Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness. The incidence of thiamine deficiency was 31% as assessed by the activation of transketolase, and 55% as assessed by the pyruvate tolerance test. The incidence of riboflavin deficiency was 23% and of ascorbic acid deficiency 91%. No cases of pyridoxine deficiency were detected. The pyruvate tolerance test was found to be a more sensitive test of thiamine deficiency than the transketolase activation, and the activation of red blood cell aspartate transaminase was found to be a poor indicator of pyridoxine deficiency. There was a poor correlation of the gamma-glutamyl transferase activity with the degree of vitamin deficiency, suggesting that alcohol exposure is only partly responsible for the observed vitamin deficiency.
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PMID:Detection and incidence of B and C vitamin deficiency in alcohol-related illness. 3 28

1. Thiamin, riboflavin and pyridoxine status of 'low-income-group' mothers and their newborn infants was assessed by analysing paired samples of maternal and umbilical cord blood for erythrocyte transketolase (EC 2.2.1.1) (ETK), erythrocyte glutathione reductase (EC 1.6.4.2) (EGR), and erythrocyte aspartate aminotransferase (EC 2.6.1.1) (EAA) activities. 2. The vitamin status of the infants was better than that of the mothers. 3. Most of the mothers and some of the infants had biochemical evidence of thiamin and riboflavin deficiency. 4. The pregnant women had a higher EAA activity and also higher stimulation with pyridoxal-5-phosphate than the non-pregnant women of the same community. 5. There was a significant correlation between maternal and umbilical blood samples for ETK and EGR activities, but not for EAA activity or any of the coenzyme stimulation tests.
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PMID:Enzymic evaluation of thiamin, riboflavin and pyridoxine status of parturient women and their newborn infants. 125

The relationship between riboflavin and pyridoxine status was studied in 40 patients with sickle cell disease (SCD) and 12 normal children by measuring activation coefficients of erythrocyte glutathione reductase (EGRAC) and aspartate transaminase (ASTAC). Prevalence of riboflavin deficiency was significantly lower in SCD (42.5%) than in control subjects (83%) and there was less pyridoxine deficiency in SCD (10.3%) than control subjects (54.5%). Aspartate transaminase (AST) activities in SCD patients were double those in control subjects. Pyridoxine status of patients, but not of control subjects, was directly affected by riboflavin status as judged from significant correlations between EGRAC and both AST activity and ASTAC. Poor riboflavin status in patients may be restricting availability of pyridoxal phosphate (PLP) due to combined effects of enhanced PLP requirements and effects of poor riboflavin status on the synthesis of PLP by pyridoxine phosphate oxidase (PPO). PPO activity was no different in the two groups.
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PMID:Dependence of pyridoxine metabolism on riboflavin status in sickle cell patients. 360 73

The formation of pyridoxal and its phosphate from pyridoxamine phosphate by red cell haemolysates was measured in a centrifugal analyser by the formation of the fluorescent adduct with semicarbazide. Pyridoxal phosphate was found to react more rapidly than pyridoxal, thus permitting a distinction between the two products, and hence the measurement of phosphatase activity. Activity of the enzyme, pyridoxamine phosphate:oxygen oxidoreductase (deaminating) EC 1.4.3.5 (PPO) was measured in haemolysates from 72 Gambian women with evidence of riboflavin deficiency, and was repeated after 6 weeks of placebo or riboflavin supplementation. Those who received the riboflavin supplement responded with a marked increase in PPO activity, which was matched by a decrease in the activation coefficient (AC) of erythrocyte NAD(P)H2:glutathione oxidoreductase, EC 1.6.4.2 (glutathione reductase, EGR). No difference between the supplemented and unsupplemented groups was observed in the capacity of haemolysates to hydrolyse pyridoxal 5-phosphate, nor in the extent of activation of erythrocyte L-aspartate:2-oxoglutarate aminotransferase EC 2.6.1.1. by pyridoxal phosphate. Although the three subjects with low levels of D-glucose 6-phosphate: NADP 1-oxidoreductase EC 1.1.1.49 (G6P-D) had, as expected, correspondingly low AC's of EGR, their unsupplemented activities of PPO were in the same low range as those of the G6P-D-normal subjects, and they responded as G6P-D-normal subjects did to riboflavin supplementation. PPO thus does not appear to resemble EGR in retaining its flavin coenzyme during riboflavin depletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A simple fluorimetric assay for pyridoxamine phosphate oxidase in erythrocyte haemolysates: effects of riboflavin supplementation and of glucose 6-phosphate dehydrogenase deficiency. 401 61

Differential enzymic analyses of the erythrocyte glutamic-oxaloacetic transaminase and the erythrocyte glutathione reductase of a patient with a 3-yr history of the carpal tunnel syndrome (CTS) revealed high deficiencies of both vitamin B-6 and riboflavin as based on approximately equal to 30% levels of the specific activities of these enzymes. Riboflavin for 5 months caused nearly complete disappearance of the CTS and caused no change in the specific activity of erythrocyte glutamic-oxaloacetic transaminase. Combined riboflavin and pyridoxine treatment increased (P less than 0.001) the specific activities of erythrocyte glutathione reductase and erythrocyte glutamic-oxaloacetic transaminase to normal levels with total disappearance of the CTS. Objectively, the strength of pinch of both hands increased (P less than 0.001) on treatment with riboflavin and further increased (P less than 0.001) on the combined treatment. For the first time, a significant riboflavin deficiency has been found to be related to CTS. Riboflavin therapy was effective biochemically, subjectively, and objectively, and riboflavin and pyridoxine were even more effective when concomitantly administered.
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PMID:Enzymology of the response of the carpal tunnel syndrome to riboflavin and to combined riboflavin and pyridoxine. 659 81

One hundred and seventy-two successive admissions to a district general hospital psychiatric unit were examined. Routine psychiatric, drug and dietary histories were taken and signs of avitaminosis B specifically noted. Red cell transketolase (for thiamine deficiency), glutathione reductase (for riboflavin deficiency) and aspartate transaminase (for pyridoxine deficiency) were measured. Of the patients, 53 per cent were deficient in at least one vitamin, 12 per cent in more than one (30 per cent in thiamine, 27 per cent in riboflavin and 9 per cent in pyridoxine). Schizophrenics and alcoholics were significantly over-represent in those patients low in thiamine and in more than one vitamin. Patients with an affective disorder had low riboflavin and low pyridoxine. It is suggested that affective changes are characteristic of riboflavin and pyridoxine deficiency.
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PMID:Thiamine, riboflavin and pyridoxine deficiency in psychiatric in-patients. 713 10