Hepatic oxidative stress in Mongolian gerbils experimentally infected with Babesia divergens.

The present study aimed to investigate oxidative stress, DNA damage, and histopathological alterations in hepatic tissues of Mongolian gerbils experimentally infected with Babesia divergens. It was found that parasitaemia reached approximately 77% at day 5 post-infection. The liver became dark-brown and extremely friable, and hepatic sinusoids were dilated and contained macrophages and parasite-containing erythrocytes. Infection also induced inflammation and injury of the liver. This was illustrated by (1) an increase in inflammatory cellular infiltrations, (2) a decrease in total antioxidant capacity, as indicated by lowered glutathione and catalase levels, (3) increased production of nitric oxide-derived products (nitrite/nitrate) and malondialdehyde, and (4) increased lactic acid dehydrogenase activity and protein carbonyl content in the liver. Infection also interfered with the normal cell cycle of the hepatic tissue, as indicated by a significant increase in the percentage of liver cells at G0/G1 from approximately 86.2% to 97.5% and in S phases from 0.28% to 2.2%. Collectively, the present data suggest that B. divergens infection could induce cell-cycle alteration following oxidative stress and DNA damage in hepatic tissue. Further work is required to investigate the mechanism by which this hepatic tissue damage takes place.