Investigation of DNA damage and protein damage caused by oxidative stress in canine visceral leishmaniasis

Abstract

Leishmaniasis, considered by the World Health Organization as one of the most important zoonotic diseases, causes death when it is not treated in its self-healing skin form. The aim of this study was to investigate DNA damage and oxidative protein damage that occurs in dogs infected with Leishmania infantum. The study group consisted of 25 dogs, including 10 clinically healthy dogs aged 2 to 6 years and 15 dogs infected with Leishmania infantum diagnosed by means of the rk39 dipstick test and the immunofluorescence antibody test (IFAT). The effects of oxidative stress on protein were evaluated in the dogs infected with Leishmania infantum by determining plasma malondialdehyde, protein carbonyl groups, nitrotyrosine, and total antioxidant capacity in blood. DNA damage, on the other hand, was determined by the COMET method. Plasma protein carbonyl content (PCO) and nitrotyrosine (NT) levels, which are considered as indicators of protein damage, were found to be higher in the dogs infected with Leishmania infantum compared to the control group, but the difference in both values was not statistically significant (p > 0.05). Plasma malondialdehyde (MDA), an indicator of lipid peroxidation, was significantly higher in the dogs infected with Leishmania infantum than in the control group. TAC levels, however, were lower in the leishmanial dogs (p < 0.05). According to the results of the COMET assay, lymphocyte cells were damaged in the leishmanial dogs, and both tail intensity (TI) and tail moment (TM) values were higher in those dogs than they were in the control group (p < 0.05, p < 0.01). The parasites caused oxidative stress through protein and DNA damage in the host and decreased the antioxidant capacity concentration that prevents destructive effects.