Showing papers on "Thiamine published in 2005"

Vitamin B1 Functions as an Activator of Plant Disease Resistance

Abstract: Vitamin B1 (thiamine) is an essential nutrient for humans. Vitamin B1 deficiency causes beriberi, which disturbs the central nervous and circulatory systems. In countries in which rice (Oryza sativa) is a major food, thiamine deficiency is prevalent because polishing of rice removes most of the thiamine in the grain. We demonstrate here that thiamine, in addition to its nutritional value, induces systemic acquired resistance (SAR) in plants. Thiamine-treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants showed resistance to fungal, bacterial, and viral infections. Thiamine treatment induces the transient expression of pathogenesis-related (PR) genes in rice and other plants. In addition, thiamine treatment potentiates stronger and more rapid PR gene expression and the up-regulation of protein kinase C activity. The effects of thiamine on disease resistance and defense-related gene expression mobilize systemically throughout the plant and last for more than 15 d after treatment. Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2. Furthermore, thiamine prevented bacterial infection in Arabidopsis mutants insensitive to jasmonic acid or ethylene but not in mutants impaired in the SAR transduction pathway. These results clearly demonstrate that thiamine induces SAR in plants through the salicylic acid and Ca2+-related signaling pathways. The findings provide a novel paradigm for developing alternative strategies for the control of plant diseases.

Outbreak of Life-Threatening Thiamine Deficiency in Infants in Israel Caused by a Defective Soy-Based Formula

Abstract: Objective. Between October and No- vember 2003, several infants with encephalopathy were hospitalized in pediatric intensive care units in Israel. Two died of cardiomyopathy. Analysis of the accumu- lated data showed that all had been fed the same brand of soy-based formula (Remedia Super Soya 1), specifi- cally manufactured for the Israeli market. The source was identified on November 6, 2003, when a 5.5-month-old infant was admitted to Sourasky Medical Center with upbeat nystagmus, ophthalmoplegia, and vomiting. Wer- nicke's encephalopathy was suspected, and treatment with supplementary thiamine was started. His condition improved within hours. Detailed history revealed that the infant was being fed the same formula, raising sus- picions that it was deficient in thiamine. The formula was tested by the Israeli public health authorities, and the thiamine level was found to be undetectable ( 25% indicates severe deficiency. Blood lactate levels (normal: 0.5-2 mmol/L) were measured in 6 infants, cerebrospinal fluid lactate in 2 (normal: 0.5-2 mmol/L), and blood pyruvate in 4 (nor- mal: 0.03-0.08 mmol/L). The diagnostic criteria for thia- mine deficiency were abnormal transketolase activity and/or unexplained lactic acidosis. Treatment consisted of intramuscular thiamine 50 mg/day for 14 days com- bined with a switch to another infant formula. Results. Early symptoms were nonspecific and in- cluded mainly vomiting (n 8), lethargy (n 7), irrita- bility (n 5), abdominal distension (n 4), diarrhea (n 4), respiratory symptoms (n 4), developmental delay (n 3), and failure to thrive (n 2). Infection was found in all cases. Six infants were admitted with fever. One pa- tient had clinical dysentery and group C Salmonella sep- sis; the others had mild infection: acute gastroenteritis (n 2); upper respiratory infection (n 2); and broncho- pneumonia, acute bronchitis, and viral infection (n 1 each). Two infants were treated with antibiotics. Three infants had neurologic symptoms of ophthalmoplegia with bilateral abduction deficit with or without upbeat nystagmus. All 3 had blood lactic acidosis, and 2 had high cerebrospinal fluid lactate levels. Patient 1, our in- dex case, was hospitalized for upbeat nystagmus and ophthalmoplegia, in addition to daily vomiting episodes since 4 months of age and weight loss of 0.5 kg. Findings on brain computed tomography were normal. Blood lac- tate levels were high, and TPPE was 37.8%. Brain mag- netic resonance imaging (MRI) revealed no abnormali- ties. Patient 2, who presented at 5 months with lethargy, vomiting, grunting, and abdominal tenderness, was found to have intussusception on abdominal ultrasound and underwent 2 attempts at reduction with air enema several hours apart. However, the lethargy failed to re- solve and ophthalmoplegia appeared the next day, lead- ing to suspicions of Wernicke's encephalopathy. Labora- tory tests showed severe thiamine deficiency (TPPE 31.2%). In patients 1 and 2, treatment led to complete resolution of symptoms. The third infant, a 5-month-old girl, was admitted on October 10, 2003, well before the outbreak was recognized, with vomiting, fever, and oph- thalmoplegia. Her condition deteriorated to seizures, ap- nea, and coma. Brain MRI showed a bilateral symmetri- cal hyperintense signal in the basal ganglia, mamillary bodies, and periaqueductal gray matter. Suspecting a metabolic disease, vitamins were added to the intrave- nous solution, including thiamine 250 mg twice a day. Clinical improvement was noted 1 day later. TPPE assay performed after treatment with thiamine was started was still abnormal (17.6%). Her formula was substituted after 4 weeks, after the announcement about the thiamine deficiency. Although the MRI findings improved 5 weeks later, the infant had sequelae of ophthalmoplegia

The potential role of thiamine (vitamin B1) in diabetic complications.

Abstract: Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycemia is one likely or potential trigger for biochemical dysfunction leading to the development of diabetic complications. This may be prevented by disposal of excess triosephosphates via the reductive pentosephosphate pathway. This pathway is impaired in experimental and clinical diabetes by mild thiamine deficiency. The expression and activity of the thiamine-dependent enzyme, transketolase--the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased. Correction of thiamine deficiency in experimental diabetes by high dose therapy with thiamine and the thiamine monophosphate prodrug, Benfotiamine, restores disposal of triosephosphates by the reductive pentosephosphate pathway in hyperglycemia. This prevented multiple mechanisms of biochemical dysfunction: activation of protein kinase C, activation of the hexosamine pathway, increased glycation and oxidative stress. Consequently, the development of incipient diabetic nephropathy, neuropathy and retinopathy were prevented. Both thiamine and Benfotiamine produced other remarkable effects in experimental diabetes: marked reversals of increased diuresis and glucosuria without change in glycemic status. High dose thiamine also corrected dyslipidemia in experimental diabetes--normalizing cholesterol and triglycerides. Dysfunction of beta-cells and impaired glucose tolerance in thiamine deficiency and suggestion of a link of impaired glucose tolerance with dietary thiamine indicates that thiamine therapy may have a future role in prevention of type 2 diabetes. More immediately, given the emerging multiple benefits of thiamine repletion, even mild thiamine deficiency in diabetes should be avoided and thiamine supplementation to high dose should be considered as adjunct nutritional therapy to prevent dyslipidemia and the development of vascular complications in clinical diabetes.

Thiamine and Thiaminase Status in Forage Fish of Salmonines from Lake Michigan

Abstract: Dietary sources of thiamine (vitamin B1) and thiamine-degrading enzymes (thiaminases) are thought to be primary factors in the development of thiamine deficiency among Great Lakes salmonines. We surveyed major forage fish species in Lake Michigan for their content of thiamine, thiamine vitamers, and thiaminase activity. Concentrations of total thiamine were similar (P ≤ 0.05) among most forage fishes (alewife Alosa pseudoharengus, bloater Coregonus hoyi, spottail shiner Notropis hudsonius, deepwater sculpin Myoxocephalus thompsonii, yellow perch Perca flavescens, ninespine stickleback Pungitius pungitius, and round goby Neogobius melanostomus) and slightly lower in rainbow smelt Osmerus mordax. Concentrations of total thiamine were all above the dietary requirements of coldwater fishes, suggesting the thiamine content of forage fish is not the critical factor in the development of thiamine deficiency in Lake Michigan salmonines. Thiamine pyrophosphate was the predominant form of thiamine in most ...

Role of mitochondrial dysfunction and oxidative stress in the pathogenesis of selective neuronal loss in Wernicke's encephalopathy.

Abstract: Thiamine deficiency results in Wernicke’s encephalopathy and is commonly encountered in chronic alcoholism, gastrointestinal diseases, and HIV AIDS. The earliest metabolic consequence of thiamine deficiency is a selective loss in activity of the thiamine diphosphate-dependent enzyme α-ketoglutarate dehydrogenase (α-KGDH), a rate-limiting tricarboxylic acid cycle enzyme. Thiamine deficiency is characterized neuropathologically by selective neuronal cell death in the thalamus, pons, and cerebellum. The cause of this region-selective neuronal loss is unknown, but mechanisms involving cellular energy failure, focal lactic acidosis, and NMDA receptor-mediated excitotoxicity have classically been implicated. More recently, evidence supports a role for oxidative stress. Evidence includes increased endothelial nitric oxide synthase, nitrotyrosine deposition, microglial activation, and lipid peroxidation. Reactive oxygen species production results in decreased expression of astrocytic glutamate transporters and decreased activities of α-KGDH, resulting in an amplification of cell death mechanisms in thiamine deficiency.

Development of Aspergillus oryzae thiA promoter as a tool for molecular biological studies.

Abstract: In filamentous fungi, the repertoire of promoters available for exogenous gene expression is limited. Here, we report the development and application of the thiamine-regulatable thiA promoter (PthiA) in Aspergillus oryzae as a tool for molecular biological studies. When PthiA was used to express the enhanced green fluorescent protein (EGFP) reporter, the fluorescence in the mycelia was either repressed or induced in the presence or absence of thiamine in the culture media, respectively. In addition, the expression level from the thiA promoter can be controlled by the concentration of external thiamine. Thiamine content in the media did not affect mycelial morphology, making the thiA promoter more useful compared with alcA and amyB promoters that depend on carbon source for regulation. Moreover, as the A. oryzae thiA promoter was also regulated by thiamine in A. nidulans, this promoter can be further applied as an inducible promoter in other Aspergilli.

High‐Dose Thiamine Therapy Counters Dyslipidemia and Advanced Glycation of Plasma Protein in Streptozotocin‐Induced Diabetic Rats

Abstract: The streptozotocin-induced (STZ) diabetic rat experimental model of diabetes on insulin maintenance therapy exhibits dyslipidemia, mild thiamine deficiency, and increased plasma protein advanced glycation end products (AGEs). The reversal of thiamine deficiency by high-dose thiamine and S-benzoylthiamine monophosphate (benfotiamine) prevented the development of incipient nephropathy. Recently, we reported that high-dose thiamine (but not benfotiamine) countered diabetic dyslipidemia. To understand further the differences between the effects of thiamine and benfotiamine therapy, we quantified the levels of the AGEs in plasma protein. We found hydroimidazolone AGE residues derived from glyoxal and methylglyoxal, G-H1 and MG-H1, were increased 115% and 68% in STZ diabetic rats, with respect to normal controls, and were normalized by both thiamine and benfotiamine; whereas N-carboxymethyl-lysine (CML) and N-carboxyethyl-lysine (CEL) residues were increased 74% and 118% in STZ diabetic rats and were normalized by thiamine only. The lack of effect of benfotiamine on plasma CML and CEL residue concentrations suggests there may be important precursors of plasma protein CML and CEL residues other than glyoxal and methylglyoxal. These are probably lipid-derived aldehydes.

Isolation and Characterization of New Thiamine-Deregulated Mutants of Bacillus subtilis

Abstract: In bacteria, thiamine pyrophosphate (TPP) is an essential cofactor that is synthesized de novo. Thiamine, however, is not an intermediate in the biosynthetic pathway but is salvaged from the environment and phosphorylated to TPP. We have isolated and characterized new mutants of Bacillus subtilis that deregulate thiamine biosynthesis and affect the export of thiamine products from the cell. Deletion of the ydiA gene, which shows significant similarity to the thiamine monophosphate kinase gene of Escherichia coli (thiL), did not generate the expected thiamine auxotroph but instead generated a thiamine bradytroph that grew to near-wild-type levels on minimal medium. From this ΔthiL deletion mutant, two additional ethyl methanesulfonate-induced mutants that derepressed the expression of a thiC-lacZ transcriptional reporter were isolated. One mutant, Tx1, contained a nonsense mutation within the B. subtilis yloS (thiN) gene that encodes a thiamine pyrophosphokinase, a result which confirmed that B. subtilis contains a single-step, yeast-like thiamine-to-TPP pathway in addition to the bacterial TPP de novo pathway. A second mutant, strain Tx26, was shown to contain two lesions. Genetic mapping and DNA sequencing indicated that the first mutation affected yuaJ, which encodes a thiamine permease. The second mutation was located within the ykoD cistron of the ykoFEDC operon, which putatively encodes the ATPase component of a unique thiamine-related ABC transporter. Genetic and microarray studies indicated that both the mutant yuaJ and ykoD genes were required for the derepression of thiamine-regulated genes. Moreover, the combination of the four mutations (the ΔthiL, thiN, yuaJ, and ykoD mutations) into a single strain significantly increased the production and excretion of thiamine products into the culture medium. These results are consistent with the proposed “riboswitch” mechanism of thiamine gene regulation (W. C. Winkler, A. Nahvi, and R. R. Breaker, Nature 419:952-956, 2002).

Thiamine deficiency in infants: MR findings in the brain.

Abstract: BACKGROUND AND PURPOSE: Thiamine deficiency is extremely rare in infants in developed countries. To our knowledge, its MR findings in the brain have not been reported. The purpose of this study was to investigate the brain MR findings in infants with encephalopathy due to thiamine deficiency. METHODS: The study group included six infants aged 2–10 months with encephalopathy who had been fed with solely soy-based formula devoid of thiamine from birth. All underwent MR evaluation at admission and follow-up (total of 14 examinations). In one patient, MR spectroscopy (MRS) was performed. RESULTS: In five patients T2-weighted, fluid-attenuated inversion recovery, or proton-attenuated sequences showed bilateral and symmetric hyperintensity in the periaqueductal area, basal ganglia and thalami. Five had lesions in the mammillary bodies, and three, in the brain stem. In all six patients, the frontal region (cortex and white matter) was clearly involved. At presentation, MRS of the periaqueductal area showed a lactate doublet. On long-term follow-up, three of four patients had severe frontal damage; in two, this occurred as part of diffuse parenchymal loss, and in one, it was accompanied by atrophy of the basal ganglia and thalami. CONCLUSION: Thiamine deficiency in infants is characterized by involvement of the frontal lobes and basal ganglia, in addition to the lesions in the periaqueductal region, thalami, and the mammillary bodies described in adults. MRS demonstrates a characteristic lactate peak.

Thiamine administration in alcohol-dependent patients

Abstract: ( Received 28 August 2004; first review notified 12 September 2004; in revised form 28 September 2004; accepted 7 October 2004 ) Thiamine (vitamin B1) is a water-soluble vitamin that is involved in the metabolism of glucose and lipids as well as in the production of glucose-derived neurotransmitters (see Cook et al ., 1998). Its deficiency leads to a variety of neurological and cardiovascular symptoms and signs. Early symptoms may include fatigue, weakness and emotional disturbance, whereas prolonged gradual deficiency may lead to a form of polyneuritis (known as dry beriberi), cardiac failure or peripheral oedema (wet beriberi) (Thomson, 2000). Severe thiamine deficiency (TD) may result in the development of Wernicke's encephalopathy (WE). The classical signs of WE are ocular motility disorders (nystagmus, ophthalmoplegia), ataxia and mental changes (confusion, drowsiness, obtundation, clouding of consciousness, pre-coma and coma), although minor episodes of 'subclinical' encephalopathies are frequent (Reuler et al ., 1985). An appropriate treatment may correct most of these abnormalities; in contrast, the lack of a diagnosis of WE may result in serious consequences (Reuler et al ., 1985 …

Can Diet-Dependent Factors Help Explain Fish-to-Fish Variation in Thiamine-Dependent Early Mortality Syndrome?

Abstract: To provide insight into the reasons why offspring of certain salmonine females exhibit early mortality syndrome (EMS) in the Great Lakes whereas others do not, we measured the egg concentrations of potential biochemical markers (stable isotopes of nitrogen and carbon, fatty acid signatures, and lipid-soluble carotenoids and vitamins) that are indicative of differing food web and trophic structure. To corroborate the presence of EMS, we also measured the egg content of thiamine vitamers. For all the stocks of coho salmon Oncorhynchus kisutch and Chinook salmon O. tshawytscha we studied, there was a very high correspondence between EMS and low concentrations of unphosphorylated thiamine in unfertilized eggs. For salmonine stocks in the Platte River, Thompson Creek, and the Swan River, Michigan, small but significant shifts occurred in measures of egg carotenoids, retinoids, δ15N depletion, and fatty acid profiles of fish producing normal offspring relative to those exhibiting EMS. Egg thiamine conc...

Brain lactate synthesis in thiamine deficiency: a re-evaluation using 1H-13C nuclear magnetic resonance spectroscopy.

Abstract: Region-selective accumulation of brain lactate occurs in TD; however, the mechanisms responsible have not been elucidated fully. (1)H and (13)C nuclear magnetic resonance (NMR) spectroscopy were therefore used to investigate de novo lactate synthesis from [1-(13)C]glucose in vulnerable (medial thalamus) and nonvulnerable (frontal cortex) brain regions of rats made thiamine deficient by administration of the central thiamine antagonist pyrithiamine. De novo synthesis of lactate was increased in the medial thalamus to 148% and 226% of pair-fed control values at presymptomatic and symptomatic stages of thiamine deficiency, respectively, whereas no such changes were observed in the frontal cortex. Administration of a glucose load selectively worsened the changes in medial thalamus. Pyruvate recycling and peripherally derived lactate did not contribute significantly to the lactate increase within the thiamine-deficient brain. Increases in immunolabeling of the lactate dehydrogenase isoenzymes (LDH1 and LDH5) were observed in the medial thalamus of thiamine-deficient animals. Metabolic impairment due to thiamine deficiency thus results in increased glycolysis, increased LDH immunolabeling of neurons and astrocytes and increased de novo synthesis of lactate in brain regions vulnerable to thiamine deficiency. These results are consistent with the notion that focal lactate accumulation participates in the worsening of neurologic symptoms in thiamine-deficient patients.

Thiamine deficiency in dogs due to the feeding of sulphite preserved meat.

Abstract: A 6-year-old dog, a 4-year-old dog and three 7-week-old puppies were diagnosed with thiamine deficiency caused by feeding sulphite treated meat. The 6-year-old dog presented with a history of inappetence, weight loss and vomiting that rapidly progressed to signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic resonance imaging revealed bilaterally symmetrical hyperintensity of the caudate nucleus and rostral colliculi. The dog recovered with thiamine supplementation. The 4-year-old dog and three 7-week-old puppies also presented with rapidly progressive multifocal central nervous system signs including ataxia, paresis, increased muscle tone, seizures, nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine deficiency.

The Effect of Thiamine Injection on Upstream Migration, Survival, and Thiamine Status of Putative Thiamine-Deficient Coho Salmon

Abstract: A diet containing a high proportion of alewives Alosa pseudoharengus results in a thiamine deficiency that has been associated with high larval salmonid mortality, known as early mortality syndrome (EMS), but relatively little is known about the effects of the deficiency on adults. Using thiamine injection (50 mg thiamine/kg body weight) of ascending adult female coho salmon Oncorhynchus kisutch on the Platte River, Michigan, we investigated the effects of thiamine supplementation on migration, adult survival, and thiamine status. The thiamine concentrations of eggs, muscle (red and white), spleen, kidney (head and trunk), and liver and the transketolase activity of the liver, head kidney, and trunk kidney of fish injected with thiamine dissolved in physiological saline (PST) or physiological saline only (PS) were compared with those of uninjected fish. The injection did not affect the number of fish making the 15-km upstream migration to a collection weir but did affect survival once fish reache...

Direct genomic PCR sequencing of the high affinity thiamine transporter (SLC19A2) gene identifies three genetic variants in Wernicke Korsakoff syndrome (WKS).

Abstract: Irene Guerrini, Allan D. Thomson, Cristopher C.H. Cook, Andrew McQuillin, Vishal Sharma, Michael Kopelman, Gerald Reynolds, Pramod Jauhar, Clive Harper, and Hugh M.D. Gurling* Molecular Psychiatry Laboratory, Windeyer Institute of Medical Sciences, Department of Mental Health Sciences, Royal Free and University College London Medical School, London, United Kingdom Kent Institute of Medicine and Health Science, University of Kent at Canterbury, United Kingdom St. Chad’s College, Durham, United Kingdom Neuropsychiatry and Memory Disorders Clinic, University Department of Psychiatry and Psychology, King’s College, St. Thomas’s Campus, London, United Kingdom Parkhead Hospital, Greater Glasgow Primary Care Trust and Department of Psychological Medicine, University of Glasgow, United Kingdom Neuropathology Department, University of Sydney and Sydney South West Area Health Service, New South Wales, Australia

Functional vulnerability of developing central nervous system to maternal thiamine deficiencies in the rat.

Abstract: Thiamine deficiency (B1 vitamin) was induced during three periods of rat central nervous system (CNS) ontogenesis. Females were fed a thiamine deficient diet such that developing offspring were exposed either to pre-, peri-, or postnatal thiamine deficiency. To control the effects of undernourishment generated by different thiamine deficiencies, every treatment group had its own pair-fed control pup from a non drug-treated but undernourished dam. Seven different developmental abilities (exploratory activity, emotional reaction, hind paws lifting reflex, wire grasping times, crawling and leap execution latencies, and nociception) were recorded in the offspring from the 10th to the 45th postnatal day. The vulnerability of developing brain to the specific lack of B1 vitamin increases from prenatal (28%) to perinatal (43%) and postnatal periods (57%).

Modification of thiamine pyrophosphate dependent enzyme activity by oxythiamine in Saccharomyces cerevisiae cells

Abstract: Oxythiamine is an antivitamin derivative of thiamine that after phosphorylation to oxythiamine pyro phosphate can bind to the active centres of thiamine-dependent enzymes. In the present study, the effect of oxythiamine on the viability of Saccharomyces cerevisiae and the activity of thiamine pyrophosphate dependent enzymes in yeast cells has been investigated. We observed a decrease in pyruvate decarboxylase specific activity on both a control and an oxythiamine medium after the first 6 h of culture. The cytosolic enzymes transketolase and pyruvate decarboxylase decreased their specific activity in the presence of oxythiamine but only during the beginning of the cultivation. However, after 12 h of cultivation, oxythiamine-treated cells showed higher specific activity of cytosolic enzymes. More over, it was established by SDS-PAGE that the high specific activity of pyruvate decarboxylase was followed by an increase in the amount of the enzyme protein. In contrast, the mitochondrial enzymes, pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase complexes, were inhibited by oxythiamine during the entire experiment. Our results suggest that the observed strong decrease in growth rate and viability of yeast on medium with oxythiamine may be due to stronger inhibition of mitochondrial pyruvate dehydrogenase than of cytosolic enzymes.

Thiamine Status of Cayuga Lake Rainbow Trout and Its Influence on Spawning Migration

Abstract: Rainbow trout Oncorhynchus mykiss in Cayuga Lake, New York, appear to be suffering from a thiamine deficiency because their progeny develop general weakness, loss of equilibrium, and increased mortality, which are prevented by treatment with thiamine Thiamine status and its effect on adults are unknown In 2000 and 2002, we captured, tagged, and released 64 and 189 prespawning rainbow trout, respectively, in Cayuga Inlet at a collection weir to evaluate their thiamine status and the effect of thiamine injection (150 nmol/g) on instream migration Half of the rainbow trout in each year (32 in 2000 and 95 in 2002) were injected with thiamine and half were uninjected; all rainbow trout were released above the weir to continue their upstream migration By means of electrofishing in 2000, we recaptured significantly more thiamine-injected (N = 7) than uninjected (N = 0) rainbow trout approximately 70–93 river kilometers upstream from the weir In 2002, the concentration of thiamine in the muscle of