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 effects of feeding a diet deficient in zinc (Zn) to male rats on histidine metabolism were studied. Results showed that significantly higher percentages of DL-histidine-carboxyl-14C and L-histidine-2-(ring)-14C were oxidized by Zn-deficient rats. The incorporation of L-histidine-2-(ring)-14C into the proteins of skin, muscle, and kidney were significantly reduced in Zn-deficient rats as compared to Zn-supplemented rats. Conversely, the radioactivity of liver protein of Zn-deficient rats was significantly increased. Zn deficiency increased the activities of liver histidase and urocanase but had no effect on the activity of liver histidine-pyruvate transaminase. The increases of enzymatic activities were not due to food intake and can be prevented upon Zn repletion. The liver of Zn-deficient rats contained normal amount of histidine but a reduced quantity of histamine. The results on urinary excretion indicated that Zn-deficient rats discharged the same amounts of one-methyl and three-methyl histidine as Zn-supplemented pair-fed rats. Overall findings support in principle the concept that Zn deficiency results in disturbances of protein metabolism and also indicate that Zn is an important factor in regulating histidine metabolism through the urocanic acid pathway.
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PMID:Effect of zinc deficiency on histidine metabolism in rats. 612 Oct 18

Effects of histidine deficiency on muscle carnosine and anserine levels and on activities of enzymes associated with histidine catabolism and protoporphyrin synthesis were investigated. Male Sprague-Dawley (150 g) rats were tube-fed isonitrogenous, isocaloric, defined diets containing 0%, low (0.013%) or adequate (0.45%) histidine for 8-13 days. While histidine-deficient animals maintained body weight, muscle and plasma histidine and carnosine concentrations decreased rapidly and remained low following a 3-day histidine repletion period. Hepatic histidine ammonia-lyase and histidine-pyruvate transaminase activities were decreased in histidine-deficient animals, whereas formiminotransferase activity was unchanged. Hematocrit levels and hemoglobin concentrations declined progressively during histidine depletion and the activity of erythrocyte and hepatic delta-aminolevulinic acid dehydratase also decreased relative to controls. Evidence is presented indicating that decreased histidine catabolism combined with carnosine and hemoglobin degradation can provide sufficient histidine to explain the slow onset of negative nitrogen balance associated with histidine deficiency and that impaired protoporphyrin synthesis may partially explain the anemia observed in the absence of dietary histidine.
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PMID:Metabolic effects of histidine-deficient diets fed to growing rats by gastric tube. 649 66

A 77-year-old, nonalcoholic man was admitted to the Omiya Red Cross Hospital with the complaint of fever and delirium state of two days' duration. Two months prior to admission he had had cough and sputum. Chest X-ray revealed honey comb lungs. Cultures of sputum revealed mycobacterium tuberculosis after eight weeks incubation. He had no liver disease in his past history. The patient appeared cachetic. His vital signs were as follows; temperature 38 degrees C, blood pressure 132/68 mmHg, with a pulse rate of 84/min. He was delirium and excited. Findings of the cranial, motor and sensory nerve examination were normal. Initial laboratory studies showed a serum sodium value of 133 mEq/l, potassium 4.5 mEq/l, chloride 98 mEq/l; a serum GOT value of 51 units, GPT 36 units; a total protein content of 7.8 g/dl and ESR rate of 87 mm/hr. Six days after admission, the patients' consciousness level began to stupor and nuchal rigidity was appeared. Spinal fluid examination revealed opening pressure 270 mm H2O, cell counts 720 (N 712, L 8)/cumm, sugar 57 mg/dl and protein 170 mg/dl. Spinal fluid cultures were positive in mycobacterium tuberculosis after eight weeks incubation. Laboratory studies showed a serum sodium value of 114 mEq/l, potassium 4.4 mEq/l, chloride 86 mEq/l, a serum osmorality (SeOs) 225 mOsm/l and urine osmorality (UOs) 958 mOsm/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine myelinolysis--pathogenesis and review of the literature]. 663 5

Some experimental and clinical studies were done from the metabolic viewpoint to elucidate the characteristics of myonephropathic-metabolic syndrome. In experimental dogs with their femoral arteries ligated and two third of femoral muscles divided, aldolase and myoglobin showed remarkable increase without significant changes in electrolytes. Slight increase of GPT and GOT was observed. Amino acids showed elevation in urea, taurin, leucin, isoleucin, valine, threonine, 3-methylhistidine, phenylalanine, histidine, lysine, methionine, tyrosine and anserin and decrease in glutamine, alanine, glycine, proline, carnosine, citrullin and arginine. In patients with acute arterial occlusion, potassium, GOT, LDH, CPK, lactate and pyruvate increased moderately and myoglobin showed remarkable increase and aldolase slight increase. Amino acids showed remarkable increase in 3-methylhistidine and beta-amino-isobutyric acid and moderate increase in phenylalanine and arginine. These results revealed that measurement of free amino acid concentration, especially that of methylhistidine as well as myoglobin, pyruvate, lactate and some other enzymes might be of great help to predict the prognosis of patients with acute arterial occlusion of the extremities.
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PMID:[Metabolic study on acute arterial occlusion of the extremities]. 667 89

Experimental studies have demonstrated preferential injury to the sinusoidal endothelium during liver preservation with University of Wisconsin (UW) or Euro-Collins solution. This endothelial cell injury has an unclear pathogenesis, and it has not yet been studied in the human liver. Therefore, we analyzed the effluent of 21 human liver allografts after cold storage. Markers of hepatocellular and nonparenchymal cell injury were assessed. After preservation with UW solution, early effluent samples contained 1823 +/- 1494 U/l lactate dehydrogenase (LDH), 493 +/- 516 U/l alanine aminotransferase (ALT) and 132 +/- 97 U/l creatine kinase (CK; 92 +/- 92 U/l CK-BB). The effluent of livers preserved in histidine-tryptophan-ketoglutarate (HTK) solution contained 3681 +/- 2009 U/l LDH, 1139 +/- 599 U/l ALT and 282 +/- 120 U/l CK (165 +/- 91 U/l CK-BB). Comparison of effluent enzyme activities with liver tissue enzyme activities indicates that the release of the endothelial cell/nonparenchymal cell marker creatine kinase was higher, by a factor of 7-8, than the release of hepatocellular enzymes. Effluent thrombomodulin concentrations were 123 +/- 248 ng/ml (UW) and 604 +/- 299 ng/ml (HTK), and effluent glucose concentrations, 40.3 +/- 27.0 mM (726 +/- 486 mg/dl; UW) and 10.4 +/- 4.5 mM (187 +/- 81 mg/dl; HTK). We conclude that prominent endothelial cell injury also occurs in human liver grafts after preservation with UW solution or HTK solution. This endothelial cell injury is unlikely to be caused by hypoxia-induced energy deficiency, as it affects a cell type with a high glycolytic capacity in the presence of high glucose levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonparenchymal cell and hepatocellular injury to human liver grafts assessed by enzyme-release into the perfusate. 793 84

The patient was a 25-year-old male doctor, who had pricked his finger with a needle contaminated with blood from a 69-year-old male patient with liver cirrhosis (HCV-Ab positive, genotype II). He was informed from the blood bank that his blood was positive for anti-HCV and his GPT being 148 IU/l on the 65th day after exposure. He was admitted on February 16, 1993 and received a liver biopsy, which was consistent with acute viral hepatitis. His genotype was the same (type II) with the donor patient. IFN-alpha-2b of total doses of 656 Megaunits resolved the hepatitis completely and the HCV-RNA became negative as early as two weeks after starting IFN therapy. Liver biopsy after IFN therapy showed convalescence of acute hepatitis. The progression of acute hepatitis C to chronicity could be prevented by interferon therapy even in unfortunate cases of HCV transmission by needlestick. In conclusion, accidental needlestick should be followed for at least six months, and serum GPT and second-generation anti-HCV ELISA tests are recommended for all infected personnel.
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PMID:[A case of needlestick-induced acute type C hepatitis]. 805 46

We report a case of sporadic acute type A hepatitis associated with acute renal failure, due to mesangioproliferative glomerulonephritis and interstitial nephritis. A 42 year-old-man was admitted to Mitsui Memorial Hospital because of jaundice and oliguria with fever in February, 1989. His serum creatinine was 12.2 mg/dl, BUN 87 mg/dl, GOT 57 U/l and GPT 358 U/l. The serum IgM antibody to hepatitis A virus was positive, which indicated recent infection with hepatitis A virus. Hemodialysis and steroidal therapy were started, and the patient's acute renal failure and liver dysfunction ameliorated within one month. Light microscopic examinations showed an increased number of mesangial cells and an increased amount of mesangial matrix, and also showed inflammatory cell invasion in the interstitium. Electron microscopic examinations showed proliferation of mesangial cells and matrix, and a dense deposit along the basement membrane. On immunofluoresent studies, fine granular deposits of IgA and Clq were observed in the mesangium.
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PMID:[A case of sporadic acute type A hepatitis associated with acute renal failure]. 807 27

Serum amino acid (AA) profiles are altered in epilepsy. It is not clear whether this is due to the disease process itself or to other variables such as seizure type, seizure frequency, duration of illness, medication, or altered liver function. We investigated serum AA profiles and liver enzymes in 73 epileptic patients and 90 healthy subjects and evaluated the data by analysis of variance to discriminate between age, sex, seizure type, duration of illness, seizure frequency, antiepileptic drug (AED) and increased serum liver enzyme levels, and their putative interaction with the serum AA profile. There was no correlation between the changes in the AA profile and age, duration of illness, seizure frequency, and seizure type. Seventy-two percent of the AED-treated patients and 33% of the unmedicated patients showed an increase in one or several serum liver enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and/or gamma-glutamyl transferase (gamma-GT)]; particularly gamma-GT. We observed a significant increase in serum concentrations of glutamine and glycine and decreased levels of taurine, threonine, serine, valine, methionine, isoleucine, leucine, phenylalanine, histidine, tryptophan, and arginine in AED-treated patients but not in unmedicated patients. These results show that the changes in the serum AA profiles of epileptic patients treated with AEDs occur in patients with alteration of serum liver enzymes; whether this implies a causal relation is still uncertain.
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PMID:Serum amino acids, liver status, and antiepileptic drug therapy in epilepsy. 809 92

We report a case of suspected liver dysfunction after general anesthesia with sevoflurane. A 30 day old male infant underwent inguinal herniorrhaphy under sevoflurane anesthesia (sevoflurane concentration: 1.3-1.5% with 50% oxygen and nitrous oxide). Two days after the operation, he developed frequent vomiting, anorexia and fever. GOT, GPT and LDH values were 242 Ku, 326 Ku and 901 Wu, respectively and peaked at 520 Ku, 709 Ku and 1000 Wu 12-16 days after the operation. Clinical symptoms and the laboratory data became normal within 2 months. The antibody titers of EB-virus, cytomegalo-virus and HA-virus were all within normal ranges and HBs antigen was negative. There were no blood transfusion or antibiotics administration before the onset, and no epidemic of hepatitis around him. His mother had no history of hepatitis during her pregnancy. Lymphocyte stimulation test for indication of sevoflurane allergy was also negative. From these evidences, toxic (not allergic) liver dysfunction due to exposure to sevoflurane was considered to be the most probable diagnosis.
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PMID:[A case of suspected liver dysfunction induced by sevoflurane anesthesia]. 832 Aug 10

A 60-year-old man with a chronic hepatitis C virus (HCV) infection and histological features of chronic active hepatitis was treated with interferon-alpha (IFN). He successfully responded to IFN with normalization of serum ALT and disappearance of serum HCV-RNA. His liver biochemistry profile remained normal and serum HCV-RNA was not detected throughout the entire follow-up period. One year later, a small hepatocellular carcinoma (HCC) was detected by routine ultrasonographic screening. Laparotomy revealed a small tumour with no metastasis and the non-tumorous liver demonstrated macronodular cirrhosis. Although no space-occupying lesions were detected by frequent radiological examinations prior to IFN therapy, the small size of the tumour suggested de novo development of HCC. Patients with chronic HCV infection, including those who have complete responses to IFN and lack clinical and histological evidence of cirrhosis, should be followed up for the potential development of HCC.
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PMID:Case report: development of hepatocellular carcinoma in a patient with chronic hepatitis C infection after a complete and sustained response to interferon-alpha. 891 34


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