To investigate the involvement of oxidative tissue damage in the pathogenes
is of murine cerebral malaria (CM), brain levels of protein carbonyls, 3,4-
dihydroxgphenylalanine (DOPA), o-tyrosine, and dityrosine were measured dur
ing Plasmodium berghei ANKA (PbA) and P. berghei K173 (PbK) infections. Dur
ing PbA infection in a CM model, brain levels of the substances were simila
r to those in uninfected mice. The role of phagocyte-derived reactive oxyge
n species in the pathogenesis of CM was examined in gp91(phox) gene knockou
t mice. The course of Chi in these mice was the same as in their wild type
counterparts. To examine whether superoxide production in the central nervo
us system could have occurred via increased xanthine oxidase activity, brai
n concentrations of urate were measured in CM mice and in mice infected wit
h PbK (which does not cause CM), Brain urate concentration increased signif
icantly in both groups of mice, suggesting that purine breakdown is not spe
cific to CM, These results indicate that reactive oxygen species probably d
o not contribute to the pathogenesis of murine CM.