A Fluorimetric Method for Measurement of Erythrocyte Transketolase Activity

Anderson, Stuart H; Nicol, A. D.

doi:10.1177/000456328602300207

Cited by 15 publications

(10 citation statements)

References 21 publications

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“…These include loss of reactivatable apoenzyme during chronic deficiency in vivo , altered binding of apoenzyme and coenzyme because of the presence of isoenzymes of TK and reduced synthesis of apoenzyme in patients with diabetes and liver disease , among other technical factors . If no appropriate controls are available, these factors may have contributed to the lack of agreement over the upper limit of the reference range for the activation assay, with values ranging from 15.5% to 40% . On the other hand, the evaluation of total thiamine content (free and bound as well as all phosphorylated forms) does not take into account the actual fraction incorporated into key enzymes of the metabolism whose inactivation results in the occurrence of symptoms .…”

Section: Methodsmentioning

confidence: 99%

Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

et al. 2014

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Alaskan Husky encephalopathy (AHE1) is a fatal brain disease associated with a mutation in SLC19A3.1 (c.624insTTGC, c.625C>A). This gene encodes for a thiamine transporter 2 with a predominantely central nervous system (CNS) distribution. Considering that brain is particularly vulnerable to thiamine deficiency due to its reliance on TPP-dependent metabolic pathways involved in energy metabolism and neurotransmitter synthesis, we characterized the impact of this mutation on thiamine status, brain bioenergetics, and the contribution of oxidative stress to this phenotype. In silico modeling of the mutated transporter indicated a significant loss of alpha-helices resulting in a more open protein structure suggesting an impaired thiamine transport ability. The cerebral cortex and thalamus of affected dogs were severely deficient in TPP-dependent enzymes accompanied by decreases in mitochondrial mass and OXPHOS capacity, and increases in oxidative stress. These results along with the behavioral and pathological findings indicate that the phenotype associated with AHE is consistent with a brain-specific thiamine deficiency, leading to brain mitochondrial dysfunction and increased oxidative stress. While some of the biochemical deficits, neurobehavior and affected brain areas in AHE were shared by Wernicke's and Korsakoff's syndromes, several differences were noted likely arising from a tissue-specific vs. that from a whole-body thiamine deficiency.

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Section: Methodsmentioning

confidence: 99%

Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

et al. 2014

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“…ETK activity was measured using a method described by Anderson & Nicol (1986). The basal activity of the enzyme was measured followed by determination of activity with excess coenzyme (thiamin pyrophosphate) added in vitro.…”

Section: Blood Collection and Preparationmentioning

confidence: 99%

Dietary intake and micronutrient status of adolescents: effect of vitamin and trace element supplementation on indices of status and performance in tests of verbal and non-verbal intelligence

Southon¹,

Wright²,

Finglas³

et al. 1994

Br J Nutr

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Relationships between micronutrient intake and status, and micronutrient status and performance in tests of intelligence were investigated in a group of adolescents (13-14 years old). Dietary intakes were assessed using a 7 d weighed dietary record method, coupled with the collection of duplicate diets.Vitamin and trace mineral intakes calculated using food composition tables were compared with those obtained by direct analysis of duplicate diets. Micronutrient status was judged via a range of biochemical indices measured in blood samples taken after a 12-15 h fast. Blood samples were taken both before and after a 16-week period of vitamin and trace mineral supplementation. Individual tests of verbal and nonverbal intelligence were also performed pre-and post-supplementation. The results of this study indicate that the use of food table data may lead to substantial over-or underestimation of the intake of several micronutrients. In general, the total calculated or analysed amount of a specific micronutrient consumed did not adequately predict status, as judged by a range of biochemical indices. There were significant changes in status measurements over the 16-week study period, irrespective of supplementation, and these changes were markedly influenced by the initial status of the subject. There was no effect of supplementation on performance in tests of intelligence. However, there was a significant association between plasma ascorbic acid and initial non-verbal intelligence quotient (IQ) in the boys, and between whole blood glutathione peroxidase (EC 1 . 11 . I .9) activity and non-verbal and verbal 1Q in both sexes.These findings are discussed in relation to other recent studies of the influence of micronutrient supplementation on the psychological performance of children.

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“…ETK activity was determined, with and without the addition of TPP, using the method of Anderson & Nicol (1986). Following the transformation of ribose-5-phosphate (yielding glycerol-3-phosphate and sedoheptulose-7-phosphate), the assay measures the secondary enzymic consumption of NADH during the production of glycerol-3-phosphate.…”

Section: Determination Of Etk" and Etk-acmentioning

confidence: 99%

Thiamin intake, erythrocyte transketolase (EC2.2.1.1) activity and total erythrocyte thiamin in adolescents

et al. 1994

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The relationships between thiamin intake, erythrocyte transketolase (EC 2.2.1.1) activity coefficient (ETK-AC) and total erythrocyte thiamin were investigated in a group of adolescents (13 to 14 years old; nineteen boys, thirty-five girls). Thiamin intakes were calculated from 7 d weighed records, using food composition tables, and compared with those obtained by direct analysis of duplicate diets. Average 7 d calculated thiamin intakes were significantly lower than analysed intakes for both sexes. On an individual basis, calculated intakes ranged from 30 to 143 % of corresponding analysed values. Analysed and calculated intakes were significantly correlated when expressed as mg/d; however, when expressed in terms of energy intake, the correlation was significant for males only. Thiamin intake appeared largely adequate when compared with current UK dietary recommendations (Department of Health, 1991), but the limitations of such comparisons are considered. The major food groups contributing to thiamin intake were examined and showed breakfast cereals to contribute more than 25% of dietary thiamin.

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A Fluorimetric Method for Measurement of Erythrocyte Transketolase Activity

Cited by 15 publications

References 21 publications

Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

Dietary intake and micronutrient status of adolescents: effect of vitamin and trace element supplementation on indices of status and performance in tests of verbal and non-verbal intelligence

Thiamin intake, erythrocyte transketolase (EC2.2.1.1) activity and total erythrocyte thiamin in adolescents

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