Oxidative stress and alteration of endogenous antioxidant enzymes play roles in the pathophysiological mechanism of trypanosomosis. The oxidative stress marker: malondialdehyde- MDA and antioxidative stress markers: Serum catalase- CAT, Serum Reduced Glutathione -GSH-Rd and Serum Superoxide dismutase- SOD of Nigerian local dogs (NLD) experimentally infected with Trypanosoma brucei were evaluated after treatments with diminazene aceturate (DA) and isometamidium chloride (IMC). Twenty dogs of age 3 – 4 months were assigned to any of the four groups of five dogs each as follows: 1 = infected and treated with DA (7.0 mg/kg); 2 = uninfected untreated; 3 = infected and untreated; 4 = infected and treated with IMC (0.5 mg/kg). DA and IMC cleared the parasites from the blood, following treatment of the dogs. Relapse was recorded in two dogs in group 1 and one dog in group 4 on days 35 and 56 post-infection (PI) respectively. No dog died except one in group 1. The levels of malondialdehyde- MDA increased significantly by day 7 post-infection in all the infected groups. However, by day 14 post-infection the malondialdehyde levels in group 4 became similar with group 2. The MDA level in group 1 remained significantly higher than in group 2. As from days 7 – 14 post-infection Catalase, Reducedg glutathionend superoxide dismutase levels in the infected groups were significantly lower than group 2. Nevertheless, both trypanocides did not return the levels of CAT, GSH, and SOD to pre-infection values before the termination of the experiment. The findings suggested that the two trypanocides could neither reverse the induced oxidative stress nor normalize the antioxidant capacity of the dogs infected with T. brucei.
Key words: Diminazene aceturate; Dogs; Isometamidium chloride; Oxidative stress; Trypanosoma brucei
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