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PubMed1984

Effects of histaminergic drugs on muricide induced by thiamine deficiency.

Male Wistar rats maintained on a thiamine deficient diet showed mouse-killing aggression (muricide). On the 30th day of experimental feeding, the incidence of this muricide was about 70%. Intracerebroventricular histamine suppressed the muricide induced by thiamine deficiency in a dose-dependent manner. Histamine H1-receptor blocking agents such as diphenhydramine, promethazine and chlorpheniramine also showed muricidal suppression, but astemizole which lacks central effects did not show muricidal suppression. Mianserin and iprindole showed muricidal suppression, but metiamide i.p. did not. On the 20th day of experimental feeding, the incidence of this muricide was 45.5%. Histamine synthesis inhibitors such as brocresine or alpha-fluoromethylhistidine could not enhance the muricide on non-killer-rats, but really suppressed the thiamine deficient killer-rats. The results of this paper suggested that muricide induced by thiamine deficiency is not mediated by the central histaminergic system, but pharmacologically characterized by antidepressants, antihistamines and histamine synthesis inhibitors.

Aggression↗
PubMed1980

[Studies on the effects of thiamine deficiency on rat testes (author's transl)].

Using male rats fed a thiamine deficient diet from the age of 35-days, an investigation was made of the effects on testicular tissue after 30 days of thiamine deficiency. It was found that: 1) In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied and there was a decrease in the number of primary spermatocytes and spermatogonium, but a moderate increase in the number of sertoli cells. Furthermore, spermatids and spermia were rarely seen in tubuli which contained multinuclear giant cells. In the group of rats not having erections, moderate interstitial edema was seen and there was notable degeneration and reduction in the number of primary spermatocytes and spermatogonium. 2) In the group injected with thiamine hydrochloride after 21 days of thiamine deficient feeding, moderate interstitial edema was seen and the seminiferous tubuli were atrophic. 3) In the pair-fed group, there was a marked edema of interstitial tissue and an atrophy of seminiferous tubulus. 4) With regard to the effects of thiamine deficiency on the polyamine contents of the testicles, there was a marked decrease in spermidine content on the 12th day of feeding and a marked increase of spermine content on the 30th day. The spermidine/spermine ratio, which is high during periods of active cell differentiation and proliferation, was found to be significantly decreased in the thiamine deficient animals on both the 12th and 30th days of thiamine deficiency. Thus, it was clarified that thiamine deficiency causes disturbances in cell differentiation and proliferation in rat testes.

Animals↗
PubMed1985

Muricidal suppression by histidine and its antagonism by alpha-fluoromethylhistidine in thiamine deficient rats.

Male Wistar rats maintained on a thiamine deficient diet showed mouse-killing behavior (muricide). On the 30th day of experimental feeding, the incidence of muricide was 70%. Intraperitoneal (ip) injection of L-histidine, a precursor of brain histamine, suppressed the muricide induced by thiamine deficiency in a dose dependent manner. The ED50 for muricidal suppression by histidine alone was 155 mg/kg (95% confidence limits; 107.6-223.2 mg/kg). Rotarod performance was concurrently examined as an index of behavioral toxicity. High doses of histidine produced insignificant changes in rotarod performance except at 30 min after administration. Histidine exhibited a specific inhibitory activity on the muricide induced by thiamine deficiency. Pretreatment with alpha-fluoromethylhistidine (alpha FMH), a potent and specific inhibitor of histidine decarboxylase, produced a reduction in the effects of histidine. The ED50 was 400 mg/kg ip (95% confidence limits; 169.5-944 mg/kg) by histidine in combination with alpha FMH 50 mg/kg ip. However, alpha FMH also exhibited specific inhibitory activity on muricide. Either activation or inhibition of the central histaminergic system resulted in muricidal suppression in thiamine deficient rats. These data support the view that muricide induced by thiamine deficiency is not mediated by the central histaminergic system.

Aggression↗
PubMed1989

Modulation of A and B cell functions by tolbutamide and arginine in the pancreas of thiamine-deficient rats.

The effects of administration of glucose orally and tolbutamide or arginine intravenously on insulin and glucagon secretion and blood glucose level were studied in normal and thiamine-deficient rats. In thiamine deficiency, insulin secretion and glucose tolerance were impaired during glucose ingestion. Tolbutamide decreased the blood glucose level in both control and thiamine-deficient rats but its stimulatory effect on insulin secretion was minimal in thiamine-deficient rats unlike the control animals. Arginine did not alter substantially the blood glucose or insulin in thiamine-deficient rats, whereas it increased the insulin level in control rats. The fasting plasma glucagon level was high in thiamine deficiency. Tolbutamide increased the plasma glucagon in control rats, but did so only marginally in thiamine-deficient rats. Arginine also increased the glucagon secretion throughout the period of study in control rats. In thiamine-deficient rats the glucagon secretion was pronounced only after 20 min of arginine administration. These results suggest that an unimpaired glucose metabolism is a prerequisite to induce proper insulin secretion. Only proper insulin secretion can check the glucagon secretion rather than the increased glucose level. Hypoglycemia can induce glucagon secretion independent of the insulin level.

Animals↗
PubMed1976

[Passive electrical constants of skeletal muscular fibres studied in different muscles of normal and thiamine deficient rats (author's transl)].

10 Some effects of thiamine deficiency were studied in three skeletal rat muscles, having different proportions of "fast" and "slow" fibres: extensor longus digiti IV (a nearly pure fast muscle), soleus (having a predominant population of slow fibres) and diaphragm muscle (mixed fibre population). 20 Cross section area of fibres (fig. 2) is reduced in thiamine deficient animals, mostly for fast fibres having a glycolytic metabolism, the histochemical profile of which tends to become similar to that of slow fibres, in which oxydative metabolism is predominant, as shown by a marked increase in succinodehydrogenase activity. 30 Measurements of resting potential E, of membranes time constant tau and of fibre input resistance R were performed in normal and thiamine deficient muscles (table I). R and tau were obtained from square pulse analysis, using a double shifted sampling method permitting the use of a single microelectrode. E is not greatly affected by thiamine deficiency. tau changes appear not to be significant, except for fast fibres from extensor longus muscle, where tau is slightly reduced. R is increased in thiamine deficient animals (fig. 3). 40 Changes in R and tau do not exactly follow the predictions of cable theory, if one assumes that a purely dimensional factor is involved. Thus, the view that thiamine deficiency does not change basic passive electrical constants of fibres (membrane specific resistance and capacity, myoplasm resistivity) can be considered only as a first approximation. 50 R and tau values obtained in normal muscles are larger than data taken from other studies. The reasons for this discrepancy are discussed. It is suggested that diet differences may play a role.

Animals↗
PubMed1990

Changes in brain lipid composition in thiamine deficient rats.

Brain lipid composition was studied in thiamine deficient rats treated with thiamine antimetabolites (oxythiamine: OT, and pyrithiamine: PT) and thiamine deficient diet (TDD). After intraperitoneal injection of OT (40 mg/kg/day) or TDD feeding for 6 days, body weight gain decreased. However, the PT (500 micrograms/kg/day) treated rats or the pair fed control (PFC: TDD + thiamine of 5 mg/kg, i.p.) showed no decrease in body weight gain compared with the regular diet control (C). Brain lipid levels (total lipid, total cholesterol, triglyceride, phospholipid, sphingomyelin and cerebroside) were examined in four brain regions (cerebral cortex, subcortical structure, brain stem and cerebellum). Total lipid level increased in four regions in OT or TDD treated rats, but total lipid level in the cerebellum in PT treated rats decreased. Total cholesterol level increased in all treated rats, while the triglyceride level in the brain stem decreased dramatically in OT or TDD treated rats. Cerebroside levels of four regions in the PT, OT or TDD group remarkably decreased, and PFC rats showed a significant improvement of the decrease in cerebroside level. It is conceivable that these changes in brain lipid composition provided some clues for the histological and morphological changes of the brain as manifested by the myelin degradation in acute thiamine deficiency.

Animals↗
PubMed1981

Thiamine deficiency and glyoxylic acid.

The effect of thiamine deficiency on glyoxylic acid metabolism in mice and rats was investigated to determine whether the vitamin deficiency results in gross effects on glyoxylate levels via an alteration in the activity of alpha-ketoglutarate:glyoxylate carboligase. Thiamine-deprived or pyrithiamine-treated mice did not show a decreased oxidation of [1-14C]glyoxylate to respiratory CO2; there was some decrease in the conversion of [2-14C]glyoxylate into CO2 by pyrithiamine-treated mice, but not by thiamine-deprived animals. Dietary thiamine deprivation caused a decrease in carboligase levels in liver but no effect on levels in three brain regions. Pyrithiamine treatment had no significant effect on liver carboligase activities, but did decrease the levels in cerebrum, cerebellum and brainstem. Thiamine-deprived and pyrithiamine-treated mice showed decreased urinary glycolic acid excretion Glyoxylic acid excretion by thiamine-deprived rats was monitored in order to re-examine a previous report by another laboratory that glyoxyluria occurs under these conditions. Trace amounts of glyoxylate could be detected in the urine of rats fed thiamine-deficient diet for 3-5 weeks, but urinary glyoxylate was not detectable at later stages of thiamine deprivation. These results do not support a significant role for alpha-ketoglutarate:carboligase activity in the primary etiology of thiamine deficiency syndromes.

Aldehyde-Ketone Transferases↗
PubMedDate not supplied

[Ultrastructure of the rat gastric mucosal parietal cells in thiamine deficiency].

The effect of the thiamine deficient diet on the ultrastructure and secretory response of parietal cells of the rat gastric mucosa was studied. The control group consisting of fasting animals showed 60% of the parietal cells to be in a presecretory state. Subcutaneous administration of histamine to the control animals was accompanied by secretion of 512 +/- 128 mkekv H+ over 3 hours, with only 18% of the parietal cells remaining not involved in the secretory process. In thiamine-free diets the number of secreting cells in fasting animals amounted to 23%, rising to 35% after histamine administration. At the same time a three-fold decrease in the secretory response (170 +/- 21 mkekv H+ over 3 h) was observed. Thiamine deficiency in the diet is also accompanied by inhibition of the transketolase activity in the gastric mucosa homogenate, which varied from 0.706 +/- 0.032 mcmole (control animals) to 0.344 +/- 0.034 mcmole of sedoheptuloso-7-phsophate/h per 1 mg protein (test animals). Potentialities of the pentose cycle participation in secretion are discussed.

Animals↗
PubMed1998

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency.

During pyrithiamine-induced thiamine deficiency (PTD), specific regions of the brain develop histological damage. The basis of this selective vulnerability is unknown but the mechanism may involve a glutamate-mediated excitotoxic process in affected structures, leading to alterations in membrane potential and disturbances in calcium homeostasis. In this study, we have examined the volume of distribution of [3H]nimodipine, an L-type voltage-sensitive calcium channel (VSCC) antagonist, in the brain of the PTD rat. An increase in specific binding of [3H]nimodipine was detected only in the posterior thalamus at the symptomatic stage, immediately following the loss of righting reflexes (P < 0.0001). There was also an increase in nonspecific binding in the medial geniculate and inferior colliculi. Replenishment with thiamine at the symptomatic stage returned [3H]nimodipine binding to normal levels. These findings provide evidence that depolarization and activation of L-type VSCCs occur in the posterior thalamus and may contribute to the appearance of histological lesions in this structure during experimental thiamine deficiency.

Animals↗
PubMed1991

Changes in blood pressure and heart rate following dietary-induced thiamine deficiency in muricide rats.

The purpose of this study was to further investigate the effects of thiamine deficiency on blood pressure and heart rate in connection with muricide in rats. The rats, maintained on a thiamine-deficient diet, showed mouse-killing response (muricide). The incidence of muricide was 72% on day 30. In this period, marked decreases in body weight, heart rate and blood pressure were observed in thiamine-deficient rats. The changes of body weight and blood pressure were statistically different from pair-fed and control groups. In thiamine-deficient group, blood pressure of thiamine-deficient killer rats was lower than that of thiamine-deficient non-killer rats. It is noteworthy that recovery of bradycardia and hypotension was observed in thiamine-deficient rats after providing them with enough thiamine, but muricide was not recovered. Thus, it is unlikely that there is a direct correlation between muricide and the disturbance of cardiovascular system in thiamine-deficient killer rats. The present findings showed that muricide induced by thiamine deficiency has different physiological bases from the other types of muricide, i.e., olfactory bulb-lesioned muricide.

Aggression↗
PubMed1985

Intrauterine growth retardation caused by dietary biotin and thiamine deficiency in the rat.

The effects on fetal development of maternal biotin deficiency, alone and in conjunction with thiamine deficiency, were investigated in rats. Fetuses from dams given biotin-deficient diet throughout gestation demonstrated only some characteristics of intrauterine growth retardation (IUGR) including abnormal liver weight and a higher brain/liver ratio. However, fetuses from dams given biotin-thiamine-deficient diet and daily pyrithiamine (a thiamine antagonist used to insure thiamine deficiency) injections demonstrated severe IUGR along all of the fetal parameters investigated. We conclude that biotin and thiamine deficiency during intrauterine growth of the fetus may be partially responsible for the development of IUGR, a frequent concomitant of fetal alcohol syndrome.

Animals↗
PubMed1991

Effects of thiamine deficiency on the biosynthesis of insulin in rats.

The effect of thiamine deficiency on insulin biosynthesis was studied. In thiamine deficient rats the total pancreatic protein content was not altered when compared to control rats whereas the pancreatic insulin content was decreased. Though the in vivo incorporation of 3H-leucine and the in vivo conversion of U-14C-glucose into proinsulin and insulin were not affected in thiamine deficient rats, the tolbutamide induced increased in vivo incorporation of 3H-leucine and in vivo conversion of U-14C-glucose into proinsulin and insulin was not seen in thiamine deficient rats. These results suggest that the biosynthesis of insulin is impaired in thiamine deficiency. Even tolbutamide could not increase the biosynthesis of insulin in this condition.

Animals↗
PubMed1976

Thiamine transport in thiamine-deficient rats. Role of the unstirred water layer.

As part of a systematic study of alcoholism and thiamine absorption, the effect of diet-induced thiamine deficiency and the role of the unstirred water layer on the thiamine transport were investigated. Using 3H-labeled dextran as a marker of adherent mucosal volume, jejunal uptake of 14C-labeled thiamine hydrochloride was measured, in vitro, in thiamine-deficient rats and pair-fed controls. Uptake of low thiamine concentrations (0.2 and 0.5 muM) was greater in the thiamine-deficient rats than in the controls. In contrast, uptake rates for high thiamine concentrations (20 and 50 muM) were similar in both groups. While Jmax was unaltered, Km was decreased in thiamine deficiency, suggesting a decrease in unstirred water layer thickness. Accordingly, the thickness of the water layer was measured in both groups of animals and correlated with Jmax and Km under unstirred and stirred conditions. Without stirring, there was no difference in Jmax between the two groups. In contrast, both Km and the water layer were reduced in the thiamine-deficient rats. With stirring, Jmax was not affected, but both Km and the water layer thickness were reduced to similar values in both groups. Reversal of thiamine deficiency resulted in the return of thiamine uptake and the unstirred water layer thickness to control values. These data support the concept of a dual system of thiamine transport and emphasize the role of the unstirred water layer as an important determinant of transport kinetics not only under physiologic situations but also in diet-induced rat thiamine deficiency, a model for a clinical patholigical state. The decrease in the unstirred water layer thickness in thiamine deficiency may be also viewed as a possible adaptive mechanism to facilitate absorption of meager supplies of thiamine.

Animals↗
PubMed1977

Milk composition and thiamine transfer in thiamine deficient rats.

Milk composition was determined in rats maintained on a thiamine deficient diet from the 10th day of pregnancy. Percentage of thiamine transfer was reduced after the 14th postpartum day. Milk composition of thiamine deficient dams 18 days postpartum revealed similar protein and amino acid levels in both thiamine deficient and control rats, whereas milk protein fractions showed some differences. Milk lactose levels were depressed in thiamine deficient rats. Fatty acid content was higher in milk of thiamine deficient than in pair fed and adlibitum controls. The supply of a larger proportion of calories from lipids rather than carbohydrates may have clinical significance.

Amino Acids↗
PubMedDate not supplied

Early edematous lesion of pyrithiamine induced acute thiamine deficient encephalopathy in the mouse.

Pyrithiamine induced acute thiamine deficient encephalopathy in the mouse is one of the possible animal models of human Wernicke-Korsakoff syndrome. In this experiment, the adult male Swiss Mice, treated with a daily subcutaneous injection of pyrithiamine in conjunction with a thiamine deficient diet, abruptly developed unique encephalopathic signs on day 10. In the animals sacrificed immediately after the onset of the disease, the gross examination of the brains revealed a small number of minute hemorrhagic lesions in the thalamus, mammilary bodies and pontine tegmentum, including the medial and lateral vestibular nuclei. When spared the hemorrhage, these regions appear intact grossly and in paraffin sections, but were found to be significantly altered in Epon sections. In semithin Epon sections of the pontine tegmentum, there was edematous swelling of all the astrocytes and oligodendrocytes and occasional myelin sheaths. By electron microscopy, the edema of astrocytes involved both nucleus and cytoplasm extensively. The oligodendroglial edema was severe in the peripheral cytoplasm, particularly in the inner loops of the myelin sheaths and only moderately in the nuclei, perinuclear cytoplasm and outer loops. Disintegration of the myelin lamellae occurred when edema of the inner loops had advanced. The axis cylinders surrounded by the edematous loops were essentially intact. In contrast to such glial cell damage, the nerve cells and blood vessels were not altered. These findings suggest that (1) astroglia and oligodendroglia are the cells most sensitive to thiamine deficiency and (2) the resultant glial cell injury is the initial change of thiamine deficient encephalopathy in man and in experimental animals.

Animals↗
PubMedDate not supplied

Comparative effects of developmental thiamine deficiencies and ethanol exposure on the morphometry of the CA3 pyramidal cells.

Maternal alcoholism and thiamine deficiency are frequently considered to be the causal agents of the central nervous system (CNS) damage associated with mental retardation in the offspring. For further understanding of pathological mechanisms underlying CNS damage in both disorders, histological studies were undertaken in developing rats to compare the hippocampus CA3 pyramidal cells measurements and density between three patterns of thiamine deficiency and chronic alcohol exposure. Female rats were given thiamine-deficient diet during different periods of gestation and lactation to obtain pre-, peri-, and postnatal thiamine-deficient pups. Twelve percent ethanol/water drinking fluid was given to mothers throughout gestation and lactation to obtain ethanol-exposed pups. Thiamine was administered during developmental ethanol exposure to assess the extent of interference between ethanol and thiamine metabolism. Nondrug-treated dams were allowed ad lib access to food and water during gestation and lactation to yield control pups. Hippocampus histology was performed in 45-day-old rats, and the CA3 pyramidal cells measurements and density assessed and compared between all treatment groups. It appears that the mean nuclear size of pyramidal cells in the field CA3 was significantly reduced in all the treatments compared to the control. While the mean nuclear size decreased more severely in development ethanol exposure than in the three patterns of thiamine deficiency, no significant difference was noted when pre-, peri-, and postnatal thiamine-deficient rats were compared. However, thiamine administration during developmental ethanol exposure partially restored the mean nuclear size. In contrast, comparisons between ethanol-exposed pups and the three patterns of thiamine-deficient pups, exhibited similar intensity in the deficit of CA3 pyramidal cells. Cell loss generated by ethanol treatment was not suppressed by thiamine administration. Common and separate mechanisms underlying the effects of alcohol intoxication and thiamine deficiency on cell death and cell atrophy were suggested.

Animals↗
PubMed1985

Enhanced sensitivity of cerebellar Purkinje cells to iontophoretically-applied serotonin in thiamine deficiency.

Electrophysiological aspects of thiamine depletion in the rat induced by dietary deficiency are described. Behavioral changes as well as qualitative and quantitative alterations in the sensitivity of cerebellar Purkinje cells to iontophoretically-applied 5-hydroxytryptamine (5-HT) were observed. Thiamine-deficient rats were characterized essentially by ataxia, piloerection, paresis, apparent weakness, and hypothermia after 4-6 weeks on a thiamine-free diet. Basal Purkinje cell firing frequency was unaffected by thiamine deficiency. The response of Purkinje cells to iontophoretically-applied 5-HT was solely inhibitory in deficient rats. In control rats, however, responses to 5-HT were excitatory, biphasic, or inhibitory. Neurons in the thiamine-deficient animals were more sensitive to the inhibitory effects of 5-HT, as demonstrated by a significant parallel shift to the left of the dose-response curve. Durations of 5-HT effects were similar in both groups. Dose-response relationships for GABA-induced inhibition of Purkinje cell firing from thiamine deficient and control rats did not differ from one another. These data demonstrate a relatively selective effect of thiamine depletion on cerebellar serotonergic neurotransmission assessed electrophysiologically. We believe there is up-regulation of 5-HT receptors on Purkinje cells caused by thiamine deficiency-induced impairment of indoleamine input to the cerebellum from raphe and related nuclei.

Animals↗