Abstract
Objective: To describe the role of oxidative/nitrosative stresses in the pathogenesis of placental malaria and complications for the fetus. Bibliographic review: Placental malaria results from the sequestration of erythrocytes infected by Plasmodium falciparum in the blood microcirculation of the placental interventional spaces, leading to the infiltration of activated leukocytes in these sites, with subsequent production of cytokines and chemokines. These mediators, associated with phagocytosis of parasites and infected cells, activate the oxidative/nitrosative stresses pathways, producing free radicals and oxidation/nitration molecules, which act by attacking compounds of the cell structure of both the parasite and the host cells, causing damage to the integrity of the placental barrier and leading to insufficiency of the placenta to support fetal development. Final considerations: Therefore, we conclude that the immune response and oxidative/nitrosative stresses play an important role not only in the defense of the patient (reducing parasitaemia), but also in the progression of the disease and placental invasion, leading to serious changes and complications to the fetus.