Assessing the mechanism of iron toxicity in isolated liver mitochondria: Oxidative damage and mitochondrial function

MUSACCO-SEBIO, ROSARIO; SAPORITO-MAGRIÑÁ, CHRISTIAN; BAJICOFF, SOFÍA; PAREDES-FLEITAS, PAOLA

Congreso; II International Congress in Translational Medicine. Maestría Internacional en Ciencias Biomédicas (IMBS).; 2015

Universidad de Freiburg (Alemania) y Universidad de Buenos Aires. Buenos Aires

Mitochondrial dysfunction and oxidative damage by copper overload in isolated rat liver mitochondriaWilson?Ls disease is a condition characterized by an alteration in hepatic excretion of copper (Cu) leading to increased metal content in the body that eventually reaches the rest of the body. The primary mechanism proposed for the toxicity of Cu overload is the production of reactive oxygen species (ROS) and oxidative damage to these species produce biomolecules. A major source of ROS in the cell?Ls mitochondria, so this organelle have an important role in the toxicity of Cu. In this work the in vitro effect of Cu2 + (0-200 mM) in mitochondrial function (O2 consumption Clark type electrode measured at 25 ?? C) and lipid peroxidation (TBARS) was studied under different conditions and metabolic state of mitochondria isolated from rat liver (male Sprague Dawley, 200 g). a decrease was observed in mitochondrial O2 consumption in the active state (state 3) to control (C), with substrates of complex I (C: 41 ?} 8 nat-g O / min.mg) and the complex II (C : 52 ?} 11 nat-g O / min.mg) 25 and 22% respectively with Cu2 + 50 mM and 54 and 75% with 100 mM Cu2 +, showing that the decline in consumption of O2 is dependent on the concentration of metal . Radio respiratory control and ADP / O were significantly decreased. Increased oxidative damage to phospholipids significantly increased (C: 0.09 ?} 0.03 nmol / mg, p