 137.5 (+/- 7.8) u/l. There were no significant changes in MDA, Cu or Zn serum concentrations. These results show that IdB1016 may improve LFTs related to hepatocellular necrosis and/or increases membrane permeability in patients affected by CAH.
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PMID:A pilot study on the liver protective effect of silybin-phosphatidylcholine complex (IdB1016) in chronic active hepatitis. 822 95

Non-alcohol-induced steatohepatitis (NASH) is characterized by elevated serum aminotransferase activities with hepatic steatosis, inflammation, and occasionally fibrosis that may progress to cirrhosis. No established treatment exists for this potentially serious disorder. Our aim was to conduct a pilot study to evaluate the safety and estimate the efficacy of ursodeoxycholic acid (UDCA) and clofibrate in the treatment of NASH. Forty patients were diagnosed with NASH based on a compatible liver biopsy with other causes of liver disease, including alcohol abuse, excluded by history, serum tests, and use of ultrasound. Twenty-four patients received 13 to 15 mg/kg/d of UDCA for 12 months. Sixteen patients with hypertriglyceridemia were placed on clofibrate, 2 g/day for 12 months. Twenty-five women and 15 men entered the study. Six of 40 patients (15%) withdrew because of side effects. Four additional patients were withdrawn because of noncompliance; one of them later required liver transplantation. In the UDCA group, the decreases in mean serum levels of alkaline phosphatase, alanine transaminase (ALT), and gamma-glutamyl transpeptidase (GGT) as well as histological grade of steatosis were significant. Among the patients treated with clofibrate, no change from baseline was found in mean ALT, aspartate transaminase (AST), GGT, bilirubin, triglycerides, and cholesterol, or in histological grade of steatosis, inflammation, or fibrosis after 12 months of treatment as compared with entry. Alkaline phosphatase activities decreased significantly from baseline. Despite the known lipid-lowering effects of clofibrate, it did not appear to be of clinical benefit in the treatment of NASH in this 1-year pilot study. However, treatment of NASH with UDCA for 12 months resulted in significant improvement in alkaline phosphatase, ALT, GGT, and hepatic steatosis. The possible benefit of UDCA therapy should be further investigated in the context of a randomized, controlled trial.
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PMID:Ursodeoxycholic acid or clofibrate in the treatment of non-alcohol-induced steatohepatitis: a pilot study. 867 65

There is no one test of liver function. Routine laboratory tests that are useful in screening for liver disease and following its course include serum AST, ALT, alkaline phosphatase, protein electrophoresis, prothrombin time, and bilirubin levels. The transaminase levels give a day-by-day account of the amount of hepatocellular injury and death that occurs. Alkaline phosphatase levels estimate the amount of impedance of bile flow. The prothrombin time and serum albumin level are excellent gauges of hepatic protein synthetic ability, whereas the bilirubin level is probably the best test of overall liver function. Many tests are now available that permit one to diagnose specific diseases of the liver.
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PMID:Evaluation of tests used to screen patients with liver disorders. 888 44

Progressive liver failure in parenteral nutrition (PN)-dependent children with short bowel syndrome carries significant morbidity and mortality. The authors retrospectively reviewed 47 consecutive patients with short bowel syndrome diagnosed from October 1985 through October 1995. All patients were treated according to a protocol designed to promote intestinal motility and discourage bacterial translocation. Elements of the protocol included the use of taurine, vigilant prevention and aggressive treatment of sepsis, meticulous catheter care, early PN cycling, appropriate enteral feeding, and measures designed to inhibit gastrointestinal bacterial translocation, especially gram-negative rods. Complete blood counts and serum liver function studies were compiled from both clinic visits and hospital admissions for each patient every 3 to 6 months while they were on PN. Three patients were lost to follow-up after they had moved out of state. The length of time on PN ranged from 3 months to 9.4 years with an average of 2.2 years. Elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and glutamyltransferase (GGT) were present in 82%, 66%, and 84% of patients, respectively. Alkaline phosphatase was elevated in 58% of patients. Eight patients (18%) are still on PN, and 31 (70%) have been weaned off PN. Five patients have died (11%). Three patients (7%) developed cholecystitis requiring cholecystectomy. No patients developed progressive liver failure. These results suggest that PN-related liver failure may be prevented in most patients with short bowel syndrome. Specific measures to prevent PN-related cholestatic jaundice need further investigation.
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PMID:Prevention of liver failure in parenteral nutrition-dependent children with short bowel syndrome. 909 21

The aim of this paper was to determine if NO modulation would influence liver damage induced by 3 day-biliary obstruction. L-Arginine (500 mg kg-1, p.o. twice a day) or L-NAME (100 mg kg-1, p.o. twice a day) or both were administered to male Wistar rats subjected to bile duct ligation (BDL). In the liver, BDL doubled lipid peroxidation and depleted glycogen (P < 0.05), L-arginine completely prevented the former and partially the latter. Alkaline phosphatase, alanine aminotransferase and gamma-glutamyl transpeptidase serum enzyme activities increased (P < 0.05) by BDL, again L-arginine treatment partially, but significantly, prevented the elevation in these three markers of liver damage. Although L-NAME treatment failed to induce a change in any marker of liver injury studied herein, it abolished the beneficial effects of L-arginine, suggesting that these effects are probably mediated by NO synthesis stimulation.
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PMID:Liver damage induced by acute cholestasis in the rat is ameliorated partially by L-arginine. 982 59


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