RESUMO
The aim of the study was to determine whether dietary iron within the normal range is (i) responsible for oxidative changes in the liver, erythrocytes and plasma; and (ii) make the heart more susceptible to ischemia/reperfusion injury. Female rats were allocated to four groups according to diet supplemented with either 15, 35, 150, or 300 mg iron/kg diet. After 4 months the following statistical difference in the two higher dietary groups were observed compared to the lower ones: (i) decreased antioxidant concentrations in liver, plasma and erythrocytes (alpha-tocopherol and ascorbic acid); (ii) increased plasma nitrite concentration; (iii) ischemia/reperfusion elevated LMWI and MDA concentrations and decreased ascorbate concentrations. This study clearly showed that increased dietary iron concentration causes oxidative changes in plasma, erythrocytes and liver. Higher dietary iron aggravated the outcome of ischemia/reperfusion injury as indicated by an elevated malondialdehyde concentration in the two higher dietary iron groups.
Assuntos
Antioxidantes/metabolismo , Eritrócitos/efeitos dos fármacos , Eritrócitos/metabolismo , Coração/efeitos dos fármacos , Ferro da Dieta/farmacologia , Fígado/efeitos dos fármacos , Fígado/metabolismo , Isquemia Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Nitritos/metabolismo , Animais , Ácido Ascórbico/sangue , Ácido Ascórbico/metabolismo , Catalase/sangue , Catalase/metabolismo , Feminino , Glutationa Peroxidase/sangue , Glutationa Peroxidase/metabolismo , Ferro/sangue , Malondialdeído/sangue , Malondialdeído/metabolismo , Mitocôndrias Hepáticas/metabolismo , Isquemia Miocárdica/induzido quimicamente , Traumatismo por Reperfusão Miocárdica/induzido quimicamente , Miocárdio/metabolismo , Nitratos/metabolismo , Óxido Nítrico/metabolismo , Nitritos/sangue , Oxirredução , Ratos , Ratos Sprague-Dawley , Superóxido Dismutase/sangue , Superóxido Dismutase/metabolismo , Vitamina E/sangue , Vitamina E/metabolismoRESUMO
There is evidence that flavonoid intake correlates inversely with coronary heart disease risk. Flavonoids are widely distributed in food and drinks and act as antioxidants and iron chelators. The aim of this study was to determine whether pycnogenol (a flavonoid extracted from the bark of Pinus pinaster) and catechin could minimise the myocardial mitochondrial damage due to ischemia/reperfusion. Using the rat heart model of ischemia/reperfusion we found that pycnogenol had no significant effect on the resultant damage, while catechin suppressed the observed elevation of low molecular weight iron during ischemia/reperfusion which might explain the significantly reduced mitochondrial injury when using catechin in the perfusate. Our results suggest that some flavonoids might be effective in minimizing ischaemic/reperfusion injury and would require further detailed investigation.