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 influence of different levels of dietary pyridoxine-HC1 (1.2, 2.4, 4.8, 9.6, 19.2, 38.4, 76.8 and 153.6 mg/kg diet) fed to dams on certain parameters of developing and mature brain was studied in rats. Brain weights and alanine aminotransferase (ALAT) activities (initial and following in vitro addition of pyridoxal phosphate, PLP) were significantly reduced in brains of 12-day-old pups of dams fed the lowest level of pyridoxine compared to other treatments; in vitro addition of PLP significantly stimulated the activities of glutamic acid decarboxylase (GAD) and ALAT. Vitamin B-6 concentrations in brain were higher for 2-day-old pups of dams fed 38.4 or 76.8 mg vitamin/kg diet and for 12-day-old pups of dams fed 2.4 to 153.6 mg compared to the 1.2 mg groups; at weaning, values were greater in groups fed 76.8 or 153.6 mg compared to the 1.2 mg group. As brain developed during the suckling period, the content of bitamin B-6 and protein increased in all groups, except the 1.2 mg group in which values remained the same. The vitamin and protein content in brain had not reached chemical maturity at weaning as evidenced by greater concentrations of each in brains of dams as compared with values for 21-day-old progeny. As brain developed, ALAT activity increased about 30 times from age 2 to 21 days when activities were similar to those observed in mature brains of dams. Activity of GAD in brain increased about four times from age 12 to 21 days.
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PMID:Influence of different levels of dietary pyridoxine on certain parameters of developing and mature brains in rats. 126 75

Theophylline administration to seven healthy male volunteers resulted in a rapid and significant decline in both plasma and erythrocyte pyridoxal-5'-phosphate levels. Total erythrocyte pyridoxal kinase levels increased during 15 wk of theophylline treatment from a mean initial activity of 19.23 +/- 5.03 (mean +/- SD) to 62.64 +/- 11.59 nmol pyridoxal-5'-phosphate formed/(g hemoglobin.h). Although plasma pyridoxal levels remained normal, the threefold increase in total erythrocyte pyridoxal kinase activity levels did not normalize plasma and erythrocyte pyridoxal-5'-phosphate levels. Pyridoxal-5'-phosphate hydrolysis was not affected by theophylline therapy. Increased pyridoxal oxidation was confirmed by elevated urinary 4-pyridoxic acid excretion after 15 wk of theophylline treatment. Mean erythrocyte alanine aminotransferase activity declined by 70%, and aspartate aminotransferase activity declined by 50%, indicating that decreased availability of pyridoxal-5'-phosphate can have widespread metabolic consequences. We conclude that the effect of theophylline on vitamin B-6 metabolism is not transitory and cannot be overcome by elevated intracellular levels of pyridoxal kinase. However, pyridoxine supplementation (10 mg/d for 1 wk) normalized indices of vitamin B-6 status and reversed the downward trend in both alanine aminotransferase and aspartate aminotransferase activity levels.
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PMID:Relationship between vitamin B-6 status and elevated pyridoxal kinase levels induced by theophylline therapy in humans. 223 Oct 24

A new, sensitive, two-step method free from interference by hemoglobin that measures erythrocyte glutamate-pyruvate transaminase (E-GPT) activity is described. Several aspects of E-GPT activity as an index of vitamin B-6 nutritional status were investigated with this method. 1) GPT shows a structural genetic polymorphism with two common alleles resulting in three phenotypes. In a population study (n = 92) E-GPT activity differed significantly (p less than 0.001) among the three phenotypic groups. Plasma pyridoxal-5'-phosphate concentrations in the three groups did not differ significantly. Therefore, E-GPT activity can only be used to assess vitamin B-6 nutritional status if GPT phenotype is accounted for. 2) Pyridoxine supplementation (10 mg/d) significantly (p less than 0.0001) increased E-GPT activity and decreased (p less than 0.0001) the percentage stimulation by pyridoxal-5'-phosphate in vitro although the absolute amount of in vitro stimulation by pyridoxal-5'-phosphate changed only marginally. 3) Inorganic phosphate inhibits in vitro activation of E-GPT by pyridoxal-5'-phosphate.
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PMID:Genetic polymorphism of glutamate-pyruvate transaminase (alanine aminotransaminase): influence on erythrocyte activity as a marker of vitamin B-6 nutritional status. 259 31

The effects of vitamin B6 on erythrocyte metabolism, erythrocyte hemoglobin O2 affinity (P50), and nonenzymatic glycosylation were studied in 15 Caucasian men with type II (non-insulin-dependent) diabetes mellitus. A control group of 13 healthy Caucasian men was also evaluated. Before treatment, diabetic subjects had low mean cell hemoglobin concentration values and increases in both erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels and erythrocyte hexokinase activities. Although all three of these changes are associated with a decrease in hemoglobin O2 (Hb-O2) affinity, P50 values were normal in diabetic subjects. Moreover, P50 values normalized to pH 7.4 (P50(7.4] were inversely related to the level of glycosylated hemoglobin (HbA1c). Both erythrocyte 2,3-DPG and erythrocyte ATP were also inversely related to HbA1c. Vitamin B6 nutriture, as determined by erythrocyte aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, was normal in all diabetic subjects before vitamin B6 therapy. Nonetheless, HbA1c levels decreased after 6 wk of treatment with 150 mg/day pyridoxine and increased again during placebo administration. These changes were not explained by changes in fasting blood glucose. Pyridoxine therapy also decreased P50(7.4) values and increased erythrocyte AST and ALT activities but had no effect on 2,3-DPG, ATP, or the activities of hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. These observations suggest that 1) nonenzymatic glycosylation may play a role in regulating both erythrocyte metabolism and Hb-O2 affinity in diabetic subjects, and 2) vitamin B6 therapy may modify nonenzymatic glycosylation of hemoglobin in this population.
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PMID:Erythrocyte O2 transport and metabolism and effects of vitamin B6 therapy in type II diabetes mellitus. 273 64

Vitamin B-6 status was assessed by measuring erythrocyte glutamic-pyruvic transaminase (EGPT) indices in 122 pregnant Hispanic teenagers. Seventeen percent were vitamin B-6 deficient (EGPT indices greater than 1.25) at the initial interview (first or second trimester). A daily supplement of 5 mg vitamin B-6, beginning at initial interview, did not reduce prevalence of vitamin B-6 deficiency at final interview (third trimester). No association was found between EGPT indices greater than 1.25 and the outcome of pregnancy. The activity of diamine oxidase (DAO), a vitamin B-6-dependent enzyme produced by the placental decidua, was measured in maternal plasma. At initial and final interviews, plasma-DAO activity was increased by in vitro addition of pyridoxal-5'-phosphate. The activity in early pregnancy was positively associated with dietary vitamin B-6 intake and was lower in teenagers with EGPT indices greater than 1.25 at the final interview. Findings suggest that plasma-DAO activity is influenced by vitamin B-6 status.
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PMID:Vitamin B-6 nutriture and plasma diamine oxidase activity in pregnant Hispanic teenagers. 309 85

The vitamin B-6 status of 62 black and 50 white adolescent girls living in Virginia and Alabama was assessed in 1981 and again in 1983, using the parameters coenzyme stimulation of erythrocyte alanine aminotransferase activities and dietary intakes of the vitamin. The subjects were 12 or 14 years old in 1981. The height and weight measurements of the subjects were within normal ranges. The mean daily vitamin B-6 intake of the girls from food was 1.25 mg both years, as estimated by two nonsequential 24-hour food recalls. Approximately half of the girls reported consuming less than 0.02 mg vitamin B-6 per gm protein during both years. Almost half of the girls had coenzyme stimulation values indicative of marginal or deficient status. Coenzyme stimulation and dietary values of the race, age, and income groups were similar. Changes in the status grouping of the girls between the 2 years as reflected by the coenzyme stimulation measurement were associated with changes in their vitamin B-6 intakes in 70% of the cases. Vitamin B-6 inadequacy seems to be prevalent among both black and white adolescent girls.
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PMID:Longitudinal assessment of vitamin B-6 status in southern adolescent girls. 381 49

The vitamin B-6 status of 583 white and black adolescent girls living in Alabama, Arkansas, North Carolina, Oklahoma, and Virginia was assessed using the parameters coenzyme stimulation of erythrocyte alanine aminotransferase activities and dietary intakes of the vitamin. The sample included 382 white and 201 black girls who were 12, 14, or 16 years of age; the sample was also divided into low, medium, and high per capita income groups. The height and weight measurements of the subjects were within normal ranges. The mean estimated daily vitamin B-6 intake of the girls from food sources was 1.20 mg daily, as indicated by evaluation of data obtained via two nonsequential 24-hour food recalls; about half of the subjects reported consuming less than 66% of the Recommended Dietary Allowance for the vitamin. Approximately 20% of the girls had marginal vitamin B-6 status and 13%, deficient status, as indicated by coenzyme stimulation values. Coenzyme stimulation and dietary values of the race, age, and income groups were similar. Vitamin B-6 inadequacy appears to be fairly prevalent among white and black southern adolescent girls.
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PMID:Vitamin B-6 status of southern adolescent girls. 396 41

Estradiol-implanted (EB) and sham-operated (SB) male rats (100-120 g Fody wt) were kept on a vitamin B6-deficient diet for 1 month along (Formula: see text) with their respective estradiol pair-fed (EPF) and sham-operated pair-fed (SPF) controls. Pyridoxine-deficient animals had higher kidney weights and increased activities of liver glycolic acid oxidase (GAO) and glycolic acid dehydrogenase (GAD) as compared to their pair-fed control animals. Kidney weights, GAO, and GAD levels in these animals are negatively correlated with erythrocyte alanine transaminase (EALT) levels, indicating that pyridoxine status regulates these two major enzymes of oxalate biosynthesis. Estradiol-treated animals showed a lower reduction in EALT levels after feeding them a pyridoxine-deficient diet for 1 month as compared to untreated animals. Estradiol administration decreased GAO levels in both normal and pyridoxine-deficient animals.
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PMID:Effect of estradiol on the oxalate metabolism in vitamin B6-deficient male rats. 639 78

Vitamin cofactor saturations of placental enzymes were assayed in 54 Kenyan women. In addition, studies were conducted to determine whether placental vitamin deficiencies were associated with deficiencies in maternal or cord blood and to determine whether neonatal birthweights were influenced by vitamin nutriture. All samples were analyzed by vitamin cofactor saturation tests of glutathione reductase, transketolase, and glutamic-pyruvic transaminase. Standard indices were used to determine vitamin deficiencies. The activity of placental diamine oxidase, a pyridoxal phosphate-requiring enzyme was also measured and examined in relation to pyridoxine nutriture. No placental riboflavin deficiencies were found although 73% of maternal red blood cells (RBC) and 35% of cord RBC were deficient. Thiamine deficiencies were found in 15% of placentas, 59% of maternal RBC and 41% of cord RBC. Pyridoxine deficiencies occurred in 24% of placentas, 35% of maternal RBC, and 15% of cord RBC. Low birth weights were found to be associated with maternal riboflavin deficiencies. Maternal RBC riboflavin and thiamine deficiencies correlated with deficiencies in cord blood, and pyridoxine deficiencies in maternal RBC were associated with deficiencies in the placenta. A trend of lower placental diamine oxidase activity was noted in pyridoxine-deficient placentas and pyridoxine-deficient mothers.
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PMID:Vitamin cofactor saturation indices for riboflavin, thiamine, and pyridoxine in placental tissue of Kenyan women. 640 9

The clinical and clinicopathologic effects of excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day) alone and in combination were evaluated in adult Beagle dogs over an experimental period of approximately 100 days. Anorexia and loss of body weight occurred in the first weeks of the trial period in each treatment group, but was most severe in dogs given both compounds. Dogs in each treatment group (10 of 10 pyridoxine-treated dogs, 6 of 13 clioquinol-treated dogs and 12 of 13 pyridoxine plus clioquinol-treated dogs) developed neurologic disease, manifested principally by ataxia. Pyridoxine-treated dogs had proprioceptive loss involving both fore- and hindquarters, characterized by stiff, spastic, dysmetric leg movements. In clioquinol-treated dogs, dysmetric leg movements were accompanied by failure to support body weight in the hindquarters, but similar forelimb involvement occurred in severely affected dogs. The neurologic disease in dogs given both compounds varied; signs in some dogs resembled those of affected dogs of the pyridoxine-treated group, and in others, those in clioquinol-treated group. Erythrocyte counts, hemoglobin concentrations and packed cell volumes were reduced in dogs in each treatment group and were lowest in dogs given both compounds. Plasma protein was mildly reduced in dogs given pyridoxine or pyridoxine plus clioquinol. Few or no differences were present in the leukocyte counts, blood urea nitrogen concentrations, in activities of serum alanine aminotransferase and aspartate aminotransferase, and in concentrations of sodium, chloride or potassium in treated dogs as compared to control dogs.
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PMID:The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. I. Clinical disease. 645 37


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