RESUMO
Toxoplasmosis caused by the protozoan parasite Toxoplasma gondii, is a zoonotic parasitic disease. Oxidative stress plays a dominant role in the host's defense against protozoan infection. In the present study the possible involvement of local oxidative stress in the pathogenesis of T. gondii were investigated. Twenty five female Wistar rats were infected with RH strain of Toxoplasma tachyzoites and twenty female rats were used as control group that only received sterile PBS. Tissue samples from liver, heart and brain on 0, 3, 5, 8 and 45 days post infection were collected. As biochemical markers of oxidative stress, endogenous concentrations of GSH, GPX and SOD activity, MDA level, protein carbonyl content and total antioxidant capacity were determined from the mentioned tissues of control and infected rats. Based on the results, on day 3, 5 and 8 post infection the level of hepatic glutathione were significantly decreased in infected rats when compared to control. There was a significant rise in hepatic glutathione peroxidase activity and malondialdehyde level on the third day post infection in comparison to uninfected rats. Significant elevation of superoxide dismutase activity and malondialdehyde level on 5 day post infection and protein carbonyls and total antioxidant capacity on 8 day post infection in infected livers were obtained. Significant changes of glutathione level, total antioxidant capacity and protein carbonyls contents were observed in cardiac homogenate on days 3, 5 and 45, respectively. Measured parameters were constant throughout all stages of experiment in brain of infected rats. Indeed increased production of reactive oxygen species accompanies Toxoplasma infection in liver and heart tissues of experimentally infected rats. Based on this study, antioxidant defense system can probably play a role in parasitic stage interconversion and shifting the toxoplasmosis into the chronic phase.
