The release of reactive oxygen intermediates (ROI), mediators of inflammatory reactions, was evaluated in murine Trypanosoma cruzi infection. In acutely infected BALB/c mice, spleen cells were stimulated, either with epimastigote or trypomastigote forms of the parasite, and the effect was enhanced by serum from infected mice. Only opsonized parasites triggered the release of ROI by normal mouse cells and this response was several times lower than in infected mice. This seems to indicate that cells from acutely infected mice reacted to T. cruzi and that neither parasites nor serum factors blocked the release of ROI. During the acute stage of the infection, both the parasitemia and the release of ROI by spleen cells were higher in BALB/c than in C3H mice (ROI generated in response to a phagocytic stimulation was 12 and 3 times the normal levels, respectively). In addition, in BALB/c mice infected with different numbers of parasites, the production of ROI was related to parasitemia. On the other hand, during the chronic stage of the infection, the inflammatory reaction in myocardium was greater in C3H than in BALB/c mice, and the increase in ROI production was 30% and 100% above the normal levels in BALB/c and C3H mice, respectively. This suggests that the increased ROI production paralleled the parasite burden in the acute phase, and could be related to inflammatory processes after the control of the parasitemia.