Absorption of glyoxylate and oxalate in thiamine and pyridoxine deficient rat intestine

Dietary deficiency of thiamine or pyridoxine has been shown to produce hyperoxaluria and renal stone formation in man and experimental animals. To determine the possible contribution of exogenous glyoxylate and oxalate, the intestinal transport of [14C] - oxalate and [14C] - glyoxylate was measured in vitamin B1 and B6 deficient rats and their respective pair-fed controls. Results indicate that glyoxylate and oxalate are passively diffused from lumen to lamina propria in thiamine deficient and their pair-fed controls with no significant change in the rate of uptake of both the substrates. However B6 deficient rats showed a significant enhancement in the rate of oxalate uptake due to development of a new biphasic transport system. The rate of glyoxylate uptake by simple passive diffusion remained unaltered in pyridoxine deficiency.     

Effects of thiamine and pyridoxine on respiratory activity in Saccharomyces carlsbergensis strain 4228

Studies were made to elucidate the relationship among the thiamine-induced growth inhibition, decrease in cellular vitamin B₆ content and respiratory deficiency in Saccharomyces carlsbergensis strain 4228 [Nakamura et al., Biochem. Biophys. Res. Commun. 59, 771–776 (1974)]. Addition of pyridoxine to the thiamine-added culture at the beginning or in the course of cultivation brought about appearance of cytochrome spectra and the increase in the activity of heme-containing enzymes and in respiratory activity (Q _{O 2}). The effects of pyridoxine occurred prior to the restoration of growth. Pyridoxine was effective even in the presence of high levels of glucose in the growth medium (not less than 3%). On the basis of these results, the mechanism of the effects of thiamine and pyridoxine was discussed.     

Inhibition of thiamine transport in Saccharomyces cerevisiae by thiamine disulfides.

Both thiamine disulfide and O-benzoyl thiamine disulfide, which are thiolfrom derivatives of thiamine, strongly inhibited thiamine transport in Saccharomyces cerevisiae. The inhibition appeared to be due to a high affinity of the analogs for yeast cell membranes, in which thiamine transport component(s) may be integrated.     

Blood thiamine and thiamine phosphate ester concentrations in alcoholic and non-alcoholic liver diseases.

Thiamine state was investigated in patients with alcoholic liver disease, patients with various non-alcoholic liver diseases, and controls using a direct technique (thiochrome assay) to measure thiamine, thiamine monophospate, and the active coenzyme thiamine pyrophosphate in whole blood after isolating the fractions by ion exchange chromatography. Overall nutrition was similar in all groups as assessed by anthropometry, and no patient had clinical evidence of thiamine deficiency. There was no significant difference among the groups in mean concentration of any form of thiamine. The scatter was much greater in patients with alcoholic liver disease but only 8.7% had biochemical thiamine deficiency (defined as a blood concentration of the active coenzyme greater than 2 SD below the mean control value). An unexpected finding was of abnormally high total thiamine concentrations (greater than 2 SD above the mean control value) in 17.4% of patients with alcoholic liver disease, the highest concentrations being found in two patients with severe alcoholic hepatitis and cirrhosis. The ratio of phosphorylated to unphosphorylated thiamine was calculated as an index of phosphorylation and, although the mean did not differ significantly among the groups, the range was greatest in alcoholic liver disease. The lowest ratios occurred in the two patients with severe alcoholic hepatitis, but neither had evidence of thiamine pyrophosphate deficiency. Contrary to studies using indirect assay techniques, these results suggest that thiamine deficiency is unusual in well nourished patients with alcoholic liver disease. The new finding of unexpectedly high thiamine concentrations in some patients may be due to abnormalities of hepatic storage or release in liver disease, particularly in severe alcoholic hepatitis. There was no convincing evidence of impaired thiamine phosphorylation in any patients with liver disease. Conclusions from studies using indirect assays on the prevalence and mechanisms of thiamine deficiency in liver diseases may not be valid.     

Inhibition of growth and increased mortality of Mexican bean beetle larvae fed with thiamine and pyridoxine antagonists and reversal of effect with vitamin supplementation

Survival and growth of Mexican bean beetle larvae was adversely affected when larvae were fed with leaves dipped in a solution of oxythiamine, pyrithiamine or desoxypyridoxine. A 0.1% solution of each of these vitamin analogs was enough to repress growth and cause total mortality of the larvae. When each corresponding vitamin, thiamine or pyridoxine was added to its antivitamin solution in a ratio of 1:1 (vitamin: antivitamin) by weight, the adverse effects of the antivitamin were reversed. Sulfanilamide and pantoyltaurine negatively affected survival only when applied as a 1% solution, while pantothenyl alcohol, 2-picolinic acid, and 3-acetyl pyridine were ineffective at the concentrations tested.

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Zusammenfassung Überleben und Wachstum der Larven des Mexikanischen Bohnenkäfers (Epilachna varivestis Muls.) wurden nachteilig beeinflußt, wenn die Larven mit Blättern ernährt wurden, die zuvor in Oxythiamin-, Pyrithiamin- oder Desoxypyridin-Lösung getaucht worden waren. Eine 0,1% ige Lösung irgendeines dieser Vitaminaloge genügte zur Unterdrückung des Wachstums und zur Abtötung aller Larven. Die nachteilige Wirkung des Antivitamins wurde aufgehoben, sobald das jeweils entsprechende Vitamin, Thiamin oder Pyridoxin, zu der Antivitaminlösung im Gewichtsverhältnis 1:1 (Vitamin: Antivitamin) beigefügt wurde. Sulfanilamid und Pantoyltaurin beeinflußten das überleben nur dann negativ, wenn sie als 1% ige Lösung angewandt wurden, während Pantothenyl-Alkohol, 2-Picolin-Säure und Acetyl-Pyridin bei den untersuchten Konzentrationen unwirksam waren.

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Florida agricultural experiment stations journal series no. 2938.     

Metabolism of tritium-labelled pyridoxine and pyridoxine 5'-phosphate in the central nervous system

Abstract— [³H]Pyridoxine and [³H]pyridoxine 5′-phosphate have been injected into rats and mice. The uptake in brain tissue has been studied by comparing the concentrations of labelled compounds in serum, cerebrospinal fluid and brain tissue. Labelled pyridoxine passes rapidly into brain tissue, whereas the uptake of pyridoxine 5′-phosphate occurs at a much slower rate. Perchloric acid extracts of brain have been fractionated by ion-exchange chromatography and the distribution of isotope between the different forms of the vitamin has been determined at different times after the administration. The time sequence of the metabolic transformation is: pyridoxine+→ pyridoxine 5′-phosphate → pyridoxal 5′-phosphate → pyridoxamine 5′-phosphate. After the initial transformation period about 40 per cent of the isotope is recovered in each of the pyridoxal 5′-phosphate and pyridoxamine 5′-phosphate fractions.