title: Mitochondrial proticity and ROS signaling: lessons from the uncoupling proteins.
abstract: Fifty years since Peter Mitchell proposed the theory of chemiosmosis, the transformation of cellular redox potential into ATP synthetic capacity is still a widely recognized function of mitochondria. Mitchell used the term 'proticity' to describe the force and flow of the proton circuit across the inner membrane. When the proton gradient is coupled to ATP synthase activity, the conversion of fuel to ATP is efficient. However, uncoupling proteins (UCPs) can cause proton leaks resulting in poor fuel conversion efficiency, and some UCPs might control mitochondrial reactive oxygen species (ROS) production. Once viewed as toxic metabolic waste, ROS are now implicated in cell signaling and regulation. Here, we discuss the role of mitochondrial proticity in the context of ROS production and signaling.
authors.affiliation: University of Ottawa, Faculty of Medicine, Department of Biochemistry, Microbiology, and Immunology, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada.
authors.forename: Ryan J
authors.initials: RJ
authors.lastname: Mailloux
authors.forename: Mary-Ellen
authors.initials: ME
authors.lastname: Harper
mesh_terms: D000818:Animals; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D000071256:Uncoupling Protein 1
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D017382:Reactive Oxygen Species; D000071256:Uncoupling Protein 1