Trypanosoma cruzi is the causative agent of Chagas’ disease, a major health problem in Central and South America. Mice infected with T. cruzi suffer a severe immunosuppression of the immune responses in the acute phase of the infection. In fact, a large number of alterations at the cellular level occur as a consequence of T. cruzi infection or a co-culture of the pathogen and cells of the immune system. The impaired immune response probably helps in the establishment of the chronic infection in animals and humans. A large number of studies have focused on the identification of the molecular mechanisms underlying the immunosuppression phenomenon [1–9]. These effects have been attributed to impaired IL-2 production due to the presence of suppressor cells, either macrophages [1–3] or T cells [4–8], or to T. cruzi immunosuppressive factors [19]. Another possible mechanism could be the polyclonal activation of lymphocytes that occur during the acute phase and that may alter the reactivity against foreign antigens thus converting the immune system into a poor responder to further antigenic challenge [11].

Glutathione (GSH) is a tripeptide thiol which plays an important role in various cellular functions [12]. Indeed, a partial depletion of the intracellular GSH pool of lymphocytes could affect blast transformation, lymphocyte proliferation and the generation of cytotoxic T cells [10, 13–15]. The limiting precursor for