Role Of Thiamine Research Articles

Action of thiamine on neuromuscular transmission in the frog

The action of thiamine on neuromuscular transmission in the frog sartorius muscle was investigated. It was found that thiamine at a concentration of 1×10−14 to 1×10−4 M increases transmitter secretion at the nerve endings. This is demonstrated by the increased frequency, amplitude, and quantal content of miniature endplate potentials, and is due to the enhanced likelihood of transmitter release. The role of thiamine in regulating synaptic transmission and the mechanism of its interaction with thiamine-sensitive receptors are examined.

Thiamin depletion after ethanol and acetaldehyde administration to rabbits.

The role of thiamin in the catabolism of ethanol and acetaldehyde has been investigated. When thiamin and subsequently ethanol were administered orally to rabbits, the thiamin concentration in blood increased slightly during the first 3 h and then decreased gradually. After 12 h, it became lower than the value before thiamin administration. Finally, it reached the lowest value after 24 h and then increased slowly to revert to normal in 72 h. It is suggested that thiamin participates in the catabolic pathway of ethanol. An oral administration of pyrazole, an inhibitor of alcohol dehydrogenase, followed by ethanol to rabbits caused a delay in ethanol elimination from blood. When acetaldehyde was injected intravenously to rabbits, thiamin concentration and the transketolase activity in blood decreased gradually and after 12 h the thiamin level reached its lowest value, then increased slowly and normalized in 72 h. Thus, it could be postulated that the decrease in thiamin after an acute ethanol ingestion linked greatly to the acetaldehyde catabolism.

ETHANOL, THIAMINE AND BRAIN DAMAGE

In this paper an attempt has been made to identify important factors governing the supply of thiamine and to examine the relative roles of thiamine and ethanol in the pathogenesis of alcoholic brain damage. Thiamine depletion occurs in alcoholics principally through decreased intake, impaired absorp tion and reduced hepatic storage. The kinetics of thiamine uptake and turnover in brain are such that any fall in circulating levels of the vitamin may significantly impair the supply to the brain. The brain depends on an adequate supply of glucose both as an energy source and as a donor of carbon fragments for protein and lipid biosynthesis. Glucose utilisation is, however, thiamine dependent and it is likely that this is a major factor in the production of thiamine deficient brain damage. Ethanol alone can cause a number of structural alterations in brain tissue and these lesions may be found in alcoholics either in association with or in the absence of thiamine deficient lesions. It is also probable that ethanol and thiamine deficiency act synergistically to produce structural damage. Recurrent deficiences of many different kinds also play a part in the production of cumulative brain damage in the alcoholic.

Possible role of thiamine in the nervous system

Possible role of thiamine in the nervous system

Role of thiamine in peripheral neuropathy following chronic alcoholism : J.K. Baruah, D. Kinder and T. Murtha (Milwaukee, Wis, USA)

Role of thiamine in peripheral neuropathy following chronic alcoholism : J.K. Baruah, D. Kinder and T. Murtha (Milwaukee, Wis, USA)

The Role of Thiamine as a Factor for the Growth of Brochothrix thermosphacta

Thiamine enhances growth of the meat spoilage organism, Brochothrix thermosphacta. It fulfils some, but not all, of the yeast‐extract requirement of this organism. Oxythiamine acts as a growth inhibitor at high concentrations and the inhibition is readily reversed by thiamine. The possible roles of thiamine in the metabolism of Br. thermosphacta are discussed.

Studies on the possible role of thiamine in the central nervous system

Studies on the possible role of thiamine in the central nervous system

The role of thiamine in nervous tissue.

The possibility that thiamine (vitamin B1) has a role in nervous tissue that is independent of its well-documented coenzyme function is discussed. After reviewing the localization and metabolism of the vitamin and its phosphate esters, the effects of either thiamine deprivation or antimetabolites of thiamine on conduction and transmission, and the relationship between thiamine triphosphate and the genetic, neurological disease, subacute necrotizing encephalomyelopathy (Leigh's disease), it is suggested that despite the lack of hard evidence, it is likely that the vitamin possesses this alternate function.

Possible role of thiamine in neuromuscular transmission

Pyrithiamine (50 mg/kg), a thiamine antagonist, decreased the muscle twitches of the rat masseter muscle at stimulation frequencies above 1 Hz 40--80 min after an i.v. injection. The post-tetanic potentiation (PTP) induced by nerve stimulation of the masseter muscle was abolished by pyrithiamine. Administration of thiamine restored the muscle twitches at stimulation frequencies above 1 Hz and the PTP. The muscle twitches elicited by direct muscle stimulation were not affected by pyrithiamine treatment. The abolishment of the PTP was accompanied by a decrease in thiamine and thiamine-diphosphate. The pyruvate level in the blood was unchanged after pyrithiamine treatment. Oxythiamine, on the other hand, had no effect on the PTP but increased the pyruvate level in the blood. Fern extract which contains thiaminase I also abolished the PTP--an effect reversible by the addition of thiamine. The frequency-induced depression of the muscle twitches induced by pyrithiamine was similar to the effect of low doses of d-tubocurarine (8 microgram/kg). The results support the hypothesis that thiamine may play a role in neuromuscular transmission.

Effects of thiamine deprivation on the growth and metabolism of the phytoflagellatePolytomella agilis

The effects of thiamine deprivation on the growth, respiration, and activity of several enzymes of the phytoflagellate protozoanPolytomella agilis were studied. Vitamin deprivation had no effect on the exponential growth rate; the peak population of cultures grown without thiamine was 50% of the control level. The rates of oxygen consumption in control and thiamine-deprived cultures were not significantly different from each other. The activities of pyruvate dehydrogenase and oxoglutarate dehydrogenase in vitamin-deprived cells were 14% and 30%, respectively, of the control values. In these cells, the succinic dehydrogenase activity was 10% and mitochondrial ATPase activity was twice that of control cells. Vitamin deprivation had no effect on the activities of malate dehydrogenase and isocitrate lyase, but pyruvic carboxylase activity increased fourfold. These results indicate a complex role for thiamine in the regulation of growth, respiration, and metabolism in this organism.

A role for thiamine in the regulation of fatty acid and cholesterol biosynthesis in cultured cells of neural origin.

Abstract— Cultured glial (C‐6) and neuronal (neuroblastoma) cells were utilized to define the role of thiamine in the regulation of fatty acid and cholesterol biosynthesis. Glial cells subjected to thiamine deficiency exhibited rates of fatty acid synthesis that were only 13% of the rates in thiamine‐supple‐mented cells. The decrease in fatty acid synthetic rate was accompanied by a comparable decrease in the activities of fatty acid synthetase and acetyl‐CoA carboxylase, the two critical enzymes in the pathway. Immunochemical techniques demonstrated that the decrease in activity of fatty acid synthetase reflected a decrease in enzyme content and that this change in content was caused by a decrease in enzyme synthesis. The disturbance of fatty acid synthesis was exquisitely sensitive to thiamine–i.e. marked improvement was evident within hours of replenishment with only 0.01 μ/ml of thiamine. Total recovery occurred in 1–2 days. Thiamine‐deficient glia also exhibited reduced rates of cholesterol biosynthesis, i.e. 60% of the rates in thiamine‐supplemented cells. This effect was accompanied by a comparable reduction in activity of 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) reductase, the rate‐limiting step in cholesterol biosynthesis. Unlike the glial cells, the neuronal cells exhibited either no or only a slight reduction in lipid synthesis under similar conditions of thiamine deficiency.The data have important implications for the genesis of the neuropathology in states of altered thiamine homeostasis and for the mechanisms of regulation of lipid synthesis.

The effect of thiamine deficiency on the turnover of lactate dehydrogenase in mouse tissues

1. 1. Groups of mice were subjected to different degrees of thiamine deprivation in their diet. In particular, the effects of complete thiamine deficiency and a continuation of minimal nutritional levels of thiamine were compared. 2. 2. The effects of these treatments on the turnover characteristics of lactate dehydrogenase and total soluble protein have been studied by means of double labelling experiments, and determinations of the relative emphases of synthesis and degradation of these tissue components. 3. 3. Marked divergences from normal were apparent with each of these nutritional regimens-complete thiamine deficiency causing a considerably increased rate of degradation for both total protein and lactate dehydrogenase in all tissues; whereas maintenance of minimal levels of thiamine led to increased degradation of total protein in liver, but reduced rates of degradation for lactate dehydrogenase in brain, heart and liver. 4. 4. The significance of these results has been discussed in relation to the relative influence of vitamin and calorie deficiencies on turnover parameters, the individuality of specific tissue behaviour, differences in protein redistribution in response to separate physiological perturbations, and the role of thiamine in specific proteolysis.

Differential effects of opiates on the incorporation of [14C] thiamine in the central nervous system of the rat

Opiate agonist (morphine), pure antagonist (naloxone), mixed agonist-antagonist (nalorphine) and analgesically inactive enantiomorph (dextrorphan) produced differential stereoselective effects on the incorporation of [14C] thiamine in the central nervous system of the rats. The possible role of thiamine in opiate effects and its implications are discussed.

Role of Thiamine in Excitable Membrane of Nerve

Role of Thiamine in Excitable Membrane of Nerve

The role of thiamine in nervous excitation.

The role of thiamine in nervous excitation.

The role of thiamine, leucine and CO 2 in the biosynthesis of carotenes by the mold Phycomyces blakesleeanus

It has been demonstrated that the mold Phycomyces blakesleeanus can metabolize thiamine ([2- 14C]thiazole) to 14CO 2. In addition, the 14CO 2 produced can be incorporated into mevalonic acid and β-carotene when the mold was incubated in the presence of non-radioactive leucine. The role of leucine in the fixation of 14CO 2 has been implicated by a study of the labeling patterns of mevalonic acid and β-carotene; thus, mevalonic acid was labeled primarily in the C-1 carboxyl group, with the remaining 11 per cent of the total 14C in the C-5 carbon atom. This labeling pattern suggests that 14CO 2 was fixed to β-methylcrotonyl CoA, a leucine metabolite, which could then give rise to [1- 14C]β-hydroxy-β-methylglutaryl CoA. [1- 14C]β-Hydroxy-β-methylglutaryl CoA could then be reduced directly to [1- 14C]mevalonic acid, the major reaction, or it could be split by the cleavage enzyme 3-hydroxy-3-methyl glutaryl CoA-acetonacetate lyase (4.1.3.4) to [1- 14C]acetoacetate and acetyl CoA. These small molecules, by a process involving activation and condensation, could then randomize the 14C to give [5- 14C]β-hydroxy-β-methylglutaryl CoA which would be reduced to [5- 14C]mevalonic acid. The loss of the C-1 carbon of mevalonic acid at the formation of isopentenylpyrophosphate would account for the low incorporation of 14CO 2 into β-carotene.

Influence of thiamine on protein biosynthesis.

The incorporation experiments with labeled serine in the crude microsomal protein fraction of normal and thiamine deficient rat liver were carried out. The liver microsomal fraction of animals kept on the thiamine deficient diet showed less incorporation of lebeled serine than the normal animals.The injection of thiamine in the thiamine deficient animals two hours before killing increased to an appreciable extent the incorporation of labeled serine in microsomal protein, indicating a possible role of thiamine in protein biosynthesis.

Enzymes and enzyme models

THE determination of mechanisms of enzyme action is among the great problems of modern chemistry (Boyer e t a l , 1960; Boyer, 1960; Westheimer, 1959). Although not one enzymatic process is today understood, and although no model system has achieved catalytic activity comparable to that of the corresponding enzyme, considerable progress has been made in elucidating the in enzymes, and in finding catalytic systems which will operate (although slowly) under experimental conditions which are comparable to those in cells and, hopefully, by mechanisms which parallel the biochemical ones. The problem is under attack from many angles: studies of peptide sequences, X-ray analysis of protein structure, determination of the coenzyme or active sites needed for reaction, kinetic studies of enzyme action, and chemical models for various enzymatic systems. All of these methods provide information relevant to the central problem; how does a protein strongly accelerate a chemical reaction between a substrate and either a coenzyme molecule or an active site on the protein itself or some other reagent. In subsequent sections of this review, some individual enzymes are considered in some detail. Before considering these systems, a few words might help set the problem in perspective. Much of our understanding of catalytic action has been gained by studies of model systems. The pioneers in such investigations (Langenbeck, 1935 ; Warburg 1949) did not have the present-day background of theoretical chemistry on which to build. In 1947, in a paper more pertinent to modern considerations of detailed mechanism, Braunstein suggested the outlines of a mechanism for transamination: this mechanism and the role of pyridoxal have been strongly substantiated (Braunstein, 1960; Metzler e t a l , 1954; Ikawa & Snell, 1954) and are generally accepted today. More recently, the role of thiamin in the decarboxylation of pyruvate (Breslow, 1958), the action of diphosphopyridine nucleotides in the direct and stereospecific transfer of hydrogen (Vennesland & Westheimer, 1954), and the role of the serine residue in the reactions of esterases (Desnuelle, 1960a, b; Cohen e t a l , 1959) and of phosphoglucomutase (Koshland & Erwin, 1957) have been discovered, and imitated with model systems. Some of these systems are here considered. The role of biotin and of several other coenzymes in enzymatic processes will be discussed in another session in this Congress. In a recent summary (Westheimer, 1959), the author stated, hopefully, in another decade, reviews may be concerned with enzymes and enzyme analogs (rather than with models) . The decade has not yet passed, and the prediction still seems reasonable.

Role of thiamine and aminoacids in the nutrition of Shigella sonnei.

Role of thiamine and aminoacids in the nutrition of Shigella sonnei.

The Role of Thiamin in Carboxylase

The Role of Thiamin in Carboxylase