Showing papers on "Thiamine published in 1972"

Thiamine-responsive lactice acidosis in a patient with deficient low-KM pyruvate carboxylase activity in liver.

Abstract: The cause of severe intermittent lactic acidosis was investigated in a female infant with profound psychomotor retardation. Hypoglycemia, hyperpyruvic acidemia, and hyperalaninemia were identified in the newborn period. A triad of lactate, pyruvate, and alanine accumulation persisted throughout infancy, and ACTH, anorexia, and high carbohydrate feeding further provoked their accumulation. Careful dietary control or thiamine-HCl supplementation (5 to 20 mg/day) ameliorated the metabolic abnormality. Pyruvate dehydrogenase activity (which is thiamine-dependent) was normal in leukocytes and cultured skin fibroblasts. Hepatic pyruvate carboxylase activity (which is biotin-dependent) was found to comprise more than one component. There was a partial deficiency of total hepatic pyruvate carboxylase activity in the patient. The loss of activity was confined to the low-Km component of the enzyme which serves pvruvate metabolism in the physiological range. A defect in glucogenesis causing hypoglycemia, pyruvate accumulation with lactic acidosis, and aberrant amino acid metabolism can be attributed to the abnormality of pyruvate carboxylase. The response to thiamine in our patients may reflect activation of a normal "shunt" mechanism for pyruvate disposal via pyruvate dehydrogenase.

Vascular Permeability to Horseradish Peroxidase in Brainstem Lesions of Thiamine-Deficient Rats

Abstract: In the early brainstem lesions of acute dietary thiamine deficiency in rats, an outstanding feature is the occurrence of edema. This study, using horseradish peroxidase as a marker, confirms and extends our previous observations using fluorescent dye-labeled albumin that vascular permeability to proteins remains essentially intact during this phase, and becomes altered only when necrosis and hemorrhage supervene. In addition, however, although a minor degree of pinocytotic transendothelial transport and pericytic uptake of horseradish peroxidase was found in both normal animals and in the early lesions, in the late lesions there was markedly enhanced pinocytotic transport but no evidence that interendothelial junctions were disrupted. Reaction product was present in the vascular basement membrane regions and in the extracellular spaces of the neuropil, as in other forms of reactive edema. The localized cerebral edema in thiamine deficiency lesions is thus a biphasic phenomenon. It occurs initially in the absence of vascular permeability change and perhaps as the result of defective active transport related to the deficiency state. In contrast, the late edema is the result of gross breakdown of barrier function to protein, with enhanced pinocytotic transport and extracellular accumulation of the marker in the neuropil.

Thiamine in neural membranes enzymic hydrolysis of thiamine diphbsphate

Abstract: — The membrane-associated diphosphatase from rat brain which catalyses the hydrolysis of thiamine diphosphate and nucleoside diphosphate is described. The parallel sub-cellular distribution of thiamine diphosphatase and nucleoside diphosphatase activity and the equal inhibition of both activities by adenosine methylenediphosphonate, a non-hydrolysable structural analogue of ADP, suggests that a single enzyme is involved. The divalent cation requirement and basic kinetic properties of this enzyme have been determined. This nucleoside diphosphatase is not activated by ATP.

Experimental thiamine deficiency in captive harp seals, Phoca groenlandica, induced by eating herring, Clupea harengus, and smelts, Osmerus mordax .

Abstract: Freshwater smelts, and Atlantic herring, both shown to contain thiaminase, were fed to harp seals under a variety of experimental conditions. When thiamine was not administered, the seals developed thiamine deficiency which, in some cases, was fatal. Red blood cell transketolase was effective in demonstrating deficiency.In a controlled experiment, three seals ingesting smelts died within 80 days; two showed terminal signs of central nervous system disturbances and concomitant plasma electrolyte imbalance. Seals fed a diet of thiamine-free herring survived despite biochemical evidence of deficiency. This is attributed to the high fat content of herring.Thiamine administered either intramuscularly or orally, during the course of deficiency, effected prompt recovery. Thereafter, seals maintained on herring required 25–33 mg thiamine/kg of ingesta, if the vitamin was consumed in the diet; if administered 2 h before feeding, 35 mg/day was sufficient for normal maintenance.

Metabolism of alcohol (ethanol) in man

Abstract: It is well recognized that the primary alcohol, ethanol, can be absorbed unchanged along the whole length of the digestive tract, that absorption takes place rapidly from the stomach (about zo%), and most rapidly from the small gut (about 80%). T h e rate of absorption after drinking is affected by several factors, for example the volume, concentration (10-2074 solutions are most rapidly absorbed) and nature of the alcoholic drink, the presence or absence of food in the stomach, rate of gastric emptying, pylorospasm, permeability of the gastric and intestinal tissues, individual variations. After absorption into the blood-stream, alcohol is distributed quickly throughout the total body water (Berggren & Goldberg, 1940; Harger & Hulpieu, I 956; Pappenheimer & Heisey, 1963) and is subsequently metabolized at a steady rate. A method which makes use of this property of ethanol has been successfully employed for measuring the total body water volume in human subjects (Pawan & Hoult, 1963 ; Pawan, 1965). After equilibration, normally 1-1.5 h after drinking, the alcohol concentration in any body fluid depends on the water content of that fluid (Pawan, 1967, 1970; Pawan & Grice, 1968). Over 90% of the absorbed alcohol is metabolized in the body, yielding some 7 kcal/g on complete oxidation to carbon dioxide and water, with a concomitant fall in the respiratory quotient; the remainder is excreted unchanged in the urine, expired air and sweat. The main site of metabolism of ethanol is the liver, although some other tissues, for example kidney, muscle, lung, intestine and possibly even the brain, may metabolize smaller quantities. Fig. I shows the main pathways of ethanol metabolism. It is generally believed that the rate-limiting step in the metabolism of alcohol is its conversion to acetaldehyde, a reaction catalysed by the zinc-containing enzyme, alcohol dehydrogenase (ADH). This process occurs chiefly in the soluble cytoplasm of liver cells, with nicotinamide adenine dinucleotide (NAD) acting as the hydrogen acceptor. However, particularly in alcoholics, some ethanol may be oxidized by the peroxidase-xanthine oxidase-catalase system, and possibly other oxidases both in liver and plasma (TrCmolikres & CarrC, 1960, 1961). Small amounts of alcohol may also be converted to ethyl glucuronide (Kamil, Smith & Williams, 1952), ethyl sulphate and other esters, and excreted in the urine. Orme-Johnson & Ziegler (1965) have described a ‘mixed-function enzyme’, and Lieber and his colleagues (Lieber & DeCarli, 1968a,b, 1969; Rubin, Hutterer & Lieber, 1968; Baraona & Lieber, 1970; Rubin, Bacchin, Gang & Lieber, 1970) have found liver microsomes, which comprise the smooth endoplasmic reticulum (SER), capable of oxidizing

Biosynthesis of Thiamine Pyrophosphate in Escherichia coli

Abstract: In Escherichia coli, thiamine pyrophosphate is synthesized from thiamine monophosphate. Free thiamine is not involved as an intermediate in de novo synthesis of thiamine pyrophosphate.

Biosynthetic Pathway of Thiamine Pyrophosphate: a Special Reference to the Thiamine Monophosphate-Requiring Mutant and the Thiamine Pyrophosphate-Requiring Mutant of Escherichia coli

Abstract: Two types of mutants of Escherichia coli were isolated, one of which (mutant 70-23-107) responded to thiamine pyrophosphate, and the other (mutant 70-23-102) to thiamine monophosphate and thiamine pyrophosphate. They were produced by further mutation of a thiamine auxotroph of E. coli 70-23 with N -methyl- N ′-nitro- N -nitrosoguanidine. The parent organism required thiamine because phosphohydroxymethylpyrimidine kinase activity was lacking in this organism, and hydroxymethylpyrimidine pyrophosphate was not permeable through the cell membrane of E. coli . Thiamine, thiamine monophosphate, and thiamine pyrophosphate were all equally active for the parent, whereas mutants 70-23-102 and 70-23-107 lost their ability to grow on thiamine. Both mutants differed only in the growth response to thiamine monophosphate: the former could grow on thiamine monophosphate, whereas the latter could not. Experimental results with the newly isolated mutants indicate that in E. coli the free form of thiamine is not involved in de novo synthesis of thiamine pyrophosphate, but thiamine monophosphate, an exclusive product formed by the reaction between hydroxymethylpyrimidine pyrophosphate and hydroxyethylthiazole monophosphate, is directly phosphorylated to form thiamine pyrophosphate. Exogenous thiamine, on the other hand, is converted to thiamine pyrophosphate via the intermediate formation of thiamine monophosphate. Images

CHEMISTRY OF THIAMINE DEGRADATION: 4‐Methyl‐5‐(β‐Hydroxyethyl) Thiazole from Thermally Degraded Thiamine

Abstract: A compound isolated from thiamine solutions brought to pH 5.0, 6.0 and 7.0 with IN NaOH or with O.1M phosphate buffer and heated in a boiling water bath open to air or in sealed tubes, or autoclaved at 121°C for 30 min, has been identified as 4-methyl-5-(β-hydroxyethyl) thiazole. Infrared, NMR and mass spectral data of this compound are presented and discussed.

Cholesterol, Pantothenic Acid, Pyridoxine and Thiamine Requirements of Honeybees for Brood Rearing

Abstract: SummaryColonies of newly emerged bees which had never eaten pollen were offered diets consisting of (A) vitamin-free casein and minerals, or A supplemented with cholesterol and the vitamins of the B group (B), or with the B vitamins but without cholesterol (C), or with cholesterol and the vitamins except pantothenic acid (D), or with cholesterol and the B vitamins except pyridoxine (E), or with cholesterol and the B vitamins except thiamine (F). The colonies reared 5 cycles of brood on diets B, D and F, and 3 cycles on diet C. No adults were produced on diet E, and no larvae were reared to the sealing stage on diet A. It therefore appears that pyridoxine is required for normal brood rearing.

Studies on the biosynthesis of the branched-chain sugars from the quinocycline complex.

Abstract: (compound 11) portion of quinocycline B produced by Streptomyces aureofaciens was investigated The methylglycosides of compounds I and I1 were subjected to periodate oxidation to yield, respectively, acetaldehyde and acetic acid from the branch carbon atoms Acetaldehyde was oxidized to acetic acid, which was then degraded by Schmidt-degradation With [2-14C]pyruvate 87 to goo/, of the radioactivity incorporated into compound I or I1 was located in the C, branch without randomization of the label In contrast, with [1-’4C]acetate only very low activity was incorporated into the sugars and no 14C was localized in the C, branch These results prove that the C, branch in compounds1 and I1 originates from C-2 and C-3 of pyruvic acid When 14C-labelled quinocycline B was incubated for 17 h with S aureofaciens, 1301, was converted to quinocycline A Under the same conditions only 2Ol0 of [14C]quinocycline A was converted to quinocycline B It can therefore be concluded that quinocycline B is the precursor of quinocycline A This result is in agreement with the assumption that hydroxyethylthiemine pyrophosphate is the immediate precursor for the oxoethyl group of the branehed sugar 11, which after transfer to the aglycone is reduced to compound I Experiments with the thiamine antagonist neopyrithiamine did not show inhibition of incorporation of radioactivity from [2-14C]pyruvate into the hydroxyethyl branch of compound I However, this result does not exclude the possibility that thiamine pyrophosphate partjicipates in the reaction

Vitamin b12, thiamine, and biotin contents of marine phytoplankton1

Abstract: SUMMARY An extraction procedure was developed for determining vitamin B12, thiamine, and biotin contents of marine phytoplankton. Phytoplankters were collected either by centrifugation or by retention on a glass fiber filter, then heated at 100 C for I hr in 100 ml of vitamin-free seawater acidified to pH 3.5 with HCl. The extract, after debris removal, was filter-sterilized and analyzed, for vitamin B12, thiamine, and biotin with standard vitamin assay procedures. The vitamin contents of haeodactylum tricornutum, Skeletonema costatum, Stephanopyxis turris, and occolithus liuxleyi were determined during growth in batch cultures. P. tricornutum (non-vitamin requirer) growing in aerated cultures contained 0.29–0.96 ng B12, 5–15 ng thiamine, and 0.45–1.70 ng biotin/mg C. Under similar conditions S. costatum (B12-requirer) contained about 0.06 ng B12, 5–36 ng thiamine, and 0.16–2.10 ng biotin/mg C. The concentrations of vitamin were generally similar during some portion of the growth curve, eg, logarithmic growth. The vitamin B12, content of S. costatum growing under nonaerated conditions decreased when medium B12, was reduced. The biotin content did not change when medium B12 was decreased. The thiamine content per unit weight of C. huxleyi (thiamine-requirer) growing with either 10 or 120 ng/liter thiamine decreased under both medium concentrations, indicating no net synthesis of the vitamin.

Effect of thiamine on serotonin levels in magnesium-deficient animals

Abstract: To clarify the relationship between thiamine metabolism and peripheral vasodilation symptoms seen in the early stages of dietary magnesium deficiency, various synthetic diets were administered to rats. After a 4-wk period of thiamine excess and magnesium-deficient diet, blood serotonin levels increased significantly. A thiamine-deficient and magnesium-deficient diet revealed no elevation of blood serotonin. Serotonin in stomach and intestine increased in the excess-thiamine, magnesium-deficient group. Blood magnesium concentration decreased markedly in thiamine-supplemented, magnesium-deficient groups but not in the thiamine-deficient magnesium-deficient group. A possible explanation of the mechanism is presented.