Liver retinol and carotenoid concentration of rats experimentally infected with trypanosoma brucei

Abstract

The acute phase response to infection has been reported to include a decline in the vitamin A status of the infected host in some disease, and the application of vitamin A supplementation in the management of these disease conditions had led to significant reductions in the severity, morbidity and mortality associated with them. Also cellular and tissue injury in trypanosome infections has partly been attributed to oxidative stress and depletion of some systemic antioxidants. This study investigated the liver retinol and carotenoid concentration of rats experimentally infected with Trypanosoma brucei. Results of the liver retinol determination showed that T. brucei infection led to a progressively significant (P < 0.01) depletion of liver retinol concentration (body vitamin A status) of infected rats from day 5 to day 25 post-infection. The decline was found to be significantly directly proportional to the degree of hepatomegaly (r = 0.778, p < 0.05) and splenomegaly (r = 0.778, p < 0.05), but not significantly related to the level of parasitaemia (r = 0.407, p > 0.05). Results of the liver carotenoids determination showed a gradual depletion of liver carotenoids from day 5 post-infection, being most severe from day 10 to day 20 post-infection when the mean liver carotenoids of infected rats was significantly (p < 0.0 1) lower than that of uninfected ones. These findings suggest prospects for trials on vitamin A supplementation in the management of T. brucei infections, and support the assertion that oxidative stress plays a significant role in cellular injury in trypanosome infections.


(Tropical Veterinarian: 2002 20(1): 1-7)