The purpose of this research is to elucidate the pathway associated with cyanide-resistant oxygen uptake in mitochondria. Cyanide-resistant respiration occurs in a wide range of plants and animals, including pathogenic protozoa of the genus Trypanosoma (sleeping sickness). There is conflicting information in the literature concerning the role of a metal, particularly iron, at the active site of the cyanide-resistant oxidase and the role of ubiquinone in the overall cyanide-resistant pathway. Research will focus on the use of the inhibitor dibromothymoquinone which seems to inhibit electron transfer in mitochondria by reducing the fluidity of the mitochondrial membrane. The effects of dibromothymoquinone on fluidity will be studied using fatty acid spin labels and EPR spectroscopic techniques. Studies of the reduction and oxidation of dibromothymoquinone in plant and animal mitochondria will also be carried out to determine why dibromothymoquinone has such different effects on mitochondria from the two sources. Optical and EPR spectroscopy will be used to study the mechanism of inhibition of the enzyme lipoxygenase by salicylhydroxamic acid and propyl gallate. Similarities exist between lipoxygenase and the cyanide-resistant oxidase so knowledge of how these two compounds inhibit lipoxygenase could give a clearer picture of the cyanide-resistant oxidase.
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