Efectos celulares del déficit de vitamina C en neuronas motoras bulbares.
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Date
2026
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Universidad de Concepción
Abstract
El déficit de vitamina C está presente en distintos grupos de la población humana. En el sistema nervioso, esta vitamina desempeña un papel fundamental como antioxidante, contribuyendo en la mantención de la homeostasis redox y la prevención del daño oxidativo, un proceso asociado a enfermedades neurodegenerativas. Basándose en un modelo de cobayo escorbútico, nuestro laboratorio evaluó el efecto del déficit de vitamina C en neuronas motoras espinales. Las observaciones evidenciaron debilidad de las extremidades y una menor frecuencia respiratoria, lo que sugiere una afección asociada al bulbo raquídeo. Para este trabajo se planteó la hipótesis de que el déficit de vitamina C o escorbuto induce daño oxidativo en las neuronas motoras bulbares, generando muerte neuronal. De esta manera, se establecieron dos objetivos: (1) Determinar si la inducción del escorbuto altera las características celulares y subcelulares de las neuronas motoras bulbares en el cerebro de cobayo. (2) Definir las características subcelulares de neuronas motoras cervicales sometidas a un déficit de vitamina C y daño oxidativo. Nuestros resultados mostraron que el déficit de vitamina se asoció con un deterioro motor, una disminución de neuronas y de SVCT2 en el bulbo raquídeo, junto con la generación de astrocitos reactivos positivos a SVCT2 en el tronco encefálico. A nivel subcelular, se identificaron alteraciones en la homeostasis del retículo endoplasmático y la organización mitocondrial. En las neuronas motoras humanas, con características cervicales diferenciadas in vitro, el déficit de vitamina C alteró la organización de los procesos neuronales y la distribución de marcadores mitocondriales, efectos que se intensificaron frente al daño oxidativo. Estos hallazgos demostraron alteraciones neuronales y efectos subcelulares asociados al déficit de vitamina C en modelos in vivo e in vitro.
Vitamin C deficiency is present in different groups of the human population. In the nervous system, this vitamin plays a fundamental role as an antioxidant, contributing to the maintenance of redox homeostasis and the prevention of oxidative damage, a process associated with neurodegenerative diseases. Using a scorbutic guinea pig model, our laboratory evaluated the effects of vitamin C deficiency on spinal motor neurons. Our observations revealed limb weakness and a reduced respiratory rate, suggesting an impairment associated with the medulla oblongata. In this study, we hypothesized that vitamin C deficiency, or scurvy, induces oxidative damage in bulbar motor neurons, leading to neuronal death. Accordingly, two objectives were established: (1) to determine whether the induction of scurvy alters the cellular and subcellular characteristics of bulbar motor neurons in the guinea pig brain; and (2) to define the subcellular characteristics of cervical motor neurons subjected to vitamin C deficiency and oxidative damage. Our results showed that vitamin C deficiency was associated with motor impairment, a reduction in neuronal number and SVCT2 levels in the medulla oblongata, together with the generation of SVCT2-positive reactive astrocytes in the brainstem. At the subcellular level, alterations in endoplasmic reticulum homeostasis and mitochondrial organization were identified. In human motor neurons with cervical characteristics differentiated in vitro, vitamin C deficiency altered the organization of neuronal processes and the distribution of mitochondrial markers, effects that were exacerbated in response to oxidative damage. These findings demonstrate neuronal alterations and subcellular effects associated with vitamin C deficiency in both in vivo and in vitro models.
Vitamin C deficiency is present in different groups of the human population. In the nervous system, this vitamin plays a fundamental role as an antioxidant, contributing to the maintenance of redox homeostasis and the prevention of oxidative damage, a process associated with neurodegenerative diseases. Using a scorbutic guinea pig model, our laboratory evaluated the effects of vitamin C deficiency on spinal motor neurons. Our observations revealed limb weakness and a reduced respiratory rate, suggesting an impairment associated with the medulla oblongata. In this study, we hypothesized that vitamin C deficiency, or scurvy, induces oxidative damage in bulbar motor neurons, leading to neuronal death. Accordingly, two objectives were established: (1) to determine whether the induction of scurvy alters the cellular and subcellular characteristics of bulbar motor neurons in the guinea pig brain; and (2) to define the subcellular characteristics of cervical motor neurons subjected to vitamin C deficiency and oxidative damage. Our results showed that vitamin C deficiency was associated with motor impairment, a reduction in neuronal number and SVCT2 levels in the medulla oblongata, together with the generation of SVCT2-positive reactive astrocytes in the brainstem. At the subcellular level, alterations in endoplasmic reticulum homeostasis and mitochondrial organization were identified. In human motor neurons with cervical characteristics differentiated in vitro, vitamin C deficiency altered the organization of neuronal processes and the distribution of mitochondrial markers, effects that were exacerbated in response to oxidative damage. These findings demonstrate neuronal alterations and subcellular effects associated with vitamin C deficiency in both in vivo and in vitro models.
Description
Tesis presentada para optar al grado de Magíster en Neurobiología.
Keywords
Ácido ascórbico, Neuronas motoras