Evidence for the existence of an inner membrane anion channel in mitochondria.
Mitochondria normally exhibit very low electrophoretic permeabilities to physiologically important anions such as chloride, bicarbonate, phosphate, succinate, citrate, etc. Nevertheless, considerable evidence has accumulated which suggests that heart and liver mitochondria contain a specific anion-conducting channel. In this review, a postulated inner membrane anion channel is discussed in the context of other known pathways for anion transport in mitochondria. This anion channel exhibits the following properties. It is anion-selective and inhibited physiologically by protons and magnesium ions. It is inhibited reversibly by quinine and irreversibly by dicyclohexylcarbodiimide. We propose that the inner membrane anion channel is formed by inner membrane proteins and that this pathway is normally latent due to regulation by matrix Mg2+. The physiological role of the anion channel is unknown; however, this pathway is well designed to enable mitochondria to restore their normal volume following pathological swelling. In addition, the inner membrane anion channel provides a potential futile cycle for regulated non-shivering thermogenesis and may be important in controlled energy dissipation.
D000818:Animals; D000838:Anions; D001692:Biological Transport; D004594:Electrophysiology; D006801:Humans; D007425:Intracellular Membranes / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology*; D008928:Mitochondria / Q000502:physiology*; D008933:Mitochondrial Swelling
D000838:Anions; D007473:Ion Channels