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At least 145 records · Page 8Linked to original sources
PubMed1980

Thiamine and cholinergic transmission in the electric organ of Torpedo. II. Effects of exogenous thiamine and analogues on acetylcholine release.

The electrogenic tissue of Torpedo was found to phosphorylate in vitro external [14C]thiamine by a saturable process. The rate of this metabolisaton was increased when acetate, an efficient precursor of acetylcholine (ACh) synthesis in this tissue, was added to the incubation medium, thus increasing the turnover of ACh. Nerve stimulation did not release significant amounts of the previously accumulated [14C]thiamine. Exogenous thiamine modified the size of the electroplaque potential (e.p.p.). At concentrations higher than 10(-3)M the nerve-electroplaque transmission was depressed after a transient increase of the e.p.p. Such a depression was due to a strong decrease of the ACh release. At concentrations equal to or lower than 10(-3)M, thiamine affected transmission in a rather complex fashion. ACh release was decreased or increased depending on concentration, time of application, and mode of stimulation. Oxythiamine, a structural antimetabolite of thiamine, affected the transmission in a very characteristic manner at 10(-5)M and higher concentrations. The amplitude of the e.p.p. was increased and, more strikingly, its duration was prolonged. These changes were not due to an inhibition of cholinesterase activity but to an enhancement of the evoked release of ACh either on single-impulse or repetitive stimulation. Another antimetabolite, pyrithiamine, had no effect on the transmission nor on ACh release. From this and our previous work, it is proposed that thiamine is involved, directly or indirectly, in the process of ACh release. The possible mechanisms of this involvement are discussed.

Acetates↗
PubMed1988

Thiamin intakes and erythrocyte thiamin levels in eleven-year-old children in the Western Cape.

Dietary intake of thiamin has been evaluated in a series of 615 eleven-year-old children in Western Cape Province, South Africa. Thiamin intakes, determined by 24-hour recall and local food composition tables, were highest in rural white children (boys 1.49 mg/day, girls 1.11 mg), followed by rural black (Xhosa) children (1.33, 1.15 mg), and lowest in rural (1.18, 1.11 mg) and urban coloured (Euro-African-Malay) subjects (1.11, 0.85 mg). The group means exceeded WHO recommended daily intakes except for urban coloured girls. Thiamin nutritional status was determined by automated microbiological assay of thiamin in erythrocytes in a subsample of 69 children. One urban coloured child was thiamin deficient. The highest mean value (69.4 micrograms/l) was found in rural coloured children, followed by their urban counterparts (64.8 micrograms/l) and black rural children (63.6 micrograms/l). Rural white children had the lowest mean value (60.3 micrograms/l). In general, thiamin stores in these children appear to be adequate.

Child↗
PubMedDate not supplied

[Thiamine- and thiamine diphosphate-binding capacity of the hyaloplasmic fraction of rat liver].

Hyaloplasmic fraction of rat liver tissue did not bind 14C-thiamin and 14C-thiamin diphosphate in vitro as shown by means of gel filtration and equilibrium dialysis. All the thiamin and 2/3 of thiamin diphosphate were in vivo in free state or in a state unbound with proteins. Hyaloplasm lost readily the endogenous thiamin diphosphate during dialysis. Endogenous thiamin diphosphate (about 1/3 of the initial content), resistent to dialysis and gel filtration, was apparently included in transketolase in hyaloplasmic fraction of rat liver tissue.

Animals↗
PubMedDate not supplied

[Free and bound thiamine pyrophosphate level in rat liver mitochondria in various saturation of the body with thiamine].

Content of tree and bound thiamine pyrophosphate (TPP) was measured by means of gel filtration and equilibrium dialysis procedures in mitochondria of normal rats, the rats under conditions of alimentary B1 avitaminosis and loading with thiamine. The content of protein-bound TPP was stable and equal to 20% of its total level in the mitochondria of control rats and in the rats loaded with thiamine. The content of free form of TPP was decreased in B1 avitaminosis; a severe form of the avitaminosis was accompanied by a decrease in content of the bound form. Concentration of the free form of TPP did not increase if the organism of the rats was loaded with thiamine. These data suggest existence of specific systems controlling the vitamin uptake in mitochondria. The active transport of thiamine across the mitochondrial membranes is considered as the most important process. Administration of the high doses of the vitamin led only to an increase in the non-coenzymatic form of the vitamin, indicating the absence of thiamine pyrophosphokinase in rat liver mitochondria. A possible mechanism of TPP transport in mitochondria is discussed.

Animals↗
PubMed1986

Content of thiamin phosphate esters in mammalian tissues--an extremely high concentration of thiamin triphosphate in pig skeletal muscle.

In relation to a high activity of thiamin diphosphate (TDP) kinase (Koyama, S. et al. (1985) Biochem. Int. 11, 371-380) in the skeletal muscle of pigs and guinea pigs, the content of thiamin phosphate esters in tissues of these animals has been determined by the method of high-performance liquid chromatography. An extremely high concentration of thiamin triphosphate (TTP), 69.2% of the total thiamin (26.1 nmol/g wet weight), was detected in adult pig skeletal muscles. One extreme case contained TTP as 88.7% of the total thiamin (19.6 nmol/g wet weight). TTP in pig skeletal muscle was found solely in cytosol fraction. This is the first report showing an unusually high level of TTP in mammals and may give a clue as to the physiological functions of TTP.

Aging↗
PubMed1982

Thiamin Metabolism in the rat during long-term alcohol administration. 1. Communication: ethanol induced changes at optimal thiamin supply.

The effect of ethanol administration on the phosphorylation of thiamin, and on the transketolase activity (TKA) in erythrocytes, heart and liver, and on the thiamin excretion in urine was investigated in rats optimally supplied with thiamin over a period of 16 weeks. Ethanol ingestion resulted in a diminished concentration of thiamin (T), thiaminmonophosphate (TMP), thiamindiphosphate (TDP) and thiamintriphosphate (TTP) in blood and organs and in a reduced excretion rate of T in urine due to an impaired intestinal absorption. An ethanol induced alteration of the degree of thiamin phosphorylation became evident only after 16 weeks resulting in a decline of T and TMP in blood and of T in heart to undetectable amounts and in an enhancement of the TDP- and TTP-pool. Despite an increasing content of TDP in erythrocytes the TKA was lowered and the alpha-TK was enhanced during the test period suggesting a partially inhibited formation of the active holoenzyme by alcohol in vivo. However, the lowered TKA and the normal alpha-TK in liver are primarily suggestive of an apo-enzyme degeneration influenced by ethanol.

Alcoholism↗
PubMed1975

Free thiamine as the likely precursor of endocellular thiamine phosphates in everted rings of rat jejunum.

Labeled and unlabeled (endogenous) free and phosphorylated thiamine were measured in isolated everted rings of rat jejunum in vitro during short incubation periods (1-10min). Shortly after the addition of thiamine-14C to the incubation medium, the intracellular specific activity of the free form was higher than the specific activity of the phosphorylated fraction. In the course of time this difference diminished and finally the two specific activities became equal. The conclusion was reached that free thiamine is the likely precursor of intracellular phosphorylated thiamine. Moreover evidence is presented which indicates that free thiamine entered actively into intestinal epithelial cells. Since free thiamine was modified into phosphorylated form inside the cells, its movement against the endocellular concentration gradient was noticeably favoured.

Animals↗
PubMed1986

Activities of thiamine-dependent enzymes in two experimental models of thiamine-deficiency encephalopathy. 2. alpha-Ketoglutarate dehydrogenase.

Chronic thiamine deprivation in the rat leads to selective neuropathological damage to pontine structures. Onset of neurological symptoms of thiamine deprivation (ataxia, loss of righting reflex) was accompanied by selective decreases (of the order of 30%) in the activity of alpha-ketoglutarate dehydrogenase (alpha KGDH) in lateral vestibular nucleus and hypothalamus. Enzyme activities were decreased to a lesser extent in medulla oblongata, striatum and hippocampus and were unchanged in other brain structures. No changes in alpha KGDH occurred prior to the onset of neurological signs of thiamine deprivation. Administration of the central thiamine antagonist, pyrithiamine, results within 3 weeks in loss of righting reflex and convulsions and in more widespread neuropathological changes than those observed following thiamine deprivation. alpha KGDH activities were found to be substantially diminished in all brain regions studied following pyrithiamine treatment with most severe changes occurring in brain regions found to be vulnerable to pyrithiamine (lateral vestibular nucleus, hypothalamus, midbrain, medulla-pons). In some cases, alpha KGDH changes preceded the appearance of neurological symptoms of pyrithiamine treatment. Such decreases in alpha KGDH may explain previous findings of region-selective changes in energy metabolism and of decreased synthesis of glucose-derived neurotransmitters (acetylcholine, GABA, glutamate) in pyrithiamine-treated rat brain. Thiamine administration to symptomatic pyrithiamine treated rats resulted in reversal of neurological signs of encephalopathy and in normalisation of defective alpha KGDH activity in all brain regions. These findings suggest that the reversible neurological symptoms associated with Wernicke's Encephalopathy in man likely result from region-selective impairment of alpha KGDH.

Animals↗
PubMed1996

Alterations of thiamine phosphorylation and of thiamine-dependent enzymes in Alzheimer's disease.

There is a growing body of evidence to suggest that thiamine neurochemistry is disrupted in Alzheimer's Disease (AD). Studies in autopsied brain tissue from neuropathologically proven AD patients reveal significantly reduced activities of the thiamine phosphate dephosphorylating enzymes thiamine diphosphatase (TDPase) and thiamine monophosphatase (TMPase) as well as the thiamine diphosphate-dependent enzymes, pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase (alpha KGDH) and transketolase. Reductions in enzyme activities are present both in affected areas of AD brain as well as in relatively well conserved tissue. Decreased TDP concentrations and concomitantly increased TMP in autopsied brain tissue from AD patients and in CSF from patients with Dementia of the Alzheimer Type suggests that CNS thiamine phosphorylation-dephosphorylation mechanisms are disrupted in AD. alpha KGDH is a rate-limiting enzyme for cerebral glucose utilization and decreases in its activity are associated with lactic acidosis, cerebral energy failure and neuronal cell loss. Deficiencies of TDP-related metabolic processes could therefore participate in neuronal cell death mechanisms in AD.

Alzheimer Disease↗
PubMed2002

Thiamine-responsive pyruvate dehydrogenase deficiency in two patients caused by a point mutation (F205L and L216F) within the thiamine pyrophosphate binding region.

The human pyruvate dehydrogenase complex (PDHC) catalyzes the thiamine-dependent decarboxylation of pyruvate. Thiamine treatment is very effective for some patients with PDHC deficiency. Among these patients, five mutations of the pyruvate dehydrogenase (E1)alpha subunit have been reported previously: H44R, R88S, G89S, R263G, and V389fs. All five mutations are in a region outside the thiamine pyrophosphate (TPP)-binding region of the E1alpha subunit. We report the biochemical and molecular analysis of two patients with clinically thiamine-responsive lactic acidemia. The PDHC activity was assayed using two different concentrations of TPP. These two patients displayed very low PDHC activity in the presence of a low (1 x 10(-4) mM) TPP concentration, but their PDHC activity significantly increased at a high (0.4 mM) TPP concentration. Therefore, the PDHC deficiency in these two patients was due to a decreased affinity of PDHC for TPP. Treatment of both patients with thiamine resulted in a reduction in the serum lactate concentration and clinical improvement, suggesting that these two patients have a thiamine-responsive PDHC deficiency. The DNA sequence of these two male patients' X-linked E1alpha subunit revealed a point mutation (F205L and L216F) within the TPP-binding region in exon 7.

Binding Sites↗
PubMed1977

The passage of thiamine across the rat placenta and its uptake by the fetal organs. I. The transport of thiamine across the placenta.

It is well known that thiamine is highly soluble in water. However, if chloroplatinic acid (H2PtCl6) is used during fixation, an insoluble, electron-dense thiamine-PtCl6 precipitate is formed. Using this method we performed electron microscope autoradiography of the placental labyrinth of rats in their 15th day of pregnancy after injection into the maternal bloodstream of 3H-thiamine, and we also measured the radioactivity of the tissues, in order to study the transport of the thiamine across the placenta. Both developed silver grains and radioactivity were found in the largest amounts 30 min after injection; the amounts of both declined after 2 hrs and declined further after 5 hrs. The majority of the developed silver grains were localized in the smooth-surfaced endoplasmic reticulum, which is generally thought to be the vehicle for the transport of materials in the cell, while in the mitochondria, Golgi apparatus, etc. the grains were few. Considering the substantial depletion of the amounts of both sivler grains and radioactivity after the relatively short time of 5 hrs, we conclude that the greater portion of the thiamine passes quickly across the placenta to the fetus, where it is used in the metabolism of the fetal organs, and that only a small part of the thiamine is retained in the placenta for its own metabolism.

Animals↗
PubMed1989

Effect of thiamine, magnesium, and sulfate salts on growth, thiamine levels, and serum lipid constituents in rats.

Six variable supplementations of thiamine magnesium, and sulfates were given to 30 male adult rats in their diets. After 3 weeks, the concentrations of thiamine in the blood and liver and those of cholesterol, phospholipids, and triglycerides in the serum were determined. Blood thiamine level did not reflect the vitamin content in liver. Sufficient and/or excessive intake of the 3 supplementations caused an increase in liver thiamine content and body weight gain; it also caused a reduction in serum cholesterol level without a change in the levels of serum triglycerides and phospholipids. Deficiency of both magnesium and sulfate salts in thiamine-supplemented groups decreased body weight gain and liver thiamine content with a significant elevation of serum triglycerides.

Animals↗
PubMed1975

Thiamine absorption in the rat. ii. intestinal alkaline phosphatase activity and thiamine absorption from rat small intestine in-vitro and in-vivo.

The correlations between intestinal alkaline phosphatase (IAP) activity and thiamine absorption and glucose absorption were studied in the rat. An everted sac in-vitro technique was used in adult rats whereas in-vitro experiments were performed in young rats 10 days old. All incubation experiments were done with 14-C-labeled thiamine. The patterns of IAP activity along the small intestines differed greatly between young and adult rats but were closely paralleled by the distribution of active thiamine transport in adult rats and thiamine absorption in young rats, respectively. When IAP was specifically inhibited in adult rats by L-phenylalanine active thiamine transport in-vitro was abolished. No correlation was found between IAP activity and active transport or glucose in-vitro, nor did inhibition of the enzyme in any way affect glucose transport capacity. It is suggested that the enzyme intestinal alkalinephosphatase is involved in the process of active thiamine absorption.

Age Factors↗
PubMedDate not supplied

[Interaction of rat brain thiamine kinase with thiamine and its derivatives].

Participation of the enzyme which provides the phosphorylation of thiamine to thiamindiphosphate (TDP) thiaminkinase (thiaminpyrophosphokinase, KF 2.7.6.2) of rat brain in the realization of thiamine action on the syntheses of acethylcholine (AC) was studied. The thiamine and its structure analogue, which differ the nature of the radicals in the 3-d and 5-e positions of the thiazollium cycle were used: 3-[(4-amino-2methylpyrimidinyl-5)methyl]-4-methylthiazolium chloride, 3-decyloxycarbonylmethyl-4-metyl-5-beta-hydrozyethylthiazolium chloride, 3-decyloxycarbonylmethyl-4-methylthiazolium chloride. All salts in the concentrations lower then Km render active influence on thiaminkinase. The analysis of data shows the presence of the regulation site on the enzyme distinguishing from the active enzyme centre and participating in the interaction with which the hydrophobic fragments of thiamine molecule participating. The comparative studies of thiamine and above mentioned derivatives influence on the inclusion of the labelled carbon with [2-(14)C] pyruvate in acethylcholine confirm an assumption about the key-role of the thiamine interaction with thiaminkinase (meaning its phosphorilation) regarding its action on the acethylcholine syntheses, and probably, on the function of the nervous cells as a whole.

Acetylcholine↗
PubMedDate not supplied

[Interrelationship between the thiamine content, thiamine diphosphate-dependent enzyme activity and reduced glutathione level in the rat liver].

Changes in the amount of thiamine, reduced glutathione, thiamine diphosphate-dependent dehydrogenase activity has been traced after thiamine injection to thiamine-deficient rats and oxythiamine to normal rats. The obtained data show that a drop in reduced glutathione level was a primary reason of the alpha-keto-acid dehydrogenase activity reduction under conditions of the thiamine deficiency. The existence of immediate connection between thiamine and glutathione metabolism is supposed.

Animals↗
PubMed1991

Thiamine responsive anemia: report of a new case associated with a thiamine pyrophosphokinase deficiency.

We report a new case of thiamine responsive anemia in a three years old boy with the characteristic association of anemia, diabetes mellitus and deafness. Thiamine therapy corrected anemia as described. A thiamine pyrophosphokinase deficiency (TPK) was found which was not influenced by treatment. However normal levels of thiamine pyrophosphate (TPP) were obtained without correction of all symptoms particularly dyserythropoïesis. Thus, etiology of the syndrome is not only a thiamine pyrophosphokinase deficiency as previously suggested.

Abnormalities, Multiple↗