title: Inhibition of corneal angiogenesis by ascorbic acid in the rat model.
abstract: OBJECTIVE
  To evaluate the effect of topically administered ascorbic acid on experimentally induced corneal neovascularization in the rat model.
  
  
  METHODS
  Corneal chemical cauterization of 72 eyes in Long-Evans male rats was performed using silver nitrate/potassium nitrate sticks. Nine groups of eight eyes were used to evaluate eight concentrations of ascorbic acid with one group of eight eyes serving as a control. Topical instillation of 100 mg/ml non-pH-neutralized ascorbic acid was performed in one group while the remaining seven groups were evaluated using pH-neutralized ascorbic acid in concentrations of 100 mg/ml, 50 mg/ml, 10 mg/ml, 5 mg/ml, 1 mg/ml, 500 microg/ml, and 250 microg/ml.
  
  
  RESULTS
  The percentage of corneal neovascularization and burn stimulus score was determined for all the eyes. The means of percent of corneal neovascularization in ascorbic acid 100 mg/ml (non-neutralized), 100 mg/ml, 50 mg/ml, 10 mg/ml, 5 mg/ml, 1 mg/ml, 500 microg/ml, 250 microg/ml, and control group were 17.50 +/- 12.80 (p = 0.001), 17.00 +/- 19.30 (p = 0.001), 15.25 +/- 13.26 (p = 0.001), 17.62 +/- 11.89 (p = 0.001), 28.87 +/- 23.08 (p = 0.001), 29.62 +/- 16.91 (p = 0.001), 60.12 +/- 8.50 (p = 0.04), 65.62 +/- 2.26 (p = 0.185), and 68.25 +/- 4.06, respectively (Tables 1 and 2). All animals had a burn score of 2+ or higher (Table 1).
  
  
  CONCLUSIONS
  Ascorbic acid applied in a topical solution appears to inhibit corneal neovascularization in the rat model of inflammatory neovascularization in concentrations in a dose-dependent manner. The optimal dose-effect relation was in our model found in concentrations between 1 mg and 500 microg/ml. At concentrations below 500 microg/ml there was no statistically significant inhibition in the degree of corneal neovascularization compared to control.
authors.affiliation: Department of Ophthalmology, University of Arizona, Arizona Health Sciences Center, 655 N. Alvernon Way, Suite 108, Tucson, AZ 85711, USA. ccole@eyes.arizona.edu
authors.forename: Gholam A
authors.initials: GA
authors.lastname: Peyman
authors.forename: Muhamet
authors.initials: M
authors.lastname: Kivilcim
authors.forename: Ana Munoz
authors.initials: AM
authors.lastname: Morales
authors.forename: John T
authors.initials: JT
authors.lastname: DellaCroce
authors.forename: Mandi D
authors.initials: MD
authors.lastname: Conway
mesh_terms: D000287:Administration, Topical; D020533:Angiogenesis Inhibitors / Q000008:administration & dosage*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001205:Ascorbic Acid / Q000008:administration & dosage*; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004338:Drug Combinations; D006863:Hydrogen-Ion Concentration; D009566:Nitrates / Q000633:toxicity; D017680:Potassium Compounds / Q000633:toxicity; D051381:Rats; D020318:Rats, Long-Evans; D012835:Silver Nitrate / Q000633:toxicity
chemical_list: D020533:Angiogenesis Inhibitors; D000975:Antioxidants; D004338:Drug Combinations; D009566:Nitrates; D017680:Potassium Compounds; D012835:Silver Nitrate; D001205:Ascorbic Acid; C023844:potassium nitrate