Efeitos de uma sobrecarga de sódio ou de antioxidantes sobre o estresse oxidativo e angiogênese placentária: repercussão sobre indicadores de estresse oxidativo no fígado fetal

Abstract

Intrauterine programmed cardiovascular disease may be linked to placental oxidative stress. It was investigated whether NaCl supplement, during pregnancy, affects placental oxidative stress and angiogenesis and imprints increased levels of oxidative stress in fetal liver. Dams were treated with 1.8% NaCl in drinking water from 20 days before and along pregnancy. Along pregnancy α-tocopherol, tempol or both were administered. Angiogenesis was evaluated throughout the expression of flt-1, the type 1 receptor for VEGF, in the villous bundles/labirinth. NaCl diminished flt-1 expression, as well as, reduced malonyldialdehide and augmented reduced gluthatione in placenta and fetal liver. α-Tocopherol led to an additional reduction in MDA levels in these organs, but diminished GSH. Otherwise, tempol increased MDA and diminished GSH in both placenta and fetal liver. No antioxidant changed the expression of flt-1. The reduced levels of MDA in placenta and fetal liver of dams under NaCl supplement might be due to reduced angiogenesis, that reduced oxygen supply, and also to the increased GSH levels. However the paradoxical pro-oxidant action of tempol indicates that the antioxidant reservoir in dams under sodium overload is limited. Furthermore, the parallel between the pattern of placental and fetal liver oxidative stress suggests that superoxide anions transferred from mothers may be important in programming cardiovascular diseases.