COPPER TOXICITY AND PROTEIN OXIDATION IN RAT HEART DUE TO CHRONIC OVERLOAD AND THE PROTECTIVE EFFECT OF VITAMIN E

FABIANA LAIRION; MARTINEZ-SARRASAGUE M; CIMATO A; LASSO M; SORENSEN M; BOGADO J; LOPEZ MONTAÑANA L; SAPORITO MAGRIÑÁ, C; MARISA GABRIELA REPETTO

CIUDAD AUTONOMA BUENOS AIRES

Congreso; 65º Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2020

Sociedad Argentina de Investigación Clínica

Departamento de Química Analítica y Fisicoquímica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires. 2. Instituto de Bioquímica y Medicina Molecular, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires. 3. Departamento de Físicomatemática, Facultad de Farma cia y Bioquímica, Universidad de Buenos Aires. Previous results indicated that chronic copper [Cu(II)] overload is toxic for liver and brain. Toxicity is associated with oxidative damage (OD) on biomolecules mediated by the generation of reactive oxy gen species, mainly hydroxyl radical and organic hydroperoxides. The objective of this work is to assess whether OD due to chronic overload of Cu(II) in rats involves changes in redox homeostasis in heart (H) and the effect of vitamin E (Vit.E) on it prevention. Male Sprague Dawley rats (80-90 g) received standard diet and drinking water with 0.5 g/L Cu(II) (0.05%w/v, n=36) as CuSO4 for 21 days, and Vit.E (100 mg/day, 5 g/kg food) over 5 days before Cu(II) overload. The following parameters were assessed in tissue homogenates: protein oxidation, measured as carbonyl groups (CO), phospholipid oxidation, measured as the content of thiobarbituric acid reactive substances (TBARS) and NADPH oxidase activity. In mitochondria, the oxygen consumption (∆O2 ) was measured with a Clark-type ox ygen electrode. A 7-fold increase of CO was observed with Cu(II) overload (day 14, p