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C E Cassidy

Publications and source records attributed to C E Cassidy.

14 recordsLinked to original sources

Thiamin deficiency and the pentose phosphate cycle in rats: intracerebral mechanisms.

Previous studies have shown that transketolase activity is decreased in the brains of thiamin deficient rats. This study assesses the effect of decreased transketolase levels on the activity of the pentose phosphate cycle in murine thiamin deficient cortex and brainstem. Thiamin deficiency was produced in newborn and adult rats by either pyrithiamin administration or by feeding a low thiamin diet. Newborn rats were killed at 22 days of age, and adults were killed at the onset of moderate to severe nurological signs. Cortices and brainstems from thiamin deficient and control rats were analyzed for activity of the two regulatory enzymes of the pentose phosphate cycle, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Flux through the pathway was measured by the differentially labeled glucose technique in the brainstems of deficient and control adult rats. In both the brainstem and cortex of thiamin dificient rats, areas in which transketolase activity was decreased up to 65%, the activities of the two regulatory enzymes, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, were unaltered. Further, flux through the pentose phosphate cycle was not decreased as compared to pair-fed control rats. These data do not support the hypothesis that in thiamin dificient rats, a decrease in cerebral transketolase activity leads to a diminished pentose phosphate cycle activity.

Age Factors↗

Adenine nucleotides in thiamine deficient rat brain.

The net levels and turnover of ATP, ADP, and AMP were measured in the cortex and brainstem of thiamine deficient and control rats. In spite of a 63% decrease in pyruvate decarboxylase activity in the brainstem of severely deficient rats, metabolism of the adenine nucleotides was unaffected. These data indicate a major reserve capacity for pyruvate decarboxylase and show that the adenylate pool is not significantly altered in thiamine deficient rat brain.

Adenine Nucleotides↗

Cardiac and renal pentose phosphate pathway activity in thiamine deficiency.

Thiamine deficiency was produced in young rats by feeding a thiamine deficient diet. At a time when neurological symptoms were severe, and cardiac and renal transketolase activities were decreased, the animals were sacrificed. Glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities, and flux through the pentose phosphate pathway were similar in pair-fed control and thiamine deficient rats. These data suggest that altered pentose phosphate pathway activity is not a vital feature of murine thiamine deficiency.

Animals↗