Oxidant stress is associated with the generation of reactive oxygen species
that are responsible for the damage of a variety of cellular components. T
he prevention of such biological damage can be achieved by dismutation of s
uperoxide to H2O2 which in turn is removed by catalase and GSH peroxidase.
However, redox-active iron released during the development of plasmodia in
the erythrocyte can mediate the conversion of H2O2 to hydroxyl radical whic
h is more reactive. The roles of SOD and the nitroxide SOD mimic 4-OH,2,2,6
,6,retramethyl piperidine-N-oxyl (Tempol) were examined in P. falciparum gr
own in vitro. Both compounds did not prevent the interference with growth i
nflicted by various inducers of oxidant stress. Moreover, Tempol inhibited
parasite growth, in agreement with previous experiments depicting accelerat
ed mortality in SOD overexpressing mouse model of malaria. Probably, effect
ive defense against ROS requires balanced increments in antioxidant enzymes
and is not necessarily improved by an increase in the activity of one enzy
me.