Protein oxidation is associated to the mitochondrial dysfunction in rat brain acute copper toxicicity.

SEMPRINE, JIMENA; MUSACCO SEBIO, ROSARIO; SAPORITO MAGRIÑÁ, CHRISTIAN; GARCÍA MAGRO, NICOLÁS; BOVERIS, ALBERTO; REPETTO, MARISA

Buenos Aires

Congreso; VIII International Congress. Society for Free Radical Biology and Medicine.; 2013

Society for Free Radical Biology and Medicine

Cu overload generates oxidative damage in the brain and is involved in the pathogenesis of neurodegenerative diseases. The aim of this work was to study the acute Cu toxicity on the mitochondrial activity of rat brain. Male Sprague Dawley rats (150 g) received Cu(II) (ip, 5 mg/kg). The oxygen consumption (∆O2) was determined in brain cortex at 6, 16 and 24 h of Cu overload, and in isolated mitochondria. A decrease of 62% in brain ∆O2 at 16 h was observed (control, 1280 ± 45 nmol O2/min g, p