Summary :The various mechanisms involved in the redox defence of norma erythrocytes are adequately known. They are herein briefly reviewed, outlining the principal enzymes and metabolic pathways, such as superoxide dismutase, catalase, glutathione peroxidase and reductase, the hexose monophosphate shunt (HMS) and glutathione synthesis and turnover. The intraerythrocytic malaria parasite is imposing an oxidative stress on its host cell. Malaria-infected cells produce O 2 -, H 2 O 2 , enhance lipide peroxidation and activate host cell HMS. This stress is produced during the digestion of host cell hemoglobin by the parasite. Hence, both parasite and host cell must be able to confront this stress. The antioxidant defence systems of the parasite and the response of those systems in the infected host cell are reviewed, underscoring unresolved problems. Nothing is virtually known on the parasite's glutathione metabolism, and on possible interactions between host cell and parasite antioxidant defence systems. The postulate that 1. host cell activated HMS in conjunction with purine salvage can provide purine nucleotides to the parasite, and 2. that glutathione transferase can participate in parasite resistance to antimalarial drugs, are also discussed.T he redox status of malaria infected erythrocytes has been the subject of intense investigations and reviews in past years (Vennerstrom & Eaton, 1988 ; Golenser & Chevion, 1989 ; Hunt & Stocker, 1990). It is generally accepted that the intraerythrocytic malaria parasite exerts an oxidative stress on its host erythrocyte ; that externally applied oxidative stress is antagonistic to survival and propagation of the malaria parasite, and that pro-oxidant agents are effective inhibitors of parasite growth in vitro and in vivo. The host's response to malaria involves, among others, oxidative attack on intraerythrocytic parasites by activated macrophages. This perception is based mostly on phenomenological observations, but relatively little is known on the redox metabolism of the parasite itself, or how the latter may affect that of the host cell. In this essay we shall briefly review our present knowledge and underscore those problems Rice-Evans, 1991), and therefore RBC are exquisitely well equipped to counteract the damage that can be produced by these radicals (Stern, 1985).Superoxide anions (O2 -) produced during the spontaneous oxidation of hemoglobin to methemoglobin are dismutated to H 2 C>2 by superoxide dismutase (SOD).