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- Antonio Dopico-López, María Pérez-Mato, Andrés da Silva-Candal, Ramón Iglesias-Rey, Aharon Rabinkov, Ana Bugallo-Casal, Tomás Sobrino, David Mirelman, José Castillo, and Francisco Campos.
- Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
- Transl Res. 2021 Apr 1; 230: 68-81.
AbstractGlutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellular glutamate that accumulates in the brain following ischemic stroke. In this study, we investigated the inhibitory effect of GOT1 on brain metabolism and on the ischemic damage in a rat model of ischemic stroke by means of a specific antibody developed against this enzyme. Inhibition of GOT1 caused higher brain glutamate and lactate levels and this response was associated with larger ischemic lesion. This study represents the first demonstration that the inhibition of the blood GOT1 activity leads to more severe ischemic damage and poorer outcome and supports the protective role of GOT1 against ischemic insults.Copyright © 2020 Elsevier Inc. All rights reserved.
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