June 1993
Volume 34, Issue 7
Free
Articles  |   June 1993
Ultrastructure of fiber cells and multilamellar inclusions in experimental diabetes.
Author Affiliations
  • M J Costello
    Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599-7090.
  • C W Lane
    Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599-7090.
  • D L Hatchell
    Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599-7090.
  • P Saloupis
    Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599-7090.
  • L M Cobo
    Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599-7090.
Investigative Ophthalmology & Visual Science June 1993, Vol.34, 2174-2185. doi:
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      M J Costello, C W Lane, D L Hatchell, P Saloupis, L M Cobo; Ultrastructure of fiber cells and multilamellar inclusions in experimental diabetes.. Invest. Ophthalmol. Vis. Sci. 1993;34(7):2174-2185.

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Abstract

PURPOSE: The goal of this ultrastructural study was to examine fiber cell shape and intercellular junctions during the early stages of fiber cell breakdown and edema in diabetic rabbit lenses. METHODS: Lens abnormalities were recorded with a slit lamp. Between 6-10 mo after drug treatment, diabetic lenses and untreated control lenses were freshly enucleated and sectioned with a vibrating knife microtome. The thick tissue sections were chemically fixed and processed for thin-section electron microscopy. RESULTS: Alloxan-induced diabetes in albino rabbits produced clinically apparent cataracts as soon as 1 mo after the animals became hyperglycemic. The cataracts displayed cortical fluid-filled vacuoles in the equatorial region and at the cortex-nucleus interface, white specks scattered throughout the cortex, and posterior subcapsular cataracts. Fiber cells just deeper than the large cortical vacuoles had oval or spindle-shaped cross sections. Multilamellar inclusions, not reported previously for diabetic lenses, were observed at or near the fiber cell interfaces and were composed of concentric or spiral rings of plasma membrane-bound cytoplasmic processes. Undulating membranes were present throughout most of the multilamellar inclusions. Transparent lenses from untreated controls did not have such multilamellar bodies or extensive membrane undulations in cells at the same distance from the lens surface. CONCLUSIONS: Fiber cells respond to the diabetic insult differently depending on their stage of differentiation and age. The observed changes are consistent with the hypothesis that hyperglycemia accelerates the formation of age-related changes in fiber cells.

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