Oxidative stress, diet, and the etiology of preeclampsia

A current theory holds that oxidative stress, ie, an imbalance between maternal prooxidants and antioxidants, is a component of preeclampsia. It is uncertain whether such an imbalance occurs before clinical recognition of the syndrome or whether it is related to diet.

We measured urinary excretion of the isoprostane 8-iso-prostaglandin F(2alpha), which is an indicator of oxidative damage to lipids, and the total antioxidant power, which is a global measure of antioxidant status, at the entry to prenatal care. We also examined the relation of these indexes to diet during pregnancy.

A cohort of 307 gravidae from Camden, NJ, was studied from entry to prenatal care (at 15.0 +/- 0.49 wk gestation). Measures of the maternal diet were obtained by 24-h recall.

Risk of preeclampsia was increased 5-fold with higher urinary isoprostane excretion and decreased 3-fold with higher total antioxidant power. Over the course of pregnancy, there were significant trends for an association of higher isoprostane excretion with increased consumption of energy-adjusted fat, polyunsaturated fat, and polyunsaturated fatty acids (n-3, n-6, and linoleic and linolenic fatty acids), whereas total antioxidant power was not related to diet.

Increased urinary excretion of isoprostane and decreased antioxidant production is an imbalance that is consistent with oxidative stress, and it precedes clinical recognition of preeclampsia. The maternal diet is an underlying factor that provides an environment for free radical generation.