Oxidative damage of erythrocytes: a possible mechanism for premature hemolysis in experimental visceral leishmaniasis in hamsters

Visceral leishmaniasis is accompanied by severe anemia and pancytopenia. Re active oxygen species are known to contribute to the pathogenesis of severa l red blood cell (RBCs) disorders. The present study reveals the extent of oxidative stress and the efficacy of the primary antioxidant system in eryt hrocytes of hamsters in the progressive anemic response at different stages of leishmanial infection. Increased intracellular precipitation of Heinz b odies secondary to oxidative denaturation of hemoglobin and enhanced format ion of malonyldialdehyde suggest oxidative damage of erythrocytes, both in the hemoglobin and cell membrane, respectively. Decreased activities of sup eroxide dismutase and catalase in the infected animals indicate the generat ion of O-2(.-) and H2O2, which in turn may produce the highly reactive (OH) -O-. species. Decreases in the reduced glutathione level along with the dec reased activities of glutathione reductase and glutathione. peroxidase poin t to a deficient antioxidant defense system during the post-infection perio d. Accentuated degradation of both cytoskeletal and integral membrane prote ins after 3 months of infection may eventually lead to membrane destabiliza tion and early lysis of erythrocytes in experimental visceral leishmaniasis .