@entity4162 cytoprotection against @entity9013 XXXX in @entity521 cells.

@entity1 @entity5212 @entity137 @entity6211 @entity19 @entity1285 @entity16 @entity26 @entity4162 @entity521 @entity9016 @entity1718 @entity9013 @entity413 @entity855
@entity4162 (ALCAR) plays an integral role in the transport of long chain @entity1718 across the inner mitochondrial membrane for oxidative phosphorylation. In non- @entity1 primates, administration of ALCAR was reported to prevent @entity5212 ( @entity5212 )-induced @entity16 to the substantia nigra. The present study investigates the effects of ALCAR against the @entity137 of @entity9013 ( @entity9016 ), the neurotoxic metabolite of @entity5212 , in @entity19 brain @entity521 cells. @entity9016 , a potent mitochondrial toxin, induced a dose-dependent reduction in mitochondrial @entity26 consumption and cell viability, corresponding to an accelerated rate of cellular @entity413 utilization. Treatment with ALCAR, but not @entity6211 , prevented @entity9016 @entity137 and partially restored intracellular @entity855 concentrations, but did not reverse the @entity9016 -induced loss of mitochondrial @entity26 consumption. These data indicate that protective effects are independent of oxidative phosphorylation. ALCAR had a substantial @entity413 sparing effect in both controls and @entity9016 -treated groups, demonstrating a potential role in enhancing @entity413 utilization through glycolysis. Antagonizing the entry of @entity1718 into the mitochondria, with either insulin or @entity1285 , did not interfere with ALCAR protection against @entity9016 . On the contrary, insulin potentiated the protective effects of ALCAR. In conclusion, these data indicate that ALCAR protects against @entity9016 @entity137 , independent of mitochondrial oxidative capacity or beta-oxidation of @entity1718 . In contrast, the protective effects of ALCAR appear to involve potentiation of energy derived from @entity413 through anaerobic glycolysis.
