Radical metabolism in the gut of blood-sucking animals

 

 

Pedro L Oliveira

 

(a) Instituto de Bioquímica Médica, Programa de Biologia Molecular e Biotecnologia, Universidade Federal do Rio de Janeiro, CEP 2a94a-590, Rio de Janeiro, Brazil.

 

 

 

Heme is a pro-oxidant molecule, which redox activity depends on the interaction with ROS produced by oxidative cell metabolism (mitochondrial respiration, NADPH oxidase, among others). Blood feeding insects generate high concentrations of heme in their midguts as a consequence of hemoglobin degradation and we have obtained evidence .that counteracting heme toxicity is a general trend in the evolution of hematophagy among blood sucking arthropods.  However, besides the toxic effects of reactive oxygen species (ROS) it has been shown that these molecules have important roles in a wide range of physiological processes, from signal transduction, modulation of cellular response to stress and infection and microbial killing.  Concerning this scenario we have characterized the production of ROS in the midgut of Ae aegypti. Using redox sensitive dyes we found that high ROS levels are present in the gut lumen of sugar-fed Ae aegypti females, which are markedly lowered immediately after a blood meal. A similar pattern was found in Rhodnius prolixus, an insect vector of Chaga’s disease, with a reduction in radical formation in the posterior midgut, the segment of digestive apparatus where hemoglobin degradation takes place. In the cattle tick, Boophilus microplus, hemoglobin is taken up by midgut cells by means of receptor-mediated endocytosis and digestion is intracellular. In tick cells, however, intense reduction of the amount and respiratory activity of mitochondria – a major source of oxygen radicals – seems to parallel hemoglobin accumulation and digest cell maturation. Taken all together, our data suggest that the control of radical production is a major antioxidant mechanism that may be operating in the gut of hematophagous invertebrates, helping to ameliorate toxic effects of heme.