Showing papers on "Thiamine published in 1981"
TL;DR: It is suggested that a low energy state is closely related to the formation of edematous lesions in thiamine-deficient encephalopathy.
Abstract: Pyrithiamine-induced acute thiamine-deficient encephalopathy was produced in adult male Wistar rats. Twenty-four hours before the onset of neurological signs the brain showed no morphological abnormalities. Encephalopathic rats had symmetrical lesions of edematous necrosis localized in the thalamus, mammillary body, and pontine tegmentum. Biochemically, encephalopathic rats had brain thiamine levels less than 20% of controls. For the assay of the concentrations of adenosine triphosphate (ATP) and phosphocreatine, the brains were fixed using 5 KW microwave irradiation and were divided into four parts: cerebral cortex, diencephalon, lower brainstem, and cerebellum. In the lower brainstem of the encephalopathic rats ATP concentrations were 89.5% of normal controls. Phosphocreatine levels were lowered to 70% of controls in the diencephalon and to 75% in the lower brainstem. Total high energy phosphate levels were decreased to 89% of controls in the diencephalon and 91% in the lower brainstem before the onset of neurological signs and to 76% and 79%, respectively, after the onset. In the cerebral cortex and cerebellum high energy phosphates were not significantly reduced. Lower high energy phosphate levels and the distribution of edematous lesions were coincident in the brain. These findings suggest that a low energy state is closely related to the formation of edematous lesions in thiamine-deficient encephalopathy.
110 citations
Journal Article•
TL;DR: Arecoline, a direct muscarinic agonist, was as effective as physostigmine or thiamine in restoring string test performance and incorporation of [2H4]choline and [U-14C]glucose into acetylcholine was decreased by 32 and 48%, respectively, relative to pair-fed controls after 12 days of pyrithiamine treatment.
Abstract: After only 1 day of treatment with a thiamine-deficient diet and pyrithiamine, a centrally and peripherally acting thiamine antagonist, 37.5% of rats performed poorly on a standardized string test. By day 12, 89.6% of the pyrithiamine-treated rats, but only 8.1% of the pair-fed controls, had decreased string test scores. Scores for rats treated with a thiamine-deficient diet and oxythiamine, a peripherally acting thiamine antagonist, did not decrease even on the day before death. The acetylcholinesterase inhibitor physostigmine improved the low string test scores in 69.2% of trials with the pyrithiamine-treated rats, whereas neostigmine, which acts peripherally, had no effect. The effect of physostigmine was inhibited by the muscarinic blocker atropine, but not by methatropine, its peripherally acting analog. Arecoline, a direct muscarinic agonist, was as effective as physostigmine or thiamine in restoring string test performance. Nicotine had no effect and the nicotinic blocker mecamylamine did not alter the effect of physostigmine. Incorporation of [2H4]choline and [U-14C]glucose into acetylcholine was decreased by 32 and 48%, respectively, relative to pair-fed controls after 12 days of pyrithiamine treatment. Acetylcholine levels were unchanged. Thiamine deficiency induces an early functionally significant central muscarinic cholinergic lesion.
79 citations
TL;DR: It is suggested that prophylactic Thiamine treatment therapy should be considered in the management of all malnourished patients.
Abstract: Four cases of acute Wernickes Encephalopathy in non-alcoholic, malnourished patients are described. In each case the administration of a glucose load precipitated a neurological crisis which was rapidly reversed by the administration of intravenous Thiamine. It is suggested that prophylactic Thiamine treatment therapy should be considered in the management of all malnourished patients.
75 citations
TL;DR: With decreasing cerebral thiamine concentrations, glucose utilization declined more rapidly in many of the structures which in humans develop histological lesions with prolongedThiamine deficiency than in structures less susceptible to the development of lesions.
Abstract: Rats maintained on a thiamine-free diet for two to seven weeks and control animals were studied by the [14C]deoxyglucose technique prior to the development of histological lesions. This technique permits measurement of local cerebral glucose utilization (LCGU) in discrete nuclei and tracts. Levels of thiamine in brain and blood were also determined. In the 41 central nervous system (CNS) structures in which it was measured, cerebral glucose utilization decreased with diminishing concentration of cerebral thiamine. Thus, the primary metabolic consequence of thiamine deficiency is a widespread reduction in cerebral glucose utilization. Furthermore, with decreasing cerebral thiamine concentrations, glucose utilization declined more rapidly in many of the structures which in humans develop histological lesions with prolonged thiamine deficiency than in structures less susceptible to the development of lesions. One determinant of the specific distribution of histological lesions occurring in human thiamine deficiency may be the variable rate at which the CNS structures lose their metabolic activity with continuing thiamine deficiency.
66 citations
TL;DR: Findings suggested that, in thiamine-deficient encephalopathy, both nervous and vascular components in the brain were involved and that the morphologic manifestations of the nervous component were far more extensive than those of the blood vessels.
Abstract: Acute encephalopathy was produced in the adult male Swiss mouse by pyrithiamine injection in conjunction with a thiamine-deficient diet. The condition of some mice was reversed within 24 hours by a treatment of a high dose of thiamine. The lesions occurred selectively in the thalamus, pontine tegmentum, and mammillary body and were manifested by hemorrhage and edematous necrosis consisting of severe edema of astrocytes, myelin sheaths, and neuronal dendrites. Before thiamine treatment, these degenerative changes were not associated with any mesenchymal reaction. At 48 and 96 hours after thiamine treatment, these edematous changes persisted. Fat-laden macrophages appeared in the lesion. Some axons showed Wallerian-type degeneration. After three weeks of thiamine treatment, macrophages became thin and rod-shaped. Wallerian-type degeneration and myelin edema persisted. The oligodendrocytes and astrocytes were hypertrophic. These lesions of thiamine-treated encephalopathy of the mouse closely resembled the non-hemorrhagic lesions of human Wernicke encephalopathy. Mice which were concomitantly-induced with hyperglycemia and encephalopathy showed no significant differences in clinical and morphologic manifestations from the encephalopathic mice with normal blood sugar levels. Vascular permeability to horseradish peroxidase was increased only slightly at the initial stage, but was reversed in the mice which clinically responded quickly to thiamine treatment. Occasionally, persistent increase of permeability was seen in 21-day-old lesions. These findings suggested that, in thiamine-deficient encephalopathy, both nervous and vascular components in the brain were involved and that the morphologic manifestations of the nervous component were far more extensive than those of the blood vessels.
65 citations
58 citations
55 citations
TL;DR: Thiamine should be given routinely to alcoholics even if their diet appears adequate and their liver disease is minimal or well compensated, perhaps reflecting failure of hte coenzyme TPP to recombine with the transketolase apoenzyme in the presence of normal thiamine stores.
Abstract: Erythrocyte transketolase activity and its stimulation in vitro by the addition of thiamine pyrophosphate (TPP effect) was measured in 64 normally nourished alcoholics with well-compensated liver disease and in 20 control subjects. Biochemical evidence of thiamine deficiency as judged by low transketolase activity was found in 19 alcoholics (29.7%). In 5 of these 19 patients the TPP effect was abnormally high, indicating depleted thiamine stores. IN the other 13 patients the TPP effect was either normal or low, suggesting a deficiency or an inability to use the transketolase apoenzyme, probably as a result o long-standing thiamine deficiency or the presence of liver disease. a further eight patients (12.5%) had normal transketolase activity but a low TPP effect, perhaps reflecting failure of hte coenzyme TPP to recombine with the transketolase apoenzyme in the presence of normal thiamine stores. There was no relationship between transketolase activity and the daily alcohol consumption, the duration of alcoholism, or the histological severity of the liver disease. Thiamine should be given routinely to alcoholics even if their diet appears adequate and their liver disease is minimal or well compensated.
48 citations
TL;DR: In order to ensure specificity, thiamine was assayed fluorometrically before and after the addition of thiaminase I (thiamin:base 2-methyl-4-aminopyrimidine-5-methenyltransferase, EC 2.1.2).
Abstract: Synaptic plasma membranes were prepared from rat cerebral cortex to determine if thiamine was localized in the membranes. The synaptosomes, prepared by discontinuous sucrose gradient centrifugation, were subjected to osmotic shock at pH 9.5 for 10--15 min and subfractionated on a discontinuous sucrose gradient. The two membrane fractions that were obtained were free of contamination by mitochondrial membrane and soluble fractions. In order to ensure specificity, thiamine was assayed fluorometrically before and after the addition of thiaminase I (thiamin:base 2-methyl-4-aminopyrimidine-5-methenyltransferase, EC 2.5.1.2). The thiamine content of the two membrane fractions was 9 and 10 pmol/mg protein.
47 citations
TL;DR: It is suggested that impaired string test performance is a central system effect of thiamine deficiency, and that it may also be a useful behavioral parameter to follow in other animal models of metabolic encephalopathies.
Abstract: Thiamine deficiency is a useful animal model of the interaction between biochemistry and behavior Although numerous biochemical changes have been detected in thiamine deficiency, studies of behavioral changes are relatively scarce We have modified and quantitated the string test, originally described by Miquel and Blasco, for application to thiamine-deficient rats The string test is reproduciblt with time, and control rats have a narrow range of scores 50% of rats treated with thiamine-deficient diet and pyrithiamine, a centrally-acting thiamine antagonist, have persistently decreased string test scores This decrease is already present on day 5 of treatment, long before the onset of weight loss or neurological symptoms Rats treated with oxythiamine, a peripherally acting thiamine antagonist, do not have decreased string test scores, even when anorectic and moribund These findings suggest that impaired string test performance is a central nervous system effect of thiamine deficiency, and that it may also be a useful behavioral parameter to follow in other animal models of metabolic encephalopathies
42 citations
TL;DR: Neither thiamine nor TTFD produced clinical improvement in the mental symptoms of Wernicke-Korsakoff psychosis unless administered early in the course of the disease.
Abstract: Erythrocyte transketolase activity and the effect of adding thiamine pyrophosphate (% TPP effect) were measured in subjects suffering from Wernicke-Korsakoff syndrome both before and during treatment with thiamine and/or thiamine tetrahydrofurfuryldisulphide (TTFD). Transketolase activity was significantly lower in untreated patients than in healthy volunteers. Treatment with either thiamine or with TTFD restored enzyme levels to control values but TTFD produced a greater increase than thiamine in enzyme activity. In a group of seven patients there was no correlation between duration of TTFD therapy and either increase in erythrocyte transketolase activity or % decrease in the TPP effect. However, when three patients were followed at intervals during treatment with TTFD, their erythrocyte transketolase increased progressively. Neither thiamine nor TTFD produced clinical improvement in the mental symptoms of Wernicke-Korsakoff psychosis unless administered early in the course of the disease.
TL;DR: The incidence of cardiac beriberi appears to be greater than is generally realized and the transketolase test and response to intravenous thiamine during catheter studies are valuable diagnostic tests.
Abstract: Five cases of cardiac beriberi occurring in chronic alcoholics are described. The clinical diagnosis was based on the presence of biventricular failure, low dietary intake of thiamine and the therapeutic response to oral thiamine. Complicating cardiac disease was excluded by haemodynamlc studies, left ventriculography, coronary angiography and endomyocardial biopsy.
Haemodynamic measurements including quantitative left ventriculography are reported. They indicate that left ventricular function is depressed despite elevated cardiac output.
Biopsy material was studied by llght and electron microscopy. No lesion specific to beriberi was detected by either technique although the biopsies were quantitatively abnormal. The histological changes resemble those in early reports based on necropsy material, and consist of vacuolation and intercellular oedema in the early stages with myofibre hypertrophy, fibrosis and cellular infiltration in the chronic cases.
The transketolase test and response to intravenous thiamine during catheter studies are valuable diagnostic tests.
Plasma renin, angiotensin II and aldosterone levels were lower than in patients with low output heart failure.
The incidence of cardiac beriberi appears to be greater than is generally realized.
TL;DR: Evidence for the importance of thiaminases in intensive beef production and the possibility of the need for thiamine supplementation in the form of aThiaminase resistant derivative is discussed.
Abstract: Thiaminases play an important role in the aetiology of CCN being responsible for the state of thiamine-deficiency which is an essential feature of the disease, evidence for which is presented here. These studies have led to a greater appreciation of the role of thiamine and thiaminases in ruminant nutrition especially as ruminal thiaminase activity is not confined to clinically affected animals but is of wider distribution. The importance of thiaminases in intensive beef production and the possibility of the need for thiamine supplementation in the form of a thiaminase resistant derivative is discussed.
TL;DR: The hypothesis that central serotonergic neurons are involved in the inhibition of the muricide aggression in thiamine deficient killer-rats is strengthened.
TL;DR: In this article, Niacin, riboflavin and thiamine (as thiochrome) were determined in enzymic hydrolysates of foods by high performance liquid chromatography.
TL;DR: The absence of auxotrophic mutants requiring an organic supplement in higher plants (other than thiamine auxotrophs) may be explained by inadequate translocation of these essential metabolites into the mutant zygotes (embryos) to enable their development to mature seeds.
Abstract: Uptake from nutrient media into the cob and translocation of various 14C-compounds from maternal tissue (cob) into developing maize seeds was examined by using caryopsis cultures. Based on relative 14C concentrations in the cob and the endosperm, it was concluded that the relative efficiencies of movement of amino acids (leucine, phenylalanine, proline), vitamins (thiamine HCl, nicotinic acid), and nucleic acid bases (adenine, thymine) from the cob to the endosperm were 11 to 250 times lower than that of sucrose. Thiamine was unique in that it was concentrated in the embryo at a level that was almost 10 times higher than in the endosperm. The absence of auxotrophic mutants requiring an organic supplement in higher plants (other than thiamine auxotrophs) may be explained by inadequate translocation of these essential metabolites into the mutant zygotes (embryos) to enable their development to mature seeds.
Journal Article•
TL;DR: It is suggested that thiamine may cause increased neutrophil migration and lymphocyte transformation by protecting these cells from toxic oxidative products generated by the peroxidase/H2O2/halide system.
Abstract: The effects of thiamine on neutrophil functions and mitogen-induced lymphocyte transformation were investigated in vitro and in vivo in adult volunteers following the injection of 50 mg thiamine intramuscularly. Thiamine caused stimulation of neutrophil motility in vitro and in vivo and increased lymphocyte transformation in vivo. Enhancement of these functions was related to inhibition of neutrophil post-phagocytic iodination of Candida albicans by the MPO/H2O2/halide system. The horseradish peroxidase/-H2O2/125 I-mediated iodination of bovine serum albumin was also inhibited by thiamine concentrations which caused increased neutrophil motility. It was found that preincubation of neutrophils and lymphocytes with the horseradish peroxidase/H2O2/halide system caused considerable inhibition of the migratory and proliferative responses respectively. Inclusion of thiamine at concentrations which were found to inhibit the peroxidase/-H2O2/halide system protected the neutrophil migratory and lymphocyte proliferative responses from inactivation by this system. It is suggested that thiamine may cause increased neutrophil migration and lymphocyte transformation by protecting these cells from toxic oxidative products generated by the peroxidase/H2O2/halide system.
TL;DR: It is likely that the carbon chain of 1-deoxy- D -threo-2-pentulose is the precursor of the five carbons chain of the thiazole moiety of theThiamine molecule in E. coli.
TL;DR: Infusion solutions containing bisulfite were found to be unsuitable vehicles for the administration of vitamin formulations containing thiamine and should be used immediately after their preparation, and the patient should be monitored for signs ofThiamine deficiency.
Abstract: The degree of degradation of thiamine hydrochloride in sodium bisulfite-containing infusion solutions was investigated. Two amino acid and one electrolyte infusion solution containing sodium bisulfite and four infusion solutions (5 and 10% dextrose, Lactated Ringer's, and 0.9% sodium chloride injections) without sodium bisulfite were obtained in 500-ml glass or plastic containers. Three thiamine sources, two commercial multivitamin preparations, and one investigational multivitamin product were added to the infusion solutions. The percentage of added thiamine remaining after storage was determined in four experiments: (1) The investigational product was added to the infusion solutions with bisulfite, and the determinations were made after 24 hours of storage at room temperature (RT) under both light and dark conditions; (2) the two commercial multivitamin preparations were mixed with an amino acid solution containing bisulfite and the determination was made after 24 hours of storage at RT under dark conditions; (3) the investigational product was added to the infusion solutions with bisulfite, and the determinations were made after 2, 4, 6, 8, and 24 hours storage at 7 degrees C and following four hours at RT under dark conditions; and (4) the investigational product was added to the four infusion solutions without bisulfite, and the determinations were made after 24 hours of storage at RT under both light and dark conditions. In the infusion solutions containing bisulfite, the stability of thiamine was inversely related to the pH. In an amino acid solution at a pH of 6.5, only 3-8% of the added thiamine was found after 24 hours storage at RT, and only 37% was found after 24 hours at 7 degrees C. In the electrolyte solution with bisulfite (pH = 5), the percentages of thiamine remaining after 24 hours RT and 7 degrees C storage were 50 and 69%, respectively. Light exposure was not found to affect the stability of thiamine in the solutions containing bisulfite. In the infusion solutions without bisulfite, a minimal loss of thiamine occurred even though the pH range was 4.7-5.6. The degradation effect of light exposure was greater for the solutions stored in plastic than in glass. Infusion solutions containing bisulfite were found to be unsuitable vehicles for the administration of vitamin formulations containing thiamine. If a patient must receive multivitamins in infusion solutions with bisulfite, the solutions should be used immediately after their preparation, and the patient should be monitored for signs of thiamine deficiency.
TL;DR: The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system.
Abstract: The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system. The incidence of thiamine deficiency was 31%, of riboflavin deficiency 22% and of pyridoxine deficiency 6%. Alcoholics in particular suffered from deficiencies of vitamin B 1, and B 2. There was a correlation of vitamin B 1 and B 2 deficiency and signs of a cerebellar and/or brainstem lesion. The most frequent symptoms in this connection were gait disturbances and oculomotor signs like spontaneous and gaze nystagmus, disturbed eye tracking, diminished optokinetic nystagmus, decreased ability to suppress vestibular nystagmus by fixation. These signs hardly ever occurred in alcoholic patients who showed no deficiency of vitamin B 1, B 2 or B 6. Whenever they do appear, a vitamin B supplementation has to be performed in order to prevent the manifestation of Wernicke's encephalopathy, cerebral or cerebellar atrophy. Alcoholics showed the same incidence of polyneuropathy, whether they suffered from a deficiency of B vitamins or not. Deficiencies of vitamin B 1, B 2 or B 6 were also found in patients with intestinal malabsorption and polyneuropathy, diabetic polyneuropathy, optic atrophy, myelopathy and cerebellar ataxia of unknown etiology, neurological manifestations of neoplasms arising outside the nervous system, B 12 myeloencephalopathy and Thevenard's syndrome.
TL;DR: The results confirm the assumption that thiamine passes through the brush border membrane of guinea-pig jejunum by simple diffusion, and Pyrithiamine, an antimetabolite of thiamines, and unlabeled thienine, both added in very excessive amounts, did not inhibit labeledThiamine transport into the membrane vesicles.
TL;DR: Abscisic acid production by Cercospora rosicola Passerini in liquid shake culture was measured with different amino acids in combination and singly as nitrogen sources and with different amounts of thiamine in the media, and single amino acids that supported the highest production of absc isic acid were asparagine and monosodium glutamate.
Abstract: Abscisic acid production by Cercospora rosicola Passerini in liquid shake culture was measured with different amino acids in combination and singly as nitrogen sources and with different amounts of thiamine in the media. Production of abscisic acid was highest with aspartic acid-glutamic acid and aspartic acid-glutamic acid-serine mixtures as nitrogen sources. Single amino acids that supported the highest production of abscisic acid were asparagine and monosodium glutamate. Thiamine was important for abscisic acid production. Leucine inhibited abscisic acid production. C. rosicola produced abscisic acid in the dark, but production more than doubled in the presence of light.
TL;DR: Thiamin status in patients with an alcohol problem was studied before and after intramuscular thiamin hydrochloride and results for erythrocyte transketolase activity and plasma thiam in pyrophosphate are compared.
TL;DR: A high-pressure liquid chromatographic assay was developed for the determination of four water-soluble vitamins: niacinamide, pyridoxine, thiamine, and riboflavin and is applicable to single-tablet assays.
TL;DR: It was found that amprolium treatment could induce thrombocytopenia, but once the sheep became accustomed to amproLium in the diet they seemed to be resistant to this effect, and depression of erythrocyte TK activity coupled with the presence of faecal thiaminase appeared to be the most reliable diagnostic biochemical parameters for PEM.
Abstract: SUMMARY Polioencephalomalacia (PEM) induced in sheep was compared with the disease found in naturally occurring cases. Blood biochemical indicators measured were pyruvate, lactate, glucose, erythrocyte transketolase (TK) and stimulation of TK by addition of thiamine pyrophosphate (TPP effect). Faeces and rumen contents were assayed for thiaminase activity. The effect of treating affected sheep with thiamine was also noted. It was found that amprolium treatment could induce thrombocytopenia, but once the sheep became accustomed to amprolium in the diet they seemed to be resistant to this effect. In sheep receiving amprolium significant weight losses preceded the onset of clinical signs. Further weight loss continued throughout the recovery period despite removal of amprolium from the diet and treatment with thiamine. Blood glucose was variable, and was elevated only when marked clinical signs were present. Pyruvate and lactate levels showed marked variation throughout the trial. TK values were depressed and TPP effects increased well before the onset of clinical signs, although some naturally occurring cases had normal levels. Faecal thiaminase activity was negligible in all the sheep on the amprolium trial but most field cases had a high level. High faecal thiaminase was observed in about 5% of clinically normal animals from affected flocks. Depression of erythrocyte TK activity coupled with the presence of faecal thiaminase appeared to be the most reliable diagnostic biochemical parameters for PEM. Treatment of PEM affected sheep with thiamine rapidly brought the biochemical status of the animals to normal. However where advanced brain lesions were present the damage was permanent and such sheep treated with thiamine remained partially decorticate. Copyright © 1981, Wiley Blackwell. All rights reserved
TL;DR: A pair of monozygotic twins, one suffering from the Wernicke-Korsakoff syndrome, verified at autopsy, and the other healthy, was studied biochemically, suggesting that an inborn error of metabolism may have been common to both twins.
Abstract: A pair of monozygotic twins, one suffering from the Wernicke-Korsakoff syndrome, verified at autopsy, and the other healthy, was studied biochemically. The erythrocyte transketolase of each twin showed abnormalities, though these differed in the two individuals. In the healthy twin, the basal transketolase was low, but responded normally to thiamine pyrophosphate (TPP) added in vitro. In the twin with the Wernicke-Korsakoff syndrome the basal level of the enzyme and its response in vitro were normal, but a period of treatment with thiamine tetrahydrofurfuryldisulphide, led to loss of the in vitro response. It is suggested that, initially, an inborn error of metabolism may have been common to both twins.
TL;DR: Thiamine pyrophosphate (cocarboxylase), a constituent component of Iso VitaleX, was found to be the only growth-promoting factor, and it could be used as a substitute for Iso vitaleX.
Abstract: The effect of a commercially available, chemically defined enrichment (Iso-VitaleX; BBL Microbiology Systems, Cockeysville, Md.) on the growth of 10 strains of Haemophilus somnus was studied. A 6- to 10-fold increase in growth, as measured turbidimetrically, was observed when Iso VitaleX was added to a basal medium of brain heart infusion broth to a final concentration of 1% (vol/vol). Thiamine pyrophosphate (cocarboxylase), a constituent component of Iso VitaleX, was found to be the only growth-promoting factor, and it could be used as a substitute for Iso VitaleX. An equimolar concentration (2.2 microM) of thiamine monophosphate promoted growth equal to that of thiamine pyrophosphate. Thiamine was nonstimulatory for all 10 strains tested. When alkaline thermal-treated brain heart infusion broth was used as the basal medium, 7 of the 10 strains had an absolute requirement for thiamine monophosphate or thiamine pyrophosphate. The three remaining strains showed minimal growth when thiamine was added to this basal medium; however, excellent growth was observed when thiamine monophosphate or thiamine pyrophosphate was utilized. Factor X (hemin) was found to further enhance the growth when concentrations of 5 to 10 micrograms/ml were coupled with thiamine pyrophosphate. No increase in growth was observed when factor V (nicotinamide adenine dinucleotide) was coupled with thiamine pyrophosphate. This is the first report of a growth factor requirement for H. somnus.
TL;DR: The hemodynamic studies done after recovery from shock revealed that the cardiac output decreased to a slightly low level and then increased to a normal level, concomitant with an increase in the peripheral vascular resistance after introductory administration of thiamine.
Abstract: A case of Shoshin beriberi found in a patient with severe metabolic acidosis and shock was presented. We believe the metabolic acidosis in this case is ascribable to overproduction of pyruvate and lactate resulting from lack of thiamine due to preferential intake of sake, precooked food, and rice, and also to shock. The hemodynamic studies done after recovery from shock revealed that the cardiac output, which was initially high, decreased to a slightly low level and then increased to a normal level, concomitant with an increase in the peripheral vascular resistance after introductory administration of thiamine. After treatment with thiamine, all abnormalities disappeared.
TL;DR: Thiamin pyrophosphokinase activity was increased on day 10 of thiamin deficiency and remained unchanged within the next period of investigation and a more (20-40% in blood) or less (5-10% in liver) pronounced TPP-stimulatory effect of transketolase activity.
Abstract: Mice were made deficient by thiamin deprivation. Thiamin pyrophosphokinase and thiamin pyrophosphatase activities were measured, and their changes were compared to transketolase (TK), pyruvate and alpha-ketoglutarate dehydrogenase (DG) activities and thiamin pyrophosphate (TPP) level in the same tissues. Thiamin pyrophosphokinase activity was increased on day 10 of thiamin deficiency and remained unchanged within the next period of investigation. Thiamin pyrophosphatase activity decreased after 5 days and was enhanced in 10, 15 and 20 days of deficiency. This fact may be related to the regulatory role of the enzyme in the intertissue vitamin distribution and transport. The liver TPP level was the earliest and most specific indicator of the thiamin status as thiamin deficiency developed, and pyruvate DG was more drastically inhibited than alpha-ketoglutarate DG. Blood TK was more sensitive to thiamin deprivation than liver TK. In both cases we obtained a more (20-40% in blood) or less (5-10% in liver) pronounced TPP-stimulatory effect of transketolase activity.
Journal Article•
TL;DR: Albino rats, injected subcutaneously with Acephate for 4 weeks and 8 weeks, showed appreciable depletion of thiamine in liver, heart, kidney, brain and blood, and there was concomitant increase in pyruvic acid and lactic acid in various tissues.
Abstract: Effect of Acephate, an organophosphorus insecticide, on tissue levels of thiamine, pyruvic acid, lactic acid, glycogen and blood sugar, has been studied. The albino rats, injected subcutaneously with Acephate (25 mg/10 gm body wt./day) for 4 weeks and 8 weeks, showed appreciable depletion of thiamine in liver, heart, kidney, brain and blood. The depletion of thiamine was found to be more after 8 weeks of Acephate injection. There was concomitant increase in pyruvic acid and lactic acid in various tissues. There was enormous depletion of glycogen in liver and slight rise in blood sugar concentration. The animals injected thiamine (120 micrograms/100 gm body wt./day) along with Acephate, showed more or less normal levels of thiamine, pyruvic acid, lactic acid, liver glycogen and blood sugar. The increase in pyruvic acid and lactic acid in tissues has been attributed to depletion of thiamine which is required of pyruvic acid oxidation. The increase in blood sugar has been attributed to the excess breakdown of glycogen.