Abstract
Toxoplasmosis is a common parasitic infection in the world. Since increased free radicals and oxidative stress are reported in many parasitic diseases the purpose of the present study was to evaluate the oxidative stress in acute and chronic toxoplasmosis. RH strains of Toxoplasma tachyzoites were used in the present study. Twenty-five female rats were infected with the parasite while 25 other rats were as the control group that received normal saline. Zero-, 5-, 7-, 10-, and 45-day postinfection (DPI) blood samples were taken. Some parameters related to oxidant and antioxidants such as antioxidant enzymes, malondialdehyde, and total antioxidant capacity were measured. On day 7 after infection, GPX activity and GSH level were significantly increased and in the mentioned day the amount of total antioxidant capacity was significantly reduced. In other cases, there were no significant differences between the groups in different days. Overall, based on the results it seems that, on day 7 after infection, in infected rats responses to oxidative stress were triggered and led to decrease of total antioxidant capacity. Furthermore, glutathione was increased to cope with stress. It seems that probably antioxidant defense system entered the infection to the chronic phase and changed the parasites stage.
Highlights
Toxoplasma gondii is an obligate intracellular protozoan parasite responsible for toxoplasmosis, a disease that affects many mammals including man [1, 2]
Mononuclear phagocytes, macrophages that have been activated by lymphokines, are the principal defense against intracellular pathogens such as T. gondii and respiratory burst plays an important role against T. gondii [18]
One of the mechanisms that protect the host cells against excess free radicals is the enzymatic antioxidant defense which includes SOD, catalase, peroxiredoxins, flavor hemoglobins, and glutathione S-transferase/GPX coupled to glutathione reductase
Summary
Toxoplasma gondii is an obligate intracellular protozoan parasite responsible for toxoplasmosis, a disease that affects many mammals including man [1, 2]. In people with immunodeficiency, such as AIDS or malignancies, rupture of tissue cysts and the transformation of bradyzoites to tachyzoites result in disease reactivation. Recent investigations indicate that parasitic infections with high tolerance of the host are the result of defense mechanisms which include enhanced generation of reactive oxygen species (ROS) [3, 4]. Even small changes in oxidant or/and antioxidant levels may disturb its balance and leads to oxidative stress. This situation becomes dangerous when the antioxidant system is unable to prevent oxidative reactions triggered by ROS and directed oxidative modification of Oxidative Medicine and Cellular Longevity lipids, proteins, and DNA [5,6,7]. Free radicals are produced continuously by normal metabolic processes, but their rate of production increases during certain parasitic infections
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