Cyanide-resistant respiration in Taenia crassiceps metacestode (cysticerci) is explained by the H 2O 2-producing side-reaction of respiratory complex I with O 2

Abstract

The nature of the cyanide-resistant respiration of Taenia crassiceps metacestode was studied. Mitochondrial respiration with NADH as substrate was partially inhibited by rotenone, cyanide and antimycin in decreasing order of effectiveness. In contrast, respiration with succinate or ascorbate plus N, N, N′, N′-tetramethyl- p-phenylenediamine (TMPD) was more sensitive to antimycin and cyanide. The saturation kinetics for O 2 with NADH as substrate showed two components, which exhibited different oxygen affinities. The high-O 2-affinity system ( K m app = 1.5 μM) was abolished by low cyanide concentration; it corresponded to cytochrome aa 3. The low-O 2-affinity system ( K m app = 120 μM) was resistant to cyanide. Similar O 2 saturation kinetics, using succinate or ascorbate–TMPD as electron donor, showed only the high-O 2-affinity cyanide-sensitive component. Horse cytochrome c increased 2–3 times the rate of electron flow across the cyanide-sensitive pathway and the contribution of the cyanide-resistant route became negligible. Mitochondrial NADH respiration produced significant amounts of H 2O 2 (at least 10% of the total O 2 uptake). Bovine catalase and horse heart cytochrome c prevented the production and/or accumulation of H 2O 2. Production of H 2O 2 by endogenous respiration was detected in whole cysticerci using rhodamine as fluorescent sensor. Thus, the CN-resistant and low-O 2-affinity respiration results mainly from a spurious reaction of the respiratory complex I with O 2, producing H 2O 2. The meaning of this reaction in the microaerobic habitat of the parasite is discussed.