Skip to main content
. 2014 Feb 20;20(6):1000–1037. doi: 10.1089/ars.2013.5447

Table 3.

Role of ROS in Protozoan Infections of Medical Importance

Pathogen Observed effects of ROS/antioxidants on pathogen's burden Model Associated mechanisms of resistance Suspected mechanisms underlying results References
Leishmania major NAC treatment of BALB/c mice reduced burden, whereas BSO (a drug that depletes gluthatione) increased burden in C57BL/6 footpads Mice were treated with NAC Increase in the frequency of IFN-γ-secreting lymphocytes in draining popliteal lymph nodes from NAC-treated mice It remains unknown whether reduction of burden is dependent on IFN-γ-secreting lymphocytes (56, 270, 276)
  Treatment of infected macrophages with GSH-depleting BSO before IFN-γ/LPS activation increased burden Elicited peritoneal macrophages(C57BL/6 mice) treated with BSO for 24 h, activated with IFN-γ/LPS GSH depletion was associated with a decrease in NO production It remains unknown whether GSH inhibited L. major growth in macrophages (276)
  NRF2-activator resveratrol reduced parasite burden of infected macrophages Elicited peritoneal macrophages or J774 murine cell line treated with resveratrol Resveratrol acts to reduce parasite burden in macrophages at lower doses than directly The mechanisms activated by resveratrol remain unknown (138)
Leishmania amazonensis NAC treatment reduced parasite burden in footpads from infected BALB/c mice NAC treatment of BALB/c mice No clues to how NAC reduced footpad parasite burden No suspected mechanism (205)
  DETC, an inhibitor of SOD activity, promoted parasite destruction in infected macrophages or reduced parasite burden in vivo, NAC reversed this effect Peritoneal macrophages from BALB/c mice Superoxide production seems to be a killing mechanism. No controls treated only with NAC IFN β increases parasite burden through induction of SOD and decrease of superoxide (141)
Trypanosoma cruzi ROS exposure of epimastigotes increased their growth Epimastigotes grow more actively in LIT medium containing H2O2 ROS affects cell signaling. No similar mechanisms are known in amastigotes (77, 226)
  Increased infection under oxidative conditions and vice versa, in macrophages and in vivo. Burden reduced in infected macrophages incubated with antioxidants, transfected with Nrf2 or HO-1, and vice versa in H2O2 or PMA. Treatment with NRF2-activators reduce parasitemia, also reduced in gp91phox−/−.mice Elicited peritoneal macrophages, BMMs or THP-1 cells; C57BL/6 and NOX2(gp91phox)−/− mice Reduction of labile iron pool associated with reduction in parasite growth by antioxidants. NO, type I IFN, and apoptosis of infected cells not involved Direct effects of ROS on amastigote proliferation were not ruled out, nor were mechanisms indirectly associated with reduction of labile iron pool (93, 210, 218, 235, 272, 285)

BSO, buthionine sulfoximine; LPS, lipopolysaccharide; NO, nitric oxide; SOD, superoxide dismutase.