title: Transmission electron microscopy and autofluorescence findings in the cornea of diabetic rats treated with aminoguanidine.
abstract: BACKGROUND
  The accumulation of advanced glycation end products (AGEs) has been implicated in the pathogenesis of diabetic keratopathy. The present study was aimed to understand if aminoguanidine (AG), an AGE inhibitor, was protective against the development of corneal complications in a diabetic rat model.
  
  
  METHODS
  Wistar rats were divided into three experimental groups: control, diabetic, and AG-treated diabetic. Diabetes was induced in rats via a single intraperitoneal injection (60 mg/kg) of streptozocin (STZ) and AG was administered in drinking water at a dose of 1 g/L. All animals were sacrificed at the end of 10 weeks and corneas from diabetic and nondiabetic rats were analyzed via transmission electron microscopy (TEM). Corneal autofluorescence measurements were also performed in all experimental groups.
  
  
  RESULTS
  Electron microscopic evaluation revealed that aminoguanidine treatment in diabetic rats prevented the formation of intracellular spaces between neighbouring cells in the superficial corneal epithelium. Hyperglycemia-induced degeneration of intracellular organelles and formation of cytoplasmic vacuoles in the corneal stroma was also prevented with the treatment of AG. Corneal autofluorescence detected in the diabetic group (5.98 +/- 2.17 Fi/mg protein) was found to be significantly greater than the control (3.92 +/- 0.56 Fi/mg protein) and the AG-treated diabetic group (4.18 +/- 0.59 Fi/mg protein) (p < 0.05).
  
  
  CONCLUSIONS
  The presented data provide evidence that AG is preventive against corneal alterations in experimental diabetes.
authors.affiliation: Department of Ophthalmology, Akdeniz University Medical School, Antalya, Turkey. iyucel@akdeniz.edu.tr
authors.forename: Iclal
authors.initials: I
authors.lastname: Yücel
authors.forename: Gültekin
authors.initials: G
authors.lastname: Yücel
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Akar
authors.forename: Necdet
authors.initials: N
authors.lastname: Demir
authors.forename: Nilgün
authors.initials: N
authors.lastname: Gürbüz
authors.forename: Mutay
authors.initials: M
authors.lastname: Aslan
mesh_terms: D000818:Animals; D003315:Cornea / Q000648:ultrastructure*; D003316:Corneal Diseases / Q000209:etiology / Q000473:pathology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D006146:Guanidines / Q000627:therapeutic use*; D008297:Male; D046529:Microscopy, Electron, Transmission / Q000379:methods*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D013050:Spectrometry, Fluorescence / Q000379:methods; D013311:Streptozocin / Q000633:toxicity
chemical_list: D004791:Enzyme Inhibitors; D006146:Guanidines; D013311:Streptozocin; D019001:Nitric Oxide Synthase; C004479:pimagedine