April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Potential Role of Superoxide Dismutase 1 in Normal-Tension Glaucoma
Author Affiliations & Notes
  • K. Yuki
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • T. Yoshida
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • T. Kurihara
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • S. Kubota
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • M. Sasaki
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • K. Noda
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
    Ophthalmology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • S. Ishida
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
    Ophthalmology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • Y. Ozawa
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • K. Tsubota
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan
  • Footnotes
    Commercial Relationships  K. Yuki, None; T. Yoshida, None; T. Kurihara, None; S. Kubota, None; M. Sasaki, None; K. Noda, None; S. Ishida, None; Y. Ozawa, None; K. Tsubota, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 6129. doi:
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      K. Yuki, T. Yoshida, T. Kurihara, S. Kubota, M. Sasaki, K. Noda, S. Ishida, Y. Ozawa, K. Tsubota; Potential Role of Superoxide Dismutase 1 in Normal-Tension Glaucoma. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6129.

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

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Abstract

Purpose: : Glaucomatous optic neuropathy is believed to be associated with oxidative stress. Moreover, normal-tension glaucoma may have predisposing condition for neuropathy. However, the underlying mechanism remains to be elucidated. In this study, we analyzed the influence of superoxide dismutase 1 (SOD-1), one of the major antioxidant enzymes which catalyze superoxide anion, as a potential pathogenic molecule for normal-tension glaucoma.

Methods: : 24 week SOD-1 -/- C57BL/6J mice were evaluated. The levels of reactive oxygen species (ROS) in the retinal ganglion cell (RGC) layer was measured by dihydroehidium. Retinal ganglion cell numbers were quantified in two ways. First, the number of RGCs in the retinal sections of hematoxylin and eosin staining was counted. Second, the number of RGCs, retrogradely labeled from the superior colliculus with Fluoro-Gold 7 days before, was examined in the whole mounted retina with fluoroscence microscopy to determine the RGC density. Function of retinal ganglion cell was evaluated using pattern electroretinogram (ERG). Intraocular pressure was measured with an induction-impact tonometer.

Results: : The levels of ROS in the RGC layer was significantly increased in SOD-1 -/- mice compared to that of WT mice (P<0.01). The number of RGCs in the section of the retina was significantly decreased in SOD-1 -/- mice (P<0.05). The number of retrogradely labeled RGCs /mm2 in SOD-1 -/- mice was significantly reduced (P<0.01).The amplitude of pattern ERG in SOD-1 -/- mice was significantly reduced compared with that of WT mice (P<0.0001). No significant difference in the amplitude of cone ERG, scotopic a-wave and b-wave ERG between SOD-1 -/- mice and WT mice was observed. There was no significant difference in the IOP levels between SOD-1 -/- mice and WT mice.

Conclusions: : SOD-1 plays a role in accumulating ROS in RGC, and RGC degeneration under the normal IOP condition. SOD-1 may have a critical role in generating glaucomatous optic neuropathy in normal tension glaucoma.

Keywords: oxidation/oxidative or free radical damage 
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