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Toxoplasma gondii, the etiological agent of toxoplasmosis, infects nucleated cells and then resides and multiplies within a parasitophorous vacuole. For this purpose, the parasite secretes many virulence factors for the purpose of invading and subverting the host microbicidal defenses in order to facilitate its survival in the intracellular milieu. Essential metals are structural components of proteins and enzymes or cofactors of enzymatic reactions responsible for these parasitic survival mechanisms. However, an excess of non-essential or essential metals can lead to parasite death. Thus, infected host cells were incubated with 20 µM ZnCl2 in conjunction with 3 µMCdCl2 or HgCl2 for 12 h in order to investigate cellular events and organelle damage related to intracellular parasite death and elimination. In the presence of these metals, the tachyzoites undergo lipid uptake and transport impairment, functional and structural mitochondrial disorders, DNA condensation, and acidification of the parasitophorous vacuole, thus leading to parasite death. Additional research has suggested that lysosome-vacuole fusion was involved in parasite elimination since acid phosphatases were found inside the parasitophorous vacuole, and vacuoles containing parasites were also positive for autophagy. In conclusion, low concentrations of CdCl2, HgCl2, and ZnCl2 can cause damage to Toxoplasma gondii organelles, leading to loss of viability, organelle death, and elimination without causing toxic effects to host cells. [ABSTRACT FROM AUTHOR]

The participation of resident, elicited, and activated macrophage surface components during internalization of tachyzoites of Toxoplasma gondii was analyzed using neuraminidase, phospholipase C, trypsin, protease, and hyaluronidase. Treatment of these macrophages with neuraminidase from Vibrio cholerae, phospholipase C from Bacillus cereus and Clostridium perfringens, protease, and hyaluronidase prior to their interaction with parasites increased the penetration of host cells by T. gondii. Incubation of macrophages with trypsin significantly inhibited the uptake of parasites. Our findings confirm previous observations that treatment of the macrophages with cytochalasin D under conditions that completely block the typical phagocytic process partially inhibits infection of the cells by T. gondii. The results of simultaneous treatment of the macrophages with enzymes and cytochalasin D suggested that the observed enhancement of cell infection by treatment with neuraminidase and hyaluronidase was attributable to a classic phagocytic process, whereas that obtained using phospholipase resulted from active penetration. [ABSTRACT FROM AUTHOR]