Blocking chloride channels in the rat lens: localized changes in tissue hydration support the existence of a circulating chloride flux.

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  • Author(s): Young MA;Young MA; Tunstall MJ; Kistler J; Donaldson PJ
  • Source:
    Investigative ophthalmology & visual science [Invest Ophthalmol Vis Sci] 2000 Sep; Vol. 41 (10), pp. 3049-55.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Association For Research In Vision And Ophthalmology (Arvo) Country of Publication: United States NLM ID: 7703701 Publication Model: Print Cited Medium: Print ISSN: 0146-0404 (Print) Linking ISSN: 01460404 NLM ISO Abbreviation: Invest Ophthalmol Vis Sci Subsets: MEDLINE
    • Publication Information:
      Publication: Brookline Ma : Association For Research In Vision And Ophthalmology (Arvo)
      Original Publication: St. Louis, Mosby.
    • Subject Terms:
      Body Water/*metabolism ; Chloride Channels/*antagonists & inhibitors ; Chlorides/*metabolism ; Lens, Crystalline/*metabolism ; Lens, Crystalline/*ultrastructure ; Nitrobenzoates/*pharmacology; 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid/pharmacology ; 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid/pharmacology ; Animals ; Lens, Crystalline/drug effects ; Microscopy, Confocal ; Organ Culture Techniques ; Organ Size ; Rats ; Rats, Wistar ; Tamoxifen/pharmacology
    • Abstract:
      Purpose: To investigate the effects of inhibitors of chloride channels on lens volume and tissue architecture under isotonic conditions.
      Methods: Rat lenses were maintained in organ culture under isotonic conditions in the presence of various putative chloride channel inhibitors. The effect of an inhibitor on lens wet mass and tissue morphology was determined by weighing and histologic examination, respectively.
      Results: Exposure to 100 microM of either 5-nitro-2- (3-phenylpropylamino) benzoic acid (NPPB) or 4, 4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) caused an increase in wet mass and severe tissue disruption in the lens equatorial region. Two distinctly different zones of tissue damage were evident: a peripheral zone of fiber cell swelling and an inner zone of extensive tissue breakdown. Extracellular space dilations caused the extensive tissue damage in the inner zone and preceded the peripheral fiber cell swellings. That the observed effects were a consequence of the inhibition of chloride channels was supported by (1) the effectiveness of NPPB at the lower dose of 10 microM, (2) the absence of any NPPB effect in chloride-free medium, and (3) an identical effect after exposure to tamoxifen, an inhibitor of the chloride channel regulator p-glycoprotein.
      Conclusions: Study results indicate that chloride channels are active in the lens under isotonic conditions. The spatial and temporal pattern of morphologic changes that was observed is consistent with a steady state efflux of chloride ions and water from peripheral fiber cells and a corresponding influx into fiber cells deeper in the lens. These observations may therefore represent the first visualization of the chloride flux postulated by others to be a component of the lens internal circulation system.
    • Accession Number:
      0 (Chloride Channels)
      0 (Chlorides)
      0 (Nitrobenzoates)
      094ZI81Y45 (Tamoxifen)
      27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid)
      3A35O9G3YZ (5-nitro-2-(3-phenylpropylamino)benzoic acid)
      Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
    • Publication Date:
      Date Created: 20000901 Date Completed: 20000914 Latest Revision: 20131121
    • Publication Date:
      20231215
    • Accession Number:
      10967063