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PubMed1986

Oral treatment of polioencephalomalacia and subclinical thiamine deficiency with thiamine propyl disulphide and thiamine hydrochloride.

Thiaminase type I production by Bacillus thiaminolyticus and activity in vitro were repressed by the primary substate thiamine and by thiamine monophosphate and thiamine propyl disulphide. At thiamine concentrations of 300-3000 mumol/l production of active enzyme by B. thiaminolyticus, and activity of purified enzyme, were totally repressed. Growth of B. thiaminolyticus was inhibited by thiamine propyl disulphide at 3000 mumol/l. Activity of purified thiaminase was lost when incubated with ruminal fluid from healthy thiaminase free sheep. Enzyme activity was also lost when exposed to mildly alkaline conditions but was stimulated and stabilized against heat denaturation if treated with dithiothreitol. Thiaminase activities in the ruminal fluids of cases of ovine polioencephalomalacia were repressed within 2 h of oral administration of thiamine propyl disulphide. Blood pyruvate levels and transketolase activities were restored to normal following treatment. Treated animals recovered clinically and were returned to pasture.

Administration, Oral↗
PubMed1987

Tissue minerals of magnesium-deficient rats with thiamine deficiency and excess.

To clarify the influence of thiamine deficiency or a dietary excess of thiamine on the mineral balance in magnesium-deficient animals, the following six different synthetic diets were fed to Wistar rats. Group 1: thiamine and magnesium-deficient; group 2: thiamine-deficient, magnesium-deficient; group 3: thiamine-sufficient, magnesium-deficient; group 4: thiamine-sufficient, magnesium-sufficient; group 5: thiamine excess, magnesium-deficient; group 6: thiamine excess, magnesium-sufficient. Rats were sacrificed after 4 weeks of these dietary regimens. In the magnesium-deficient groups, magnesium levels in serum, bone and heart decreased; calcium levels in serum and heart increased and, in contrast, calcium levels in bone decreased. These changes in mineral concentration seen in magnesium-deficient animals, as well as kidney weight changes, were alleviated significantly when the animals were also deficient in thiamine. It can be presumed that thiamine deficiency inhibits magnesium depletion and, consequently, the influence of magnesium deficiency is less significant in the thiamine- and magnesium-deficient animals. In regard to trace elements, the significant changes seen in magnesium-deficient rats were as follows: zinc in liver, muscle and blood increased and that in bone decreased. Copper in blood, kidney, muscle and heart increased and that in liver decreased. Iron in serum, liver, spleen and kidney increased and that in whole blood decreased.

Animals↗
PubMed1987

Increased axonal transport in peripheral nerves of thiamine-deficient rats.

Thiamine deficiency has been implicated as a significant contributing factor in the development of peripheral neuropathies in chronic alcoholic patients. We hypothesized that thiamine deficiency may lead to an alteration in axonal transport because it has been associated with "dying-back" neuropathies and its importance in neural tissue has been demonstrated with antimetabolites. To test this possibility rats were made thiamine-deficient by feeding a liquid diet lacking thiamine. Control rats were pair-fed a complete liquid diet. The deficiency developed after 3 to 4 weeks and was evidenced by anorexia, weight-loss, and a significant increase in the erythrocyte transketolase activity ratio. Also, the sural nerve conduction velocity was found to be significantly reduced in these animals (18.74 m/s) relative to that of pair-fed control rats (31.99 m/s). In vitro transport experiments utilizing dorsal root ganglia-sciatic nerve preparations indicated that twice as much [35S]methionine-labeled protein accumulated at a ligation by fast transport in the thiamine-deficient rats as in nerves of their pair-fed controls. There was no difference in the level of incorporation of radioactive precursor into the dorsal root ganglia. The increase in transport suggests that thiamine deficiency per se has no detrimental effects on the transport machinery and process, but may indicate extensive regenerative activity in the distal portions of these axons.

Animals↗
PubMed1998

Increased neuronal cell survival after L-deprenyl treatment in experimental thiamine deficiency.

Experimental thiamine deficiency results in a reproducible pattern of selective neuronal cell death. Events such as blood-brain barrier breakdown, N-methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity, and increased reactive oxygen species have been implicated in thiamine deficiency-induced neural loss. L-deprenyl protects dopaminergic, noradrenergic, and acetylcholinergic neurons from neurotoxic, mechanical, and excitotoxic damage. In the present study, the effects of l-deprenyl on neuronal cell survival were examined in rats made thiamine deficient by daily administration of the central thiamine antagonist pyrithiamine (0.5 mg/kg s.c.). Rats assigned to thiamine deficient or control groups received daily injections of l-deprenyl (0.25, 0.5, or 1.0 mg/kg/day i.p.) or vehicle until they reached a state of severe thiamine deficiency (loss of righting reflex). At this stage, thiamine status was restored by daily injections of thiamine (10 mg/kg s.c.) for 3 days, after which the animals were killed, and their brains were processed for neuronal cell counts (cresyl violet staining), astrocytic proliferation [glial fibrillary acidic protein (GFAP) immunohistochemistry], and monoamine oxidase B (MAO-B) activity. All rats receiving l-deprenyl (all doses) had significantly decreased neuronal cell loss in thalamic nuclei, in the inferior colliculus, and in the inferior olive and had a concomitant decrease in reactive astrocytic proliferation compared with the thiamine-deficient, vehicle-treated rats. The neuroprotective effects of l-deprenyl in thiamine deficiency induced brain damage most likely result from its properties other than its effects as an MAO-B inhibitor.

Animals↗
PubMed2004

Fatal metabolic acidosis caused by thiamine deficiency.

Acute thiamine deficiency, an uncommon cause of hemodynamic instability in Western countries, may be manifested by acute heart failure and neurological deficits. Severe metabolic acidosis is one of its least recognized features. We present a report of foreign workers who complained of weakness and lower limb edema and were found to have acute thiamine deficiency. One died of refractory metabolic acidosis and shock, and the diagnosis was reached post mortem. Thiamine deficiency should be considered in every case of severe lactic acidosis without an obvious cause, especially in high-risk populations (malnourished, alcoholics, Far-East workers, etc). Whenever it is suspected, empiric treatment with thiamine should be initiated immediately. Physicians who care for populations at risk should be familiar with the clinical spectrum of nutritional deficits, and monitor the nutritional habits of these patients carefully. The treatment is inexpensive and devoid of adverse effects. Moreover, delaying thiamine administration in patients with deficiency may cause severe life-threatening metabolic acidosis and affect recovery. The prophylactic use of thiamine in a high-risk population, even before blood levels are received, may be cost effective.

Acidosis↗
PubMed1995

Blood-brain barrier abnormalities in vulnerable brain regions during thiamine deficiency.

Experimental thiamine deficiency (TD) is a classical model of metabolic encephalopathy and selective cell loss in the brain resulting from a generalized, low-grade oxidative deficit. Late stages of TD are characterized by hemorrhages in the brain indicating a disruption of the blood-brain barrier (BBB). However, the relation of the breakdown of the BBB to selective cell loss in TD is not understood. The current studies examined the BBB at different stages of TD using immunoglobulin G (IgG) as an indicator of BBB integrity. Adult rats received thiamine-deficient diet ad libitum and daily injections of the thiamine antagonist pyrithiamine. IgG immunoreactivity increased in the inferior colliculus and inferior olive as early as 10 days after the initiation of TD and prior to the onset of cell death and hemorrhage. After 11 or 12 days, IgG immunoreactivity increased in multiple vulnerable regions. On Day 13, intense IgG immunoreactivity was found in regions of tissue damage and hemorrhage such as the thalamus, inferior colliculus, mammillary body, medial geniculate nucleus, medial vestibular nucleus, and inferior olive. Nonvulnerable regions displayed little or no IgG immunoreactivity. Immunoblotting analysis confirmed the presence of IgG in vulnerable areas such as the thalamus and inferior colliculus but not in preserved regions such as the cortex. Preliminary electron microscopy of capillary endothelia in areas of IgG accumulation in the thalamus at Day 13 revealed perivascular edema and intact interendothelial tight junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Novel neuritic clusters with accumulations of amyloid precursor protein and amyloid precursor-like protein 2 immunoreactivity in brain regions damaged by thiamine deficiency.

Experimental thiamine deficiency (TD) is a classical model of a nutritional deficit associated with a generalized impairment of oxidative metabolism and selective cell loss in the brain. In rats, TD-induced cell degeneration is accompanied by an accumulation of amyloid precursor protein (APP)/amyloid precursor-like protein 2 (APLP2) immunoreactivity in abnormal neurites and perikarya along the periphery of, or scattered within, the lesion. Prompted by these data and our previous findings of a genetic variation in the development of TD symptoms, we extended our studies to mice. C57BL/6, ApoE knockout, and APP YAC transgenic mice received thiamine-deficient diet and pyrithiamine injections. Unlike rats, APP/APLP2-immunoreactive neurites in all strains of mice were sparsely scattered within damaged areas and did not delimit the thalamic lesion. In addition, abnormal clusters of intensely immunoreactive neurites occurred only in areas of damage including the thalamus, mammillary body, and inferior colliculus. The clusters appeared as either irregular clumps or round or oval rosettes that strikingly resembled the neuritic component of Alzheimer amyloid plaques. However, immunostaining using various antisera to synthetic amyloid beta-protein (A beta 1-40) and thioflavine S histochemistry failed to show evidence of a component of A beta Neither APP/APLP2-immunoreactive clusters nor amyloid plaques were observed in the brain from patients with Wernicke-Korsakoff syndrome, the clinical manifestation of TD in man. Our results demonstrate species (i.e., genetic) differences in the response to TD-induced damage and support a role for APP and APLP2 in the response to brain injury. This is the first report that chronic oxidative deficits can lead to this novel pathology.

Amyloid beta-Protein Precursor↗
PubMed2004

[Dysfunction of serotonergic systems in thiamine-deficient diet fed mice: effects of SSRI on abnormality induced by thiamine deficiency].

Mice fed a thiamine deficient (TD) diet, showed some abnormal behaviors such as amnesia and mood abnormality. It is known that several neurons, especially marked in serotonergic neuron, are damaged in humans and rodents in the earlier phase of TD. The symptoms derived from dysfunction of serotonergic neurons are observed in Wernicke-Korsakoff patients (WKS)-derived TD, and it is known that fluvoxamine is effective for WKS. However, the mechanism of this dysfunction is still unclear. For that reason, we studied the relative mechanism between abnormal behaviors and selective dysfunction of serotonergic neurons in TD animals. As a result, this dysfunction by TD is much affected by the brainstem region. But the effect of fluvoxamine on depressive symptoms in WKS patients is not reported; therefore we also studied the effects of fluvoxamine on the depressive behaviors in TD mice as a model of WKS. The increase of immobility time in a forced swimming test as depressive behavior in TD mice was significantly inhibited by fluvoxamine, suggesting an improvable effect on depressive symptoms. With those results of ours, the possible mechanisms between the abnormal behaviors derived from the dysfunction of serotonergic neurons and the role of serotonin in TD and WKS are reviewed here.

Animals↗
PubMed1997

Apoptosis is restricted to the thalamus in thiamine-deficient rats.

Thiamine deficiency (TD) produces lesions in the thalamus, mamillary and medial geniculate nuclei, and inferior colliculus. To clarify the pathogenesis of these lesions, we examined the occurrence of hallmarks of apoptosis following TD in rat brain. Histological assessment showed apoptotic cells in the thalamus and medial geniculate nucleus but not in the inferior colliculus. We used terminal deoxynucleotidyl transferase-mediated deoxyuridine (dUPT)-biotin nick-end labelling (TUNEL) and gel electrophoresis to demonstrate that TD is associated with apoptotic cell death. In the thalamus, DNA fragmentation appeared from day 14 of deficiency and preceded the appearance of ataxia. The inferior colliculus and mamillary nucleus were without electrophoretic DNA fragments, and only rare TUNEL-positive labelling was observed. This model shows a rare combination of both apoptosis and necrosis in the same lesioned brain.

Animals↗
PubMed2000

Prevalence of thiamin deficiency in anorexia nervosa.

OBJECTIVE: Deficiency of thiamin (vitamin B1) causes a range of neuropsychiatric symptoms that resemble those reported in patients with anorexia nervosa (AN) but the prevalence of thiamin deficiency in AN has not been reliably established. This study was designed to investigate the prevalence of thiamin deficiency in AN. METHOD: Thirty-seven patients attending a specialist eating disorders unit and meeting all or some of the DSM-IV criteria for AN were compared with 50 blood donor controls. All subjects underwent measurement of erythrocyte transketolase activation following the addition of thiamin pyrophosphate, the standard biochemical test for thiamin deficiency. Deficiency was defined as a result more than 2 SD above the mean of the control population. RESULTS: Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption. DISCUSSION: Thiamin deficiency may account for some of the neuropsychiatric symptoms of AN and routine screening or supplementation may be indicated.

Adolescent↗
PubMed1996

Regional reductions of transketolase in thiamine-deficient rat brain.

Thiamine deficiency impairs oxidative metabolism and causes metabolic encephalopathy. An early reduction in transketolase (TK) activity may be an important pathogenic event. To assess the role of TK, we have delineated the regional/cellular distribution of TK protein and mRNA in adult rat brain in pyrithiamine-induced thiamine deficiency. TK activity declined in both vulnerable and spared regions. Immunoblots showed a parallel reduction of TK protein. With a few exceptions, immunocytochemistry indicated an overall decline of TK immunoreactivity and the decrease was not specific to vulnerable areas. In contrast to the pronounced, general decline of TK protein, in situ hybridization revealed a regional decrease of 0-25% of TK mRNA in thiamine deficiency. Northern blots indicated a similar level of TK mRNA in whole brain in thiamine deficiency. These results show that the decline of TK activity results from a proportional decrease of TK protein, and the deficiency may be due to an instability of TK protein or an inhibition of TK mRNA translation. The lack of correlation of the distribution, and the absence of specific alteration, of TK in affected regions suggest that the reduced TK may not be linked directly to selective vulnerability in thiamine deficiency.

Animals↗
PubMedDate not supplied

[Isoenzyme spectrum and kinetic properties of pyruvate kinase from the liver of thiamine-deficient rats].

Thiamine-deficiency in animals induced by everyday subcutaneous administration of oxythiamine in a dose of 4, 40 and 100 mg/kg of weight for 10 days results in a decrease of the total activity of pyruvate kinase in the liver tissue and does not affect the mentioned index in the kidney and heart tissues. It is shown that as a result of the enzyme fractionation in the column with DEAE-cellulose the total activity of pyruvate kinase in the liver tissue of rats with thiamine-deficiency decreases due to L-isoform while the content of M-isoform remains unchanged. Thiamine deficiency does not affect kinetic characteristics of the L-isoform, extracted from the liver and this shows the absence of changes in the degree of phosphorylation of pyruvate kinase L-isoform under these conditions.

Animals↗
PubMed1963

Pharmacological responses of thiamine-deficient rat tissues.

Rats were rendered deficient in thiamine by feeding a synthetic diet free of the vitamin. Responses of the isolated heart to acetylcholine, adrenaline, noradrenaline and isoprenaline, and of the phrenic nerve-diaphragm preparation to tubocurarine, gallamine and eserine, were compared with responses of tissues obtained from littermate rats pair-fed an identical diet with the addition of 25 mug of thiamine hydrochloride per day. In thiamine-deficient tissues eserine failed to produce sustained potentiation of the twitch response of the phrenic nerve-diaphragm preparation to single supramaximal nerve stimuli. The perfused thiamine-deficient heart was more sensitive to acetylcholine, adrenaline, noradrenaline and isoprenaline, which produced greater negative or lesser positive chronotropic and inotropic effects. There was no significant difference in the response of the phrenic nerve-diaphragm preparation to tubocurarine and gallamine, or to eserine with faradic stimulation.

Acetylcholine↗
PubMed1975

Reversible impairment of cerebral DNA synthesis in thiamine deficiency.

The effect of thiamine deficiency on rat brain DNA and RNA synthesis was investigated. Thiamine deficiency, culminating in encephalopathy (symptomatic stage) was induced by dietary thiamine deprivation of 4 to 5 weeks. The encephalopathy could be completely reversed within 6 hours by paranteral administration of thiamine. Controls consisted of pair-fed and ad libitum-fed littermates given the same diet supplemented with thiamine. Brain DNA and RNA synthesis was determined by administration of labeled thymidine, orotic acid, or adenine into the cerebral ventricle and measuring the incorporation of the appropiate labeled precursor into DNA or RNA. Thiamine deficiency(symptomatic stage) had no effect on net DNA and RNA level in any brain area studied. Also, no consistent alteration of brain RNA synthesis was shown in severe thiamine seficiency. By contrast, DNA synthesis in symptomatic thiamine-deficient ratswas reduced to 22, 37, 31, and 19 percent, respectively; of pair-fed control values in the cortex, brain stem, cerebellum, and subcortical structures (p less than 0.05). Thedegree of depressed DNA synthesis increased with the extent and duration of thiaminedeprivation. Following reversal of the encephalopathy with parenteral thiamine, DNAsynthesis in all brain areas increased markedly to and above control values. Thses data indicate that the thiamine deficiency state interferes with the synthesis ofsome discrete DNA pool(s) in the brain. This effect may be due to thiamine deficiency per se and /or some thiamine-induced impaired food assimilation or utilization.

Adenine↗