Vitamin E supplementation in the diet protects liver oxidative damage associated to chronic overload of copper

PAREDES FLEITAS, PAOLA; MUSACCO SEBIO ROSARIO; BAJICOFF SOFÍA; FUDA JULIÁN; TORTI HORACIO; BOVERIS ALBERTO; REPETTO MARISA

Buenos Aires

Congreso; LXII Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica.; 2017

Sociedad Argentina de Investigación Clínica.

Copper (Cu) is a bioelement that responds to the hormesis concept.At physiological concentration is essential for enzymatic reactions(in humans 50±5 μg/g liver and 5-10 μM plasma for diets of 1.4to 2.0 mg Cu/day; in rats, 7.3±0.5 μg/g liver and 3.6±0.2 μg/g brain)but at pathological levels becomes toxic for living organisms. Chronicpathologies as Wilson, Parkinson and Alzheimer diseases are associatedto higher than normal Cu levels in liver (L) and brain (B),oxidative stress (OS) and damage (OD), cognitive and neurologicaldisorders. In L of Wilson patients, the Cu content is higher than 1000μg/g, and in transgenic rats (ATP7B-/-), 300 μg/g. The aim of this researchis to evaluate if vitamin E supplemented diet (Vit.E) preventsthe OD associated to toxicity of Cu. Sprague Dawley male rats (200g) received Vit.E (100 mg/day,5 g/kg food) over 5 days before Cuchronic overload (0.05% P/V water, 0-42 days). Rats survival, Cucontent in L and B, phospholipid and protein oxidation (measured asTBARS and carbonyl (CO) protein) and glutathione (GSH) contentwere determined. Results indicated that chronic overload of CuSO4decreased rat survival after 28 days of treatment (75%, p