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Luciano Ferrada

Researcher at University of Concepción

Publications -  21
Citations -  297

Luciano Ferrada is an academic researcher from University of Concepción. The author has contributed to research in topics: Ascorbic acid & Dehydroascorbic acid. The author has an hindex of 8, co-authored 16 publications receiving 198 citations.

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Vitamin C Transporters, Recycling and the Bystander Effect in the Nervous System: SVCT2 versus Gluts.

TL;DR: This review will compare the molecular and structural aspects of vitamin C and glucose transporters and their expression in endothelial or choroid plexus cells, which form part of the blood-brain barrier and blood-cerebrospinal fluid (CSF) barrier, respectively and describe SVCT and GLUT expression in different cells of the brain.
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The oxidized form of vitamin C, dehydroascorbic acid, regulates neuronal energy metabolism

TL;DR: DHA is a novel modulator of neuronal energy metabolism by facilitating the utilization of glucose through the PPP for antioxidant purposes by stimulating the rate of lactate uptake by neurons in a time‐ and dose‐dependent manner.
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Dehydroascorbic Acid Promotes Cell Death in Neurons Under Oxidative Stress: a Protective Role for Astrocytes

TL;DR: The effects of oxidative stress and DHA uptake on neuronal cell death in vitro indicate that DHA promotes the death of stressed neurons and that astrocytes are essential for the antioxidant defense of neurons, participating in the antioxidative defense of the brain.
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Vitamin C controls neuronal necroptosis under oxidative stress

TL;DR: It is shown that treatment with AA regulates the expression of pro- and antiapoptotic genes, whereas the oxidation of AA in neurons induces morphological alterations consistent with necroptosis and MLKL activation, suggesting that ne croptosis is a target for cell death induced by vitamin C.
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SVCT2 Is Expressed by Cerebellar Precursor Cells, Which Differentiate into Neurons in Response to Ascorbic Acid

TL;DR: Stable over-expression of SVCT2 in C17.2 cells enhances β III tubulin expression, but it also increases cell death, suggesting that AA transporter levels must be finely tuned during neural stem cell differentiation.