May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Author Affiliations & Notes
  • L.–R. Lin
    Ophthalmology, Univ of Michigan, Ann Arbor, MI
  • E. Kasahara
    Ophthalmology, Univ of Michigan, Ann Arbor, MI
  • Y.–S. Ho
    Institute of Environmental Health Sciences, Wayne State University, Detroit, MI
  • V. Reddy
    Ophthalmology, Univ of Michigan, Ann Arbor, MI
  • Footnotes
    Commercial Relationships  L. Lin, None; E. Kasahara, None; Y. Ho, None; V. Reddy, None.
  • Footnotes
    Support  EY00484
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 399. doi:
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      L.–R. Lin, E. Kasahara, Y.–S. Ho, V. Reddy; REGULATION OF THE EXPRESSION OF Sod2 IN A MOUSE MODEL AND ITS EFFECT ON OXIDATIVE STRESS . Invest. Ophthalmol. Vis. Sci. 2004;45(13):399.

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

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Abstract: : Purpose: To study the protective role of Sod2 on oxidative stress in lens epithelium from mice expressing varying levels of the enzyme and derive primary cultures of lens epithelium from these strains to examine oxidation–induced apoptosis. Methods: Mice with three different levels of Sod2 were generated. Heterozygous (Sod2 half knockout) mice obtained from Jackson Labs (strain B6.129s7 Sod2) were used as breeding pair to derive additional heterozygotes, enzyme deficient; 25% wild–type, normal enzyme level and 25% homozygotes. However, all animals null to the enzyme died within 2–3 days of birth. Transgenic mice with elevated enzyme level were obtained by injection of human Sod2 cDNA into B6C3 mouse oocytes. These mice were mated with wild–type mice to generate hemizygotes, which had about 60% higher expression of the enzyme level compared to wild–type. The lenses removed from the three groups of mice were cultured for 30 minutes in the presence of 25 µM H202 and DNA strand breaks were assayed. Primary cultures of lens epithelium from the heterozygotes and wild type mice were established and their susceptibility to photochemically generated O2 was also evaluated by measuring apoptosis. Results: Lens epithelium from partially–deficient Sod2 (heterozygotes) showed much greater DNA damage compared to those from wild–type (normal enzyme level) or lenses from transgenic mice (hemizygotes) with three times higher Sod2 than heterozygotes. Similar to the findings with epithelium of in situ lenses, primary cultures of lens epithelium derived from these animals showed a direct relationship between enzyme level and resistance to oxidative stress in terms of apoptosis. Conclusions: The present studies extend our previous findings on the role of Sod2 in protection against oxidative damage in lens epithelium in situ as well as in primary cultures derived from respective animal lenses. The results demonstrate that the protective effect of Sod2 against oxidation–induced DNA damage and cell apoptosis is directly related to the enzyme level. Support: NIH (EY00484); Vision Core Grant (EY07003). CR: None

Keywords: antioxidants • apoptosis/cell death • cataract 

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