Determination of the binding constant of thiamine diphosphate in transketolase from Baker's yeast by circular dichroism titration.
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Thiamine and its phosphorylated derivatives reacted with hypochlorite with reaction rates following the order: thiamine greater than thiamine monophosphate greater than thiamine diphosphate from pH 4.0 to 6.5. At least one unknown transient intermediate was formed and at least one non-thiochrome product was fluorescent. Chemiluminescence was also observed.
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Galactosamine, a selective hepatotoxin, produces in rats histologic alterations, which show the characteristics of severe human viral hepatitis. In the present study the efficacy of two different cofactor regimens (coenzyme A, NAD, alpha lipoic-acid, cocarboxylase) in rats with fulminant galactosamine hepatitis were tested. The results showed an improvement of the short-term survival with a short-term treatment and definitely better survival with a long-term regimen with cofactors.
Active uptake of [32P]thiamine diphosphate by E. coli was analyzed using an improved method of gel filtration chromatography. The radioactive coenzyme was accumulated without dephosphorylation. From this result it was concluded that thiamine kinase is not involved in the membrane transport of thiamine in E. coli.
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Drinking of both green and black tea as the only liquid ingested resulted in significant decreases in the activity of transketolase in whole blood of rats both before and after the in vitro addition of thiamin diphosphate. Liver transketolase activity was decreased only by green tea. Mucosal transketolase activity was not affected by either type of tea. The activity of lactate dehydrogenase (LDH) was not affected by either type of tea, while whole blood LDH was decreased by both green and black tea. Neither tea had any affect on mucosal alkaline phosphatase, but thiamin diphosphatase activity was decreased by both teas. An increase in liver total thiamin resulted from the drinking of both types of tea.
Thirty two cases of acute Wernicke's encephalopathy were observed in a period of 33 months, and prior to the mandatory thiamine enrichment of Australian bread-making flour in 1991. These cases were carefully assessed by multiple tests at specified intervals prior to, and following thiamine administration until discharge from hospital. Structured scoring of neurological signs and symptoms, CT scans, psychometry, nutritional measurements, and liver biopsies were performed. There was variation in the presentation and severity of clinical signs and symptoms and in response to treatment. All patients had alcohol-related liver disease, and the results indicated that fatty liver was important in presentation and in response to treatment with thiamine. Other forms of alcohol related brain damage were present in these patients, most of whom were in the 4th or 5th decade of life and had been drinking beer to excess for more than 20 years.
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