Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed retrospectively a cohort of 80 patients with hyperemesis gravidarum hospitalized between 1976 and 1986 for the presence of abnormal liver enzymes and ketonuria. Thirteen (16%) had abnormal liver enzymes, generally less than four times the upper limit of normal. In this group, hyperemesis gravidarum began at the 14th week of pregnancy as compared to the 6th week in the normal enzyme group (p less than 0.01). Both groups were similar with regard to age, number of children and pregnancies, and duration of vomiting. Ketonuria was significantly more severe (p less than 0.01) in the abnormal enzyme group, implying a more severe state of starvation and dehydration. The correlation coefficient between the degree of ketonuria and level of liver enzymes was low for alkaline phosphatase (r = 0.18), GPT (r = 0.15), and GOT (r = 0.28). The concept that dehydration and starvation are important factors for the induction of liver cell injury is supported by our data. Lack of correlation between the degree of ketonuria and liver enzyme levels is suggestive of other mechanisms (hormonal, genetic) that may interact to produce transaminasemia.
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PMID:Abnormal liver enzymes and ketonuria in hyperemesis gravidarum. A retrospective review of 80 patients. 236 99

Iron overload is found clinically in such conditions as hemochromatosis and sideroblastic anemia, and after long term repeated transfusion in aplastic anemia. An animal model of iron overload was successfully developed in rats and rabbits by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe3+-NTA). This procedure induced a diabetic state with hyperglycemia, ketonemia, glycosuria and ketonuria. Blood venesection on these rats reduced the iron load in the liver and pancreas, and ameliorated the general diabetic symptoms. A single injection of Fe3+-NTA in rats induced a temporary elevation in plasma iron concentration, lipid peroxidation in the perfused liver homogenate expressed by malondialdehyde (MDA) formation, blood GOT, GPT, ALP and gamma-GTP sequentially. Fe3+-NTA uptake in the liver caused membrane lipid peroxidation, and subsequently produced a transit liberation of liver cell enzymes, although the incorporated liver Fe3+-NTA was only 1% of the injected dosage (7.5 mg iron/kg BW) at 3 hr after injection. The direct toxic effect of Fe3+-NTA to living cells was examined using cultured normal rat liver parenchymal cells (RL-34). Marked cytolysis was found in cells exposed to more than 25 micrograms of iron through Fe3+-NTA/ml. At 50 micrograms iron of Fe3+-NTA/ml, most cells were lethally injured and the remaining cells were piled up and aggregated at 15 days. They grew on soft agar culture, and when inoculated subcutaneously to five newly born rats a subcutaneous tumor developed in all animals within three weeks. Lung metastases were found in three of five inoculated rats. A spin trapping technique with electron spin resonance (ESR) on Fe3+-NTA employing 5, 5-dimethyl-l-pyrroline-N-oxide (DMPO) yielded a spin adduct with three doublets (DMPO-Z) which corresponded to singlet oxygen. By ESR in the presence of H2O2, the Fe3+-NTA solution strongly generated hydroxyl radical. The production of active oxygen species by Fe3+-NTA solution may explain the toxicity and carcinogenicity of Fe3+-NTA. The majority of stainable iron in the iron overloaded tissue was hemosiderin (Hs). We tried to purify the Hs from multi-transfused human spleen by the method of Weir et al. The purified Hs did not show a DMPO-OH adducts in the presence of H2O2 and DMPO on ESR measurement. The Hs iron was solubilized with several biological ligands in an acidic state in the presence of a reducing reagent like glutathione. Solubilized Hs iron produced iron chelate complexes which resulted in OH radicals production in the presence of H2O2 in acidic conditions below pH 5.5.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathogenesis and mechanism of iron overload: ferric nitrilotriacetate, hemosiderin, active oxygen, and carcinogenesis]. 268 76

Investigations were carried out with a total of 276 high-producing and clinically healthy cows that had freshly calved on 11 farms, being divided into groups according to the extent to which ketonuria was present if al all. Whole blood and blood serum were sampled to determine the ketone bodies, blood sugar, erythrocyte and leukocyte counts, hemoglobin, inorganic phosphorus, Ca, Mg, total protein, carotene, and activity of the GOT and GPT enzymes as well as the activity of lactic acid dehydrogenase, alkaline phosphatase, aldolase, and leucine aminopeptidase. Studied were the body temperature, the pulse rate, and the respiration rate. It was found that on farms with ketosis in cows ketonuria was manifested most often after the ketone bodies in the blood rose to 10-12 mg%. At the same time the blood sugar level was lowered and as a rule it showed reverse correlation with the levels of ketonemia and ketonuria. In such cows there was a lowering trend with the Ca and carotene contents and the erythrocyte count, and the respiration rate was higher. There were no changes in the body temperature, pulse rate, leukocyte count, Ca, Mg, hemoglobin, protein, and the activity of aldolase. The activity of the other enzymes mentioned was higher, and it correlated positively with the rise of ketonemia and ketonuria. With diseased cows the activity of alkaline phosphatase only was shown to be lower, negatively correlating with ketonuria.
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PMID:[Changes in the serum enzymes and clinical and clinico-biochemical indices of cows with subclinical ketosis]. 653 57