Energy and glucose pathways in thiamine deficient primary rat brain microvascular endothelial cells

Rok, strany: 2005, 467 - 474

Thiamine deficiency (TD) results in lactate acidosis, which is associated with neurodegeneration. The aim of this study was to investigate this alteration in primary rat brain endothelia. Spectrophotometric analysis of culture media revealed that only a higher concentration of pyrithiamine, which accelerates the intracellular blocking of thiamine, significantly elevated the lactate level and lactate dehydrogenase activity within 7 days. The medium without pyrithiamine and with a thiamine concentration comparable to pathophysiological plasma levels mildly reduced only the activity of transketolase. This suggests that significant metabolic changes may not occur at the early phase of TD in cerebral capillary cells, while anaerobic glycolysis in capillaries may be mediated during late stage/chronic TD.

ISO 690:

Ham, D., Karska-Wysocki, B. 2005. Energy and glucose pathways in thiamine deficient primary rat brain microvascular endothelial cells. In General Physiology and Biophysics, vol. 24, no.4, pp. 467-474. 0231-5882.

APA:

Ham, D., Karska-Wysocki, B. (2005). Energy and glucose pathways in thiamine deficient primary rat brain microvascular endothelial cells. General Physiology and Biophysics, 24(4), 467-474. 0231-5882.