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Glucose 6‐Phosphate and Fructose 1,6‐Bisphosphate Can Be Used as ATP‐Regenerating Systems by Cerebellum Ca 2+ ‐Transport ATPase
Author(s) -
Ramos Renata C. S.,
De Meis Leopoldo
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0720081.x
Subject(s) - fructose 2,6 bisphosphate , hexokinase , fructolysis , fructose , biochemistry , glycolysis , atpase , glucose 6 phosphate , chemistry , phosphate , phosphofructokinase , biology , metabolism , enzyme
: In this work, it is shown that theCa 2+ ‐transport ATPase found in the microsomal fraction of thecerebellum can use both glucose 6‐phosphate/hexokinase and fructose1,6‐bisphosphate/phosphofructokinase as ATP‐regenerating systems. The vesiclesderived from the cerebellum were able to accumulate Ca 2+ in amedium containing ADP when either glucose 6‐phosphate and hexokinase orfructose 1,6‐bisphosphate and phosphofructokinase were added to the medium.There was no Ca 2+ uptake if one of these components was omittedfrom the medium. The transport of Ca 2+ was associated with thecleavage of sugar phosphate. The maximal amount of Ca 2+ accumulatedby the vesicles with the fructose 1,6‐bisphosphate system was larger than thatmeasured either with glucose 6‐phosphate or with a low ATP concentration andphosphoenolpyruvate/pyruvate kinase. The Ca 2+ uptake supported byglucose 6‐phosphate was inhibited by glucose, but not by fructose 6‐phosphate.In contrast, the Ca 2+ uptake supported by fructose 1,6‐bisphosphatewas inhibited by fructose 6‐phosphate, but not by glucose. Thapsigargin, aspecific SERCA inhibitor, impaired the transport of Ca 2+ sustainedby either glucose 6‐phosphate or fructose 1,6‐bisphosphate. It is proposedthat the use of glucose 6‐phosphate and fructose 1,6‐bisphosphate as anATP‐regenerating system by the cerebellum Ca 2+ ‐ATPase may representa salvage route used at early stages of ischemia ; this could be used toenergize the Ca 2+ transport, avoiding the deleterious effects derived from the cellular acidosis promoted by lactic acid.