Effect of vitamin C depletion on UVR-B induced cataract in SMP30/GNL knockout mice

Yohei Ishikawa, Kouhei Hashizume*, Seishi Kishimoto, Yu Tezuka, Hideo Nishigori, Naoki Yamamoto, Yoshitaka Kondo, Naoki Maruyama, Akihito Ishigami, Daijiro Kurosaka

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

36 Citations (Scopus)


We investigated whether decreased vitamin C (VC) in a mouse model increases lens opacity (cataract) induced by invivo exposure to ultraviolet radiation type B (UVR-B).Senescence marker protein-30 (SMP30) knockout (KO) mice, which cannot synthesize VC due to genetic disruption of the gluconolactonase (GNL) gene, were divided into 2 groups: VC sufficient (VC (+)) and VC deficient (VC (-)). Starting at 1 month of age, these groups had free access to water containing 0.0375 and 1.5g/L of VC, respectively. SMP30 KO VC (-), SMP30 KO VC (+), and wild-type (WT) mice, all 14 weeks of age, were unilaterally exposed invivo to UVR-B (200mW/cm 2) for 100s twice a week for 3 weeks (total: 1200mJ/cm 2). At 48h after the last UVR-B exposure, cataract morphology was documented, and the ratio of cataract induction was quantified as the cataract area ratio (opacity area/anterior capsule).UVR-B exposure induced cataract mainly at anterior sub-capsular in SMP30 KO VC (-), SMP30 KO VC (+), and WT mice. In SMP30 KO VC (-) lenses the opacities were more extensive than in SMP30 KO VC (+) or WT lenses (cataract area ratios: 59.3%±10% vs. 32.2%±11.7% or 29.0%±9.0%; P<0.01).In conclusion, VC depletion may increase the susceptibility to develop UVR-B induced cataracts in mice unable to endogenously produce VC.

Original languageEnglish
Pages (from-to)85-89
Number of pages5
JournalExperimental Eye Research
Issue number1
Publication statusPublished - 2012 Jan
Externally publishedYes


  • Cataract
  • Lens
  • UV radiation
  • Vitamin C

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


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