Copper overload: oxidative damage and mitochondrial dysfunction in rat brain cortex, hippocampus and striatum.

SAPORITO MAGRIÑÁ, CHRISTIAN; MUSACCO SEBIO, ROSARIO; SEMPRINE, JIMENA; ARAUJO, JAVIER; REPETTO, MARISA

Buenos Aires

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

Society for Free Radical Biology and Medicine

Chronic copper overload causes neurotoxicity, oxidative damage and mitochondrial dysfunction in brain. The objective of this work is to determine the brain areas affected in Cu mitochondrial toxicity to characterize the biochemical changes associated to oxidative damage. Sprague Dawley male rats (150 g) received Cu(II) in the drinking water (0.5 g/L) over 21 days. Spontaneous brain chemiluminescence (CL) increased 125% (control, 16 ± 2 cps/g, p < 0.001). After Cu overload, the oxygen uptake (∆O2) of brain cortex mitochondria with malate-glutamate as substrate increased 13% in active state (control, 76 ± 3 nmol O2/min.mg protein, p < 0.01) and 19% in resting state 4 (Control, 13.5 ± 0.5 nmol O2/min.mg protein) (p < 0.01). In similar conditions, hippocampus mitochondria decreased ∆O2 36% (control, 1215 ± 18 nmol O2/min.g, p < 0.001) and striatum mitochondria 32% (control, 175 ± 16 nmol O2/min.g, p < 0.001). In cortex, the mitochondrial ∆O2 increase indicates that under physiological conditions, with ADP and substrate, electron transport operate at a higher rate after Cu overload.