Oxidative Stress in Huntington's Disease Models: BDNF Antioxidant Effect

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

Buenos Aires

Congreso; LXVI Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2021

Sociedad Argentina de Investigación Clínica (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 isassociated with neuronal death. Glutathione (GSH) is an antioxidant molecule secreted by astrocytes that can protectneurons from death by reducing ROS levels. Superoxide dismutase 2 (SOD2) is a mitochondrial antioxidant enzyme thatreduces ROS levels and its overexpression provides neuroprotection. We have shown that brain-derived neurotrophicfactor (BDNF) reduces ROS levels induced by 3NP in astrocytes and increases intracellular GSH while 3NP reducesextracellular GSH levels. Now, we have studied BDNF effect on ROS production in cortical astrocytes, and GSH levelsand SOD2 expression in cortical and striatal astrocytes. We found that BDNF reduces ROS levels induced by 3NP incortical astrocytes (p