It was observed, in vitro, that the water extract of the fermented-tea customarily chewed by Thai people has a similar thermostable thiamine-inactivating factor to that found in the water extract of fern. It was also observed that the percentage of thiamine disulfide formed from thiamine with some flavones, catechol, pyrogallol, caffeic acid, dihydroxyphenylalanine, and hemin is greater at pH 7.5 than at pH 7.0. With some flavonoids, such as quercetin, rutin, and 6, 7, 4'-trihydroxyisoflavone, and pyrogallol, hemin, catechol and caffeic acid at pH 7.5, around 30-100% of thiamine is changed into thiamine disulfide. Water extract of shiitake, okra, coffee, black tea and fukinoto have only weak activities of thermostable thiamine-inactivating factors as a large percentage of thiamine disulfide is formed from thiamine even at pH 7.0. 2-Methyl-4-amino-5-aminomethylpyrimidine was isolated from the reaction mixture of 1g thiamine with 20mg catechol (1:0.5mole) at pH 7.0, 45°C, and identified with the synthesized pyrimidine.
Electrophysiological and biochemical studies were performed to determine the role of thiamine in the excitable membrane of the crayfish giant axons, as it has been suggested that thiamine plays a role in the excitability of the membrane which is unrelated to the metabolic process. Thiamine (5mM) significantly increased the rising rate of the action potential without affecting the resting membrane potential and threshold potential. A recovery of the enhancement was evidenced by a wash of the axon with physiological solution. Pyrithiamine (10 mM) reduced the rising rate of the action potential without affecting the membrane and threshold potential. The reduction of dV/dt by pyrithiamine remained unchanged after a wash of the axon with physiological solution, while dV/dt increased after thiamine treatment. The amount of thiamine found in the crayfish axons was comparable to that observed in the rat sciatic nerve. In addition, pyrithiamine reduced the thiamine content in axons and protein binding thiamine of the axons. It is thus concluded that thiamine in the excitable membrane of crayfish axons plays a significant role in production of the action potential and is essential for maintaining the membrane excitability of crayfish axons.
Oral administration of lipidsoluble allithiamines [thiamine propyl disulfide (TPD) and thiamine tetrahydrofurfuryl disulfide (TTHF)] rapidly increased thiamine activity in whole blood, red blood cells, cerebrospinal fluid, and urine in normal and thiamine-deficient subjects. These thiamine congeners also restored red blood cell transketolase to normal in alcoholics with thiamine deficiency. Such repletion equaled that produced by parenteral, water-soluble thiamine hydrochloride (THCl) or thiamine pyrophosphate (TPP). Oral administration of water-soluble thiamines (THCl, TPP) neither elevated thiamine activity in biological fluids nor restored transketolase activity to normal in alcoholics with thiamine deficiency presumably due to their rate-limited intestinal transport. Oral administration of TPD eliminated lateral rectus palsy in patients with Wernicke's encephalopathy. Orally administered allithiamine vitamers are therefore recommended for prophylaxis and treatment of thiamine deficits because while having essentially the same biological properties as parenterally administered water-soluble thiamines they have not produced any untoward effects after long-term administration and are far more efficiently utilized.
A series of children with Leigh's disease had normal hepatic pyruvate carboxylase activity, increased cerebral thiamine diphosphate, and decreased cerebral thiamine triphosphate. These thiamine esters were normal in liver. The author suggests that the histologic changes of Leigh's disease, as well as the similar changes of Wernicke's disease, could be due to a deficiency of cerebral thiamine triphosphate.