Intracellular redox homeostasis in liver and brain associated to histopathologycal damage in acute copper overload

LAIRION, FABIANA; ACOSTA, JUAN MANUEL; MORALES, CELINA; RODRÍGUEZ, MANUEL; CASTRO PARODI, MAURICIO; DAMIANO, ALICIA; SAPORITO MAGRIÑÁ, CHRISTIAN; FUDA, JULIÁN; TORTI, HORACIO; GELPI, RICARDO; BOVERIS, ALBERTO; REPETTO, MARISA

Mar del Plata

Congreso; LXIII Reunión anual de la Sociedad Argentina de Investigación Clínica; 2018

Sociedad Argentina de Investigación Clínica

Acute copper (Cu(II)) overload generates histopathological lesions (HL), oxidative damage (OD), mitochondrial dysfunction and antioxidant enzymes response to oxidative stress, mediated by the nuclear transcription factor (Nrf2-ARE) signaling pathway. The aim of this study is to evaluate if HL in liver and brain correlates with redox homeostasis, Cu organ content and dose. Sprague Dawley male rats (200 g) were sacrificed at 1h, 6h and 16h after received 5.0; 6.5 and 7.5 mg Cu(II)/kg (ip). The organs were excised and sampleswere processed for obtaining histopathological preparations that were stained with hematoxylin-eosin. The congestion index (CI) was calculated for each organ and dose. Superoxide dismutase activity (SOD1) was evaluated using spectrophotometric method. Nrf2 expression in cells (cytosol and nucleus) was determined by western blot. Results shows that congestion increased with dose,CI2: moderate-strong (7.5mg/kg). In liver, CI increased from 0 to 2 with Cu content from 1.1 to 8.0 μg Cu/g organ, with no significant changes in SOD1 after 6h (5mg/kg); Nrf2 decreased 48% (p