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Rabbits infected with Trypanosoma brucei brucei (Basa isolate) were intraperitoneally administered with vitamins C and E at 100 mg/kg and 10 mg/kg body weight, respectively, from day 7 before infection to day 12 post-infection (p.i.). Another group of rabbits were similarly infected, but received no vitamin treatment. The uninfected (control) rabbits were either untreated or treated with vitamins like the infected group. Treatment of the infected animals did not affect the onset and level of parasitaemia. On day 12 p.i., the anaemia tended to be ameliorated, but insignificantly, by the treatment. The infection increased (p0.05) serum urea and creatinine concentrations to similar levels in treated and untreated groups. However, the increase (p0.05) in alanine and aspartate transaminases in the untreated infected animals was prevented in the treated infected ones. Therefore, it seemed that the treatment with antioxidant vitamins boosted their storage in hepatic cells, but not in erythrocytes and glomeruli, to annul any cellular injury due to infection. It is concluded that this may be an indirect evidence that the hepatic damage may be principally due to oxidative injury.

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 (P0.05) 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 (P0.05) 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 (P0.05) in GSH concentration occurred on Day 12 pi at the second peak of parasitaemia followed by a significant (P0.05) 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.

Intraperitoneal inoculation of rats with Trypanosoma congolense (Federe strain) produced a sustained parasitaemia from days 7 to 23 post-infection (pi). The fasting tail-blood glucose (FBG) concentrations in the infected animals increased (p0.05) from 3.8+/-0.2 mmol/l on day 0 pi to 4.6+/-0.2, 4.9+/-0.2 and 5.8+/-0.3 mmol/l on days 7, 10 and 17 pi and decreased (p0.05) to 3.1+/-0.8 and 2.9+/-0.7 mmol/l on days 20 and 23 pi, but the values in the uninfected controls varied between 3.8+/-0.3 mmol/l on day 0 pi and 3.9+/-0.2 mmol/l on day 23 pi. After oral glucose intake (1.0 g/kg) and determination of tail-blood glucose (BG) concentrations after 2 h, the percentage increase in BG from FBG was either comparable in infected and uninfected groups (days 7, 20, 23 pi) or lower (p0.05) in the infected group (days 10, 17), suggesting the same rate of tissue glucose delivery in both groups or a faster rate in the infected group. Therefore, oral glucose tolerance in the infected rat was not impaired, but there was initial fasting hyperglycaemia followed by fasting hypoglycaemia in the later stage.

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.