title: Free radical tissue damages in the anterior segment of the eye in experimental autoimmune uveitis.
abstract: OBJECTIVE
  To investigate increased free radical activity and the accumulation and localization of lipid peroxidation in the anterior segment of the eye with uveitis.
  
  
  METHODS
  Experimental autoimmune uveitis (EAU) was induced in rats using human S-antigen peptide. Conjugated dienes (CD) and keto-dienes (KD) were then extracted from the cornea, iris-ciliary body and lens of the EAU eyes. The quantity of CD and KD were determined by measuring ultraviolet absorption and estimating by means of a molar extinction coefficient. Frozen sections of EAU eyes were reacted with 3-hydroxy-2-naphthoic acid hydrazide (NAH), and NAH-carbonyl compounds were detected using a confocal laser scanning microscope. Statistical comparisons of CD and KD products between the EAU groups and controls were performed using the Student's t-test.
  
  
  RESULTS
  Compared to controls, CD and KD were significantly increased in the cornea and iris-ciliary body of EAU eyes. Lenses of EAU eyes showed a tendency to elevated levels of CD and KD. In EAU, primarily the anterior border layer and the posterior epithelium of the iris--and, to a lesser extent, the trabecular meshwork and corneal endothelium--revealed positive fluorescence staining for peroxidized carbonyl products. No staining was observed on the ciliary epithelium.
  
  
  CONCLUSIONS
  Free radicals and lipid peroxidation products are generated in the anterior segment of the eye in EAU. Because the individual tissues in the anterior segment are composed of various levels of fatty acids and different concentrations of antioxidants, the extent of tissue damage from lipid peroxidation may represent a balance between the fatty acid composition and the antioxidant distribution in each of the tissues.
authors.affiliation: Doheny Eye Institute, University of Southern California, School of Medicine, Los Angeles, CA 90033, USA.
authors.forename: S
authors.initials: S
authors.lastname: Ishimoto
authors.forename: G S
authors.initials: GS
authors.lastname: Wu
authors.forename: S
authors.initials: S
authors.lastname: Hayashi
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: N A
authors.initials: NA
authors.lastname: Rao
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D000869:Anterior Eye Segment / Q000378:metabolism / Q000473:pathology*; D000941:Antigens / Q000737:chemistry; D019393:Arrestin; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D002924:Ciliary Body / Q000378:metabolism / Q000473:pathology; D003315:Cornea / Q000378:metabolism / Q000473:pathology; D005136:Eye Proteins / Q000737:chemistry; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D005260:Female; D005609:Free Radicals; D007498:Iris / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation; D018613:Microscopy, Confocal; D008969:Molecular Sequence Data; D010446:Peptide Fragments / Q000737:chemistry; D010726:Phosphodiesterase Inhibitors / Q000737:chemistry; D051381:Rats; D011917:Rats, Inbred Lew; D014606:Uveitis, Anterior / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*
chemical_list: D000941:Antigens; D019393:Arrestin; D005136:Eye Proteins; D005231:Fatty Acids, Unsaturated; D005609:Free Radicals; D010446:Peptide Fragments; D010726:Phosphodiesterase Inhibitors