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)

Coenzymes participate in many of the enzyme analyses performed in the clinical laboratory. Supplementation of assay systems with optimal levels of coenzymes has recently been recommended as part of efforts to achieve interlaboratory standardization of enzyme measurements. Aspartate aminotransferase and alanine aminotransferase require pyridoxal phosphate for expression of enzyme activity. The role of this coenzyme in enzymatic transamination and the effects of its supplementation on the clinical estimation of these two enzymes is reviewed. Other coenzymes discussed are flavins, coenzymes for glutathione reductase, glucose oxidase, cholesterol oxidase and diaphorase, as well as thiamine pyrophosphate, coenzyme for transketolase. Catalase and peroxidase are used as examples of hemoproteins utilized in clinical measurements. Two peptide coenzymes, colipase and glutathione, are also considered. Measurement of apoenzyme stimulation upon supplementation with specific coenzymes is discussed as a valuable technique for quantitative coenzyme measurements or assessment of vitamin nutritional status.
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PMID:Review: the role of coenzymes in clinical enzymology. 33 88

This paper reports a study of changes in red blood cell enzymes and some serum parameters during and after treatment of protein-calorie malnutrition. The red cell GSH levels were low during the crisis, together with the levels of GSSG:NADPH reductase, GSH:H2O2 peroxidase, aspartate aminotransferase and alanine aminotransferase. After treatment the levels of all these enzymes increased significantly to normal values. Of the serum parameters investigated, significant reduction in the activity of the enzymes cholinesterase, catecholamine oxidase, total proteins, albumin, urea and electrolytes were obvious, and returned to normal values after treatment. Ceruloplasmin activity remained low even after three weeks' treatment and could not be related to copper levels. The results are discussed in relation to anemia and liver damage that may accompany the syndrome.
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PMID:Protein-calorie malnutrition: a study of red blood cell and serum enzymes during and after crisis. 82 Apr 94

The study on the embryotrophic action of phosalon insecticide preparation is conducted against the background of its comprehensive and thorough hygiene-toxicologic assay. Pregnant white rats undergo treatment per os with 1/10 and 1/100 LD50 throughout the entire gravidity period. Recordings are made of the quantity of corpora lutea, pre- and postimplantation lethality; the pedigree development is traced up to the end of the second postnatal month with readings being made of weight and length in the first postnatal day, presence or not of external malformations, weight increase and survival up to the end of the lactation period, day of eye cleft opening and hairing, and sex ratio. The presence of phosalon and phosalon-oxone in whole embryo homogenates is estimated. Enzyme activity of GOT, GPT, catalase, LDH, G-6-PD, RNA and DNA quantity are studied in the liver of newborns on the second postnatal day. Within 21 days of birth, the peripheral blood picture and visceral weight coefficient are also studied. Investigation of the peripheral blood picture, activity of catalase, GOT and GPT in the liver and serum, alkaline and acid phosphatase, and peroxidase in the serum is performed at the end of the second month. The results point to the presence of an embryotoxic effect at the level of the investigated hepatic indicators, detected on the 2nd day of the postnatal period, only at 1/10 LD50 dose.
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PMID:[Embryotropic action of phosalone]. 103 14

Ubiquinol-1 in aerated aqueous solution inactivates several enzymes--alanine aminotransferase, alkaline phosphatase, Na+/K(+)-ATPase, creatine kinase and glutamine synthetase--but not isocitrate dehydrogenase and malate dehydrogenase. Ubiquinone-1 and/or H2O2 do not affect the activity of alkaline phosphatase and glutamine synthetase chosen as model enzymes. Dioxygen and transition metal ions, even if in trace amounts, are essential for the enzyme inactivation, which indeed does not occur under argon atmosphere or in the presence of metal chelators. Supplementation with redox-active metal ions (Fe3+ or Cu2+), moreover, potentiates alkaline phosphatase inactivation. Since catalase and peroxidase protect while superoxide dismutase does not, hydrogen peroxide rather than superoxide anion seems to be involved in the inactivation mechanism through which oxygen active species (hydroxyl radical or any other equivalent species) are produced via a modified Haber-Weiss cycle, triggered by metal-catalyzed oxidation of ubiquinol-1. The lack of efficiency of radical scavengers and the almost complete protection afforded by enzyme substrates and metal cofactors indicate a 'site-specific' radical attack as responsible for the oxidative damage.
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PMID:Enzyme inactivation by metal-catalyzed oxidation of coenzyme Q1. 135 46

A deceased 59-year-old woman with insulin dependent diabetes mellitus complicated by chronic thyroiditis and chronic hepatitis was autopsied. She had had diabetes mellitus since she was 30 years old, and insulin therapy was started at 34 years. Laboratory findings were as follows: s-GOT 85, s-GPT 31, gamma-globulin 2.45 g/dl. Immunological tests were positive for anti-smooth muscle antibody and anti-ENA antibody with high titers of antithyroglobulin and anti-microsome antibodies. HLA analysis revealed the presence of DR-4. The thyroid biopsy specimen showed microscopic features characteristic of chronic thyroiditis at 52 years of age. She had been repeatedly admitted for the control of diabetes mellitus. She was admitted for the 9th time in June, 1987 following complaints of abdominal pain. After admission, her general condition became gradually worse, and she died of peritonitis in September, 1987. Pathological examination of the liver revealed an expansion of fibrous tissue on Glisson's capsule accompanied by lymphocytic infiltration and was diagnosed to be chronic inactive hepatitis. As for the thyroid gland, fibrous tissue replaced an extensive area of the thyroid gland, and normal thyroid tissue was not observed. Lymphocytic infiltration was less in comparison with that in the previous biopsy. As for the pancreas, atrophy of exocrine pancreatic tissue and fibrous change in interstitial tissue was observed. Lymphocytic infiltration was also seen in the interstitial exocrine tissue but not in the islet. Immunohistochemical examination of the islets using anti-insulin, glucagon and somatostatin antibodies by ABC peroxidase method showed the selective disappearance of B cells in the islets. The pathological changes in the thyroid gland, liver and pancreas suggest that autoimmune mechanism may be involved in the pathogenesis of chronic thyroiditis, chronic hepatitis and IDDM with exocrine pancreatic impairment in this case.
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PMID:[An autopsied case of insulin dependent diabetes mellitus complicated by chronic thyroiditis and chronic hepatitis]. 259 7

The intrahepatic expression of hepatitis-B core antigen (HBcAg) was investigated in 54 liver biopsy specimens from 24 chronic type-B hepatitis patients, by the peroxidase-anti-peroxidase technique. The HBcAg localization pattern in the hepatocyte correlated with the evolution of serum alanine aminotransferase (ALAT) values. The clinical course were classified into three phases, as follows: pre-exacerbation phase (A phase), with minimal abnormal range of ALAT (40-100 KU) for 6 to 12 months; exacerbation phase (B phase) with elevated ALAT (more than 100 KU) for 3 to 6 months; and post-exacerbation and subsiding phase (C phase) for 3 months after phase B, showing decreased ALAT values. Nineteen of the 54 biopsied specimens belonged to the A phase, 21 to the B phase, and 14 to the C phase. In the A phase the hepatocytic HBcAg was variably expressed as nuclear, cytoplasmic, and membranous in location in the same specimens. In the B phase, HBcAg expression decreased in the nucleus, but increased in the cytoplasmic-membranous pattern. The intrahepatic HBcAg expression in the C phase decreased in all patterns. The mean level of ALAT in cases of cytoplasmic-membranous HBcAg expression was higher than that in cases of nuclear HBcAg expression. Four of six patients who underwent liver biopsies in the A, B, and C phases showed remarkable decreases of cytoplasmic and membranous HBcAg expression in the C phase. These findings suggest that cytoplasmic and membranous localization of HBcAg can be related to both liver cell injury and active inflammatory processes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Change of intrahepatic expression of hepatitis-B core antigen during the clinical course of type-B chronic hepatitis. 267 3

We have previously shown that the rapid clearance of intravenously injected lactate dehydrogenase M4 from plasma is mainly due to endocytosis by macrophages in liver, spleen, and bone marrow. We have now studied endocytosis of lactate dehydrogenase M4 in detail, using freshly isolated rat liver macrophages (Kupffer cells) in vitro. 125I-lactate dehydrogenase M4 rapidly accumulated in the cells and was subsequently degraded to trichloroacetic acid-soluble material. Degradation was inhibited by leupeptin, an inhibitor of lysosomal proteases. Breakdown of the protein was also greatly diminished by treatment of the cells with chloroquine, a weak base which inhibits proteolysis by raising the pH in endosomes and lysosomes. High concentrations of chloroquine inhibited uptake. Lactate dehydrogenase M4 was not endocytosed by liver endothelial cells, although, under the same conditions, these cells were shown to accumulate horse radish peroxidase via a mannose-specific receptor. Uptake of lactate dehydrogenase M4 by Kupffer cells was strongly reduced after pretreatment of the cells with low concentrations of proteases. Endocytosis of lactate dehydrogenase M4 exhibited saturation kinetics (Km = 0.8 microM) and was competitively inhibited by mitochondrial and cytosolic malate dehydrogenase, alcohol dehydrogenase, adenylate kinase, and creatine kinase MM, enzymes which are rapidly cleared in vivo. Enzymes with long half-lives in plasma, namely lactate dehydrogenase H4, alanine aminotransferase, and cytosolic aspartate aminotransferase did not compete at concentrations up to 10 microM. Our results indicate that Kupffer cells contain a receptor that is involved in the clearance of lactate dehydrogenase M4 and a number of other tissue-derived enzymes from plasma. Uptake of lactate dehydrogenase M4 does not occur via a receptor that recognizes carbohydrate residues, for the enzyme is not a glycoprotein.
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PMID:Receptor-mediated endocytosis of lactate dehydrogenase M4 by liver macrophages: a mechanism for elimination of enzymes from plasma. Evidence for competition by creatine kinase MM, adenylate kinase, malate, and alcohol dehydrogenase. 282 Sep 61

Using a monoclonal antibody to bromodeoxyuridine, we studied the cell kinetics of human hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis. Specimens were taken either by biopsy or surgery and immediately incubated with 0.1% bromodeoxyuridine solution at 37 degrees C for 45 min. After in vitro labeling, the bromodeoxyuridine taken up by the nuclei of S-phase cells was determined by the avidin-biotin-peroxidase complex method, using an anti-bromodeoxyuridine monoclonal antibody as the first antibody. The number of positive nuclei in 1,000 hepatic cells was counted, and the bromodeoxyuridine labeling index was expressed per thousand. The mean bromodeoxyuridine labeling index +/- S.D. of the cancerous portion of hepatocellular carcinoma, the noncancerous portion of hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis were 64.1 +/- 31.3, 33.6 +/- 14.4, 23.2 +/- 20.8, 9.1 +/- 6.1 and 21.6 +/- 13.0, respectively. The mean bromodeoxyuridine labeling index of the hepatocellular carcinoma cancerous portion was statistically higher than that of any other group. There was no statistical difference by the t test or the Wilcoxon test between the noncancerous portion of hepatocellular carcinoma and liver cirrhosis, and these two groups were proved interdependent by chi 2 test (Fisher's exact test), whether they were subdivided by bromodeoxyuridine labeling index greater than or equal to 10 or not. Bromodeoxyuridine labeling index was not significantly correlated with the usual biochemical parameters such as serum AST, ALT, gamma-GTP, alkaline phosphatase, lactate dehydrogenase, cholinesterase, albumin, and alpha-fetoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-phase cells in diseased human liver determined by an in vitro BrdU-anti-BrdU method. 284 68

During an evaluation of the IFCC reference method for alanine aminotransferase (ALT, EC 2.6.1.2), we noted that the specimen blank activity reaction was markedly increased. Experience with five different lots of D-alanine from four commercial sources indicated that substantial and varying negative bias (up to -10%) could be introduced into the blank-corrected ALT activity, depending on the lot of D-alanine used. Although the IFCC procedure for ALT mentions the possibility of this L-alanine contamination, we believe that the degree of contamination in commercial reagents is underestimated. Analyzing the five lots of D-alanine for L-alanine, we found the magnitude of negative bias to be correlated directly with L-alanine contamination. Here, we describe a quick, sensitive assay based on coupled reactions of L-amino acid oxidase/peroxidase for quantifying L-alanine in the concentration range of 0-15 mmol/L without a sample-dilution step. Results by this alternative L-alanine assay agreed well with those recommended in the IFCC ALT procedure. Further examination suggested an even simpler solution to the L-alanine contamination problem, because we found no difference in the blank-corrected ALT activity determined in Tris HCl buffer, with or without D-alanine (free of L-alanine). We therefore propose that D-alanine be omitted from the IFCC reference ALT procedure.
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PMID:Evaluation of the IFCC reference method for alanine aminotransferase: spurious blank ALT activity due to contamination of D-alanine with L-alanine, and recommendations for a correction. 291 May 58

Sera and biopsied liver specimens from 45 hepatitis B surface antigen (HBsAg) carriers both with or without overt liver diseases and negative for anti-delta antibody, were examined for markers of hepatitis B virus (HBV) infection: hepatitis B e antigen (HBeAg), hepatitis B virus deoxyribonucleic acid (HBV-DNA) in serum and hepatitis B core antigen (HBcAg) in liver. HBV-DNA in serum was assayed by the spot hybridization technique, and HBcAg in the liver was investigated by the peroxidase anti-peroxidase method. Among the parameters showing active replication of HBV, serum HBeAg, serum HBV-DNA and intrahepatic HBcAg were found in 27 (60%), 27 (60%) and in 22 (48.9%) of 45 HBsAg carriers, respectively. The presence of serum HBV-DNA and of intrahepatic HBcAg in HBeAg positive cases and the absence of serum HBV-DNA and of intrahepatic HBcAg in anti-HBe positive cases was the rule with few disparate cases among those with chronic liver disease. These parameters were not useful in predicting the histology on liver biopsy. The activity of hepatic inflammation in the HBsAg chronic carriers assessed by serum alanine aminotransferase level closely paralleled HBV-DNA in serum but not HBeAg in serum, HBcAg in liver or histologic picture on biopsy. HBV-DNA may be the most sensitive parameter of replication of hepatitis B virus and of the activity of inflammation in the liver.
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PMID:Relationship between hepatitis B virus deoxyribonucleic acid, HBeAg/anti-HBe status in serum and HBcAg in liver: its clinical significance in chronic HBsAg carriers. 305 67


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