title: Role of water and electrolyte influxes in anoxic plasma membrane disruption.
abstract: The role of water and electrolyte influxes in anoxia-induced plasma membrane disruption was investigated using rabbit proximal tubule suspension. The results indicated that normal proximal tubule (PT) cells have a great capacity for expanding cell volume in response to water influx, whereas anoxia increases the susceptibility to water influx-induced disruption, and this was attenuated by glycine. However, resistance of anoxic plasma membranes to water influx-induced stress is not lost, although their mechanical strength was diminished, compared with normoxic membranes. Anoxic membranes did not disrupt under an intra-to-extracellular osmotic difference as great as 150 mosM. Potentiating or attenuating water influx by incubating PT cells in hypotonic or hypertonic medium, respectively, during anoxia, did not affect anoxia-induced membrane disruption. After the transmembrane electrolyte concentration gradient was eliminated by a "intracellular" buffer or by permeabilizing the plasma membrane to molecules <4 kDa using alpha-toxin, anoxia still caused further membrane disruption that was prevented by glycine or low pH. These results demonstrate that 1) water or net electrolyte influxes are probably not a primary cause for anoxia-induced membrane disruption and 2) glycine could prevent the plasma membrane disruption during anoxia independently from its effect on transmembrane electrolyte or water influxes. The present data support a biochemical rather than a mechanical alteration of the plasma membrane as the underlying cause of membrane disruption during anoxia.
authors.affiliation: Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.forename: L J
authors.initials: LJ
authors.lastname: Mandel
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D002478:Cells, Cultured; D004573:Electrolytes / Q000378:metabolism*; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D007424:Intracellular Fluid / Q000502:physiology; D007672:Kidney Cortex / Q000166:cytology / Q000502:physiology*; D007687:Kidney Tubules, Proximal / Q000166:cytology / Q000502:physiology*; D007700:Kinetics; D007770:L-Lactate Dehydrogenase; D009994:Osmolar Concentration; D011817:Rabbits; D010738:Type C Phospholipases / Q000494:pharmacology
chemical_list: D004573:Electrolytes; D007770:L-Lactate Dehydrogenase; D010738:Type C Phospholipases