RESUMO
The common bed bug Cimex lectularius (Linnaeus 1758) is an ectoparasite that feeds preferably on human blood, being considered an important public health issue. Blood-feeding is a challenging process for hematophagous organisms, and one of the inherent risks with this kind of diet is the liberation of high doses of free heme after the digestion of hemoglobin. In order to deal with this potent cytotoxic agent, such organisms have acquired different defense mechanisms. Here, we use UV-visible spectrophotometry and infrared spectroscopy to show that C. lectularius crystalizes free heme to form the much less dangerous compound, hemozoin. According to our results, the peak of formation of hemozoin in the intestinal contents occurred 4-5 days after the blood meal, primarily in the posterior midgut. The quantification of the rate of conversion of heme to hemozoin revealed that at the end of digestion all the heme was in the form of hemozoin. Inhibition of the synthesis of hemozoin using the anti-malarial drug quinine led to an increase in both catalase activity in the intestinal epithelium and the mortality of the bed bugs, indicating that the insects were unable to cope with the oxidative stress generated by the overload of free heme. The data presented here show for the first time how C. lectularius deals with free heme, and how the process of formation of hemozoin is essential for the survival of these insects. Since resistance to insecticides is a common feature among field populations of bed bugs, there is an urgent need to develop alternative control methods. Thus, targeting the synthesis of hemozoin emerges as a possible novel strategy to fight bed bugs.