Poly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) is an abundant nuclear 
protein that is involved in DNA repair, cell cycle control, programmed cell 
death and transcriptional regulation. It also plays critical roles in the 
pathogenesis of inflammatory disorders. Here we have performed a detailed 
analysis of the interplay between the apicomplexan parasite Toxoplasma gondii 
and host cell PARP and its consequences for the host-parasite relationship. Our 
results have shown that T. gondii significantly decreased PARP expression in its 
host cells within 10min of infection but that the amount of PARP normalized 
during prolonged infection. Importantly, down-regulation of PARP expression 
after infection abrogated the ADP-ribosylation of acceptor proteins in response 
to oxidative stress. Overexpression of PARP in RAW264.7 cells revealed that 
elevated amounts of PARP neither affected host cell invasion nor intracellular 
development of T. gondii in non-stimulated or IFN-gamma/LPS-stimulated 
monocytes/macrophages. Furthermore, measurements of the activities of effector 
caspases 3 and 7 indicated that the blockade of host cell apoptosis by T. gondii 
occurs independently of the inhibition of PARP after infection. These findings 
suggest that the prominent decrease of host cell PARP and poly(ADP-ribos)ylation 
after parasitic infection do not affect the intracellular development of T. 
gondii in vitro.