title: Mitochondrial permeability transition in the crustacean Artemia franciscana: absence of a calcium-regulated pore in the face of profound calcium storage.
abstract: When mammalian mitochondria are exposed to high calcium and phosphate, a massive swelling, uncoupling of respiration, and release of cytochrome c occur. These changes are mediated by opening of the mitochondrial permeability transition pore (MPTP). Activation of the MPTP in vivo in response to hypoxic and oxidative stress leads to necrotic and apoptotic cell death. Considering that embryos of the brine shrimp Artemia franciscana tolerate anoxia for years, we investigated the MPTP in this crustacean to reveal whether pore opening occurs. Minimum molecular constituents of the regulated MPTP in mammals are believed to be the voltage-dependent anion channel, the adenine nucleotide translocators, and cyclophilin D. Western blot analysis revealed that mitochondria from A. franciscana possess all three required components. When measured with a calcium-sensitive fluorescent probe, rat liver mitochondria are shown to release matrix calcium after addition of >/=100 microM extramitochondrial calcium (MPTP opening), whereas brine shrimp mitochondria continue to take up extramitochondrial calcium and do not release internal stores even up to 1.0 mM exogenously added calcium (no MPTP opening). Furthermore, no swelling of A. franciscana mitochondria in response to added calcium was observed, and no release of cytochrome c could be detected. HgCl(2)-dependent swelling and cytochrome c release were readily confirmed, which is consistent with the presence of an "unregulated pore." Although the absence of a regulated MPTP in A. franciscana mitochondria could contribute to the extreme hypoxia tolerance in this species, we speculate that absence of the regulated MPTP may be a general feature of invertebrates.
authors.affiliation: Division of Cellular, Developmental and Integrative Biology, Department of Biological Sciences, Louisiana State University, 202 Life Sciences Bldg., Baton Rouge, LA 70803, USA. menze@lsu.edu
authors.forename: Michael A
authors.initials: MA
authors.lastname: Menze
authors.forename: Kirk
authors.initials: K
authors.lastname: Hutchinson
authors.forename: Susan M
authors.initials: SM
authors.lastname: Laborde
authors.forename: Steven C
authors.initials: SC
authors.lastname: Hand
mesh_terms: D000818:Animals; D001156:Artemia / Q000378:metabolism*; D002118:Calcium / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000378:metabolism*; D008297:Male; D008628:Mercury / Q000494:pharmacology; D008928:Mitochondria / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D008933:Mitochondrial Swelling / Q000187:drug effects; D010539:Permeability / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013395:Sucrose / Q000494:pharmacology
chemical_list: D007473:Ion Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D013395:Sucrose; D045304:Cytochromes c; D008628:Mercury; D002118:Calcium