title: Effect of vitamin C depletion on UVR-B induced cataract in SMP30/GNL knockout mice.
abstract: We investigated whether decreased vitamin C (VC) in a mouse model increases lens opacity (cataract) induced by in vivo 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 1.5 g/L of VC, respectively. SMP30 KO VC (-), SMP30 KO VC (+), and wild-type (WT) mice, all 14 weeks of age, were unilaterally exposed in vivo to UVR-B (200 mW/cm(2)) for 100 s twice a week for 3 weeks (total: 1200 mJ/cm(2)). At 48 h 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.
authors.affiliation: Department of Ophthalmology, Iwate Medical University, School of Medicine, Uchimaru 19-1, Morioka, Iwate 020-8505, Japan.
authors.forename: Yohei
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Kouhei
authors.initials: K
authors.lastname: Hashizume
authors.forename: Seishi
authors.initials: S
authors.lastname: Kishimoto
authors.forename: Yu
authors.initials: Y
authors.lastname: Tezuka
authors.forename: Hideo
authors.initials: H
authors.lastname: Nishigori
authors.forename: Naoki
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Kondo
authors.forename: Naoki
authors.initials: N
authors.lastname: Maruyama
authors.forename: Akihito
authors.initials: A
authors.lastname: Ishigami
authors.forename: Daijiro
authors.initials: D
authors.lastname: Kurosaka
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000502:physiology*; D001206:Ascorbic Acid Deficiency / Q000150:complications* / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000235:genetics; D002265:Carboxylic Ester Hydrolases / Q000235:genetics; D002386:Cataract / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D007908:Lens, Crystalline / Q000528:radiation effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018384:Oxidative Stress; D011833:Radiation Injuries, Experimental / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D002135:Calcium-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C513324:Rgn protein, mouse; D002265:Carboxylic Ester Hydrolases; C020579:gluconolactonase; D001205:Ascorbic Acid