April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Apoptosis in the Rat Lens After in vivo Exposure to UV-B Radiation
Author Affiliations & Notes
  • K. Galichanin
    Section for Ophthalmology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
    Section of Ophthalmology, Department of Neuroscience, Uppsala University, Uppsala, Sweden
  • L. Meyer
    Section for Ophthalmology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
    Department of Ophthalmology, University of Bonn, Bonn, Germany
  • S. Löfgren
    Section for Ophthalmology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
  • J. P. Bergmanson
    Texas Eye Research and Technology Center, University of Houston College of Optometry, Houston, Texas
  • P. G. Söderberg
    Section of Ophthalmology, Department of Neuroscience, Uppsala University, Uppsala, Sweden
  • Footnotes
    Commercial Relationships  K. Galichanin, None; L. Meyer, None; S. Löfgren, None; J.P. Bergmanson, None; P.G. Söderberg, None.
  • Footnotes
    Support  Karolinska Institute Eye Research Foundation, Gun och Bertil Stohnes Stiftelse, Swedish Radiation Protection Authority, Swedish Research Council
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2127. doi:
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      K. Galichanin, L. Meyer, S. Löfgren, J. P. Bergmanson, P. G. Söderberg; Apoptosis in the Rat Lens After in vivo Exposure to UV-B Radiation. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2127.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To investigate apoptosis in the lens after in vivo close to threshold ultraviolet-B radiation (UVR-B) around 300 nm.

Methods: : Six-week-old albino Sprague-Dawley rats were familiarized to a rat restrainer five days prior to exposure. Non-anaesthetized rats received double threshold dose (8 kJ/m2) UVR (max = 300 nm) unilaterally for 15 minutes. The animals were sacrificed at 1, 7, 48 and 336 h following exposure, depending on the group belonging. Thereafter, the lenses were extracted and examined with light and transmission electron microscopy.

Results: : Sections of control lenses had a normal single layer of epithelial cells with regular architecture of the nuclear bow, and the lens fibers were packed and oriented in order. One hour after UVR exposure, apoptotic epithelial cells appeared in the central zone and small vacuoles were seen in the outer anterior and posterior cortex. The peripheral epithelium was normal. At 7 hours post-exposure, apoptotic cells and bodies were spread all over the epithelium and the order of the anterior cortical fibers was disturbed at outer anterior cortex. At 48 hours after exposure, the epithelium was full of apoptotic cells with pathologic appearance, apoptotic bodies, debris and extracellular spaces. Closer to the nuclear bow region epithelial cells aggregated in multiple layers. The nuclear bow was deteriorated and cortical fiber cells throughout appeared swollen, partly fused and contained vacuoles. Deeper fiber cells remained accurately organized. After 336 hours, the central epithelium was normalized. Superficial equatorial cortex was composed of disoriented, heavily swollen fiber cells with large intercellular vacuoles. Anterior and posterior deeper fiber cells were swollen. Adjacent cells were involved into phagocytosis of apoptotic cells.

Conclusions: : Lens epithelium is the primary target of UVR exposure. Apoptosis in the lens epithelial cells leads to cataract development after UVR-B exposure. Maximum damage appears at 48 hours after exposure. Adjacent epithelial cells remove apoptotic epithelial cells by phagocytosis. By 336 hours after exposure, the lens epithelium was fully repaired whereas fiber cells remained unrecovered.

Keywords: cataract • apoptosis/cell death • radiation damage: light/UV 
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