Effect of acute Trypanosoma vivax infection on cattle erythrocyte glutathione and susceptibility to in vitro peroxidation.

During acute Trypanosoma vivax infection of calves, produced by intravenous inoculation, the mean packed cell volume and red blood cell counts of the infected animals decreased significantly (P < 0.05) between Days 6 and 13 post-infection (pi). The moderately severe normocytic anaemia started to develop during the first wave of parasitaemia which occurred from Day 2 pi and peaked between Days 4 and 5 pi. The mean erythrocyte glutathione (GSH) concentration of the infected calves decreased significantly (P < 0.05) from 58.4 +/- 11.4 mg 100ml-1 red blood cells (RBC) on Day 0 pi to 44.5 +/- 12.8 mg 100ml-1 RBC on Day 5 pi. As the GSH values recovered on Day 6 pi and increased thereafter, another slight decrease (P > 0.05) in GSH concentration occurred on Day 12 pi at the second peak of parasitaemia followed by a significant (P < 0.05) increase to 79.1 +/- 14.6 mg 100ml-1 RBC on Day 13 pi. In the uninfected calves, the mean GSH values ranged from 47.7 +/- 7.0 to 60.8 +/- 6.8 mg 100ml-1 RBC. When washed, erythrocytes of the infected and uninfected calves were separately challenged with hydrogen peroxide. They produced comparable amounts of thiobarbituric acid reactive substances as a measure of by-products of lipid peroxidation. This suggested that the ability of the erythrocytes to prevent peroxidative injury was not reduced, because GSH regeneration was probably enhanced and the antioxidant capacity of the erythrocytes was maintained.

Increased susceptibility of erythrocytes to in vitro peroxidation in acute Trypanosoma brucei infection of mice.

Trypanosoma brucei, Wamba strain, produced an acute infection in mice, and mortality was observed 2 days after the onset of parasitaemia which occurred 3-5 days postinfection. Anaemia was observed in the tail blood of the survivors. When washed erythrocytes from the heart blood were incubated in physiological saline containing 1.5% hydrogen peroxide, the erythrocytes of the infected mice produced significantly greater amounts of by-products of lipid peroxidation (measured as thiobarbituric acid reactive substances) than the erythrocytes of the control mice. This observation suggested that the infected mice may have a reduced ability in the prevention of free radical mediated lipid peroxidation in the erythrocyte membrane. It is concluded that peroxidative injury to the erythrocytes may contribute to the pathogenesis of anaemia in trypanosomosis.