title: Prevention of UV-induced damage to the anterior segment using class I UV-absorbing hydrogel contact lenses.
abstract: OBJECTIVE
  To determine whether class I ultraviolet (UV) light-blocking contact lenses prevent UV-induced pathologic changes in a rabbit model.
  
  
  METHODS
  Twelve rabbits were assigned to 1 of 3 treatment groups (n = 4), as follows: senofilcon A (class I UV blocking) contact lenses; lotrafilcon A contact lenses (no reported UV blocking); no contact lens. The contralateral eye was patched without a contact lens. Animals received UV-B (1.667 J/cm(2)) exposure daily for 5 days. Postmortem tissue was examined as follows: in the cornea, the expression of matrix-metalloproteinases (MMPs) was evaluated by zymography, and apoptosis was evaluated by TUNEL and caspase-3 ELISA; ascorbate in the aqueous humor was evaluated by nuclear magnetic resonance spectroscopy; crystalline lens apoptosis was evaluated by TUNEL and caspase-3 ELISA.
  
  
  RESULTS
  Exposed corneas showed a significant increase in MMP-2 and -9, TUNEL-positive cells, and caspase-3 activity in the lotrafilcon A group compared with the senofilcon A group (all P = 0.03). A significant decrease in aqueous humor ascorbate was observed in the exposed lotrafilcon A lens-wearing group compared with the exposed senofilcon A lens-wearing group (P = 0.03). Exposed crystalline lenses had significantly increased caspase-3 activity in the lotrafilcon A group compared with the senofilcon A group (P = 0.03). Increased numbers of TUNEL-positive cells were noted in both the lotrafilcon A and the non-contact lens groups.
  
  
  CONCLUSIONS
  The authors show that senofilcon A class I UV-blocking contact lenses are capable of protecting the cornea, aqueous humor, and crystalline lens of rabbits from UV-induced pathologic changes.
authors.affiliation: Ohio State University, College of Optometry, Columbus, Ohio, USA. chandler.111@osu.edu
authors.forename: Heather L
authors.initials: HL
authors.lastname: Chandler
authors.forename: Kathleen S
authors.initials: KS
authors.lastname: Reuter
authors.forename: Loraine T
authors.initials: LT
authors.lastname: Sinnott
authors.forename: Jason J
authors.initials: JJ
authors.lastname: Nichols
mesh_terms: D000818:Animals; D000869:Anterior Eye Segment / Q000378:metabolism / Q000528:radiation effects*; D017209:Apoptosis; D001082:Aqueous Humor / Q000378:metabolism / Q000528:radiation effects; D001205:Ascorbic Acid / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D003263:Contact Lenses, Hydrophilic; D003315:Cornea / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D004797:Enzyme-Linked Immunosorbent Assay; D005128:Eye Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D020100:Hydrogels; D020287:In Situ Nick-End Labeling; D007908:Lens, Crystalline / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D009682:Magnetic Resonance Spectroscopy; D020782:Matrix Metalloproteinases / Q000378:metabolism; D011446:Prospective Studies; D011817:Rabbits; D011833:Radiation Injuries, Experimental / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D011835:Radiation Protection / Q000379:methods; D012828:Silicones; D014466:Ultraviolet Rays / Q000009:adverse effects*; D005466:Fluorocarbons
chemical_list: D001205:Ascorbic Acid; D053148:Caspase 3; D020100:Hydrogels; D020782:Matrix Metalloproteinases; D012828:Silicones; C481129:lotrafilcon A; D005466:Fluorocarbons; C523196:senofilcon A