OXIDATIVE STRESS IN HUNTINGTON DISEASE MODELS: BDNF ANTIOXIDANT EFFECT

LÓPEZ COUSELO, FEDERICO; CARNIGLIA, LILA; CARLA CARUSO; JULIETA SABA; DANIELA DURAND; BRUNO, JULIETA; LASAGA, MERCEDES

CABA

Congreso; Reunion conjunta SAIC SAI AAFE NANOMED.ar; 2021

SAIC

Huntington disease (HD) involves oxidative stress and mitochondrial dysfunction which can be mimicked by 3-nitropropionic acid (3NP), a phenotypic model of HD. Reactive oxygen species (ROS) generate oxidative stress which is associated with neuronal death. Glutathione (GSH) is an antioxidant molecule secreted by astrocytes that can protect neurons from death by reducing ROS levels. Superoxide dismutase 2 (SOD2) is a mitochondrial antioxidant enzyme that reduces ROS levels and its overexpression provides neuroprotection. We have shown that brain-derived neurotrophic factor (BDNF) reduces ROS levels induced by 3NP in astrocytes and increases intracellular GSH while 3NP reduces extracellular GSH levels. Now, we have studied BDNF effect on ROS production in cortical astrocytes, and GSH levels and SOD2 expression in cortical and striatal astrocytes. We found that BDNF reduces ROS levels induced by 3NP in cortical astrocytes (p