Leishmania infantum devoid of mitochondrial peroxiredoxin are capable of surviving and proliferating in culture at wildtype levels

#Castro, H., #Romão, S., #Sousa, C., *Gadelha, F.R. & #Tomás, A. 

Leishmania infantum is a trypanosomatid with relevance as human pathogen.  Like in other aerobes, the Leishmania mitochondrion constitutes an important source of reactive oxygen species (ROS) and possibly also of reactive nitrogen intermediates (RNI).   Together these species can cause irreversible damage to mitochondrial components, but they can also regulate important cell signaling pathways.  To keep the concentration of ROI and RNI at harmless levels, the mitochondrion is equipped with efficient antioxidant devices. In these parasites, mitochondrial peroxiredoxin, LimTXNPx, presumably participates in ROI and RNI removal from this organelle.  Using a DNA recombination strategy, L. infantum mutants lacking LimTXNPx were produced.  The growth curve of transformants did not significantly differ from wild-type (WT) cells indicating that this enzyme does not control cell proliferation.  Endogenous H₂O₂ generation by inhibition of the mitochondrial respiratory chain by antimycin A did not show any significant differences between LimTXNPx null mutants and WT cells.  In face of these results we conclude that the physiological functions of LimTXNPx appear to be compensated by alternative antioxidants and/or repair mechanisms.

 Supported by: FCT (Portugal), FAPESP and CNPq