May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
d––Tocopherol Reduces Diabetes–Induced Retinal Vascular Leakage and ERG Abnormalities in the Rat
Author Affiliations & Notes
  • N.H. Timothy
    Beetham Eye Institute,
    Joslin Diabetes Center, Boston, MA
  • A.C. Clermont
    Beetham Eye Institute,
    Joslin Diabetes Center, Boston, MA
  • K.M. Della Vecchia
    Beetham Eye Institute,
    Joslin Diabetes Center, Boston, MA
  • G.L. King
    Vascular Cell Biology,
    Joslin Diabetes Center, Boston, MA
  • L.P. Aiello
    Beetham Eye Institute,
    Joslin Diabetes Center, Boston, MA
  • S.E. Bursell
    Beetham Eye Institute,
    Joslin Diabetes Center, Boston, MA
  • Footnotes
    Commercial Relationships  N.H. Timothy, None; A.C. Clermont, None; K.M. Della Vecchia, None; G.L. King, None; L.P. Aiello, None; S.E. Bursell, None.
  • Footnotes
    Support  Mass. Lions Eye Res. & Biomedical Research Partnership EY14106
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1099. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      N.H. Timothy, A.C. Clermont, K.M. Della Vecchia, G.L. King, L.P. Aiello, S.E. Bursell; d––Tocopherol Reduces Diabetes–Induced Retinal Vascular Leakage and ERG Abnormalities in the Rat . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1099.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Abstract: : Purpose: Mediators of diabetic retinal vascular abnormalities include the activation of the diacylglycerol (DAG)/protein kinase C (PKC) pathway, as well as the generation of reactive oxygen intermediates. The anti–oxidant, d–α–tocopherol (Vitamin E), inhibits PKC by enhancing DAG kinase activity. This study examines whether Vitamin E can ameliorate the diabetes–induced impairment in retinal vascular permeability (RVP) and electroretinogram (ERG). Methods: Sprague–Dawley non–diabetic (NDM) and STZ–induced diabetic (DM) rats were treated with 40 mg/kg d–α–tocopherol (Eisai, Tokyo, Jpn) or placebo QOD from onset of diabetes for 4 weeks. Plasma hydroperoxide levels were measured (PeroXOquant, Pierce). Single flash ERGs with a flash time of 5 ms and an illumination of 14000 cd/m2 were performed after 1 hour dark adaptation to evaluate a–wave, b–wave, and oscillatory potential (OP) amplitude and peak latency. RVP was measured using the Evans–blue albumin permeation technique. Results: Plasma hydroperoxide was increased 2.4 fold in DM (20.6±9.5 µmol/l, n=7) versus NDM animals (4.9±4.1 µmol/l, p<0.05) and was totally normalized by Vitamin E treatment in DM rats (3.7±3.7 µmol/l, n=7, p<0.05). Peak latency was prolonged (p<0.05) in DM for OP1–4, b–wave, and summation of OP1–4 as compared to NDM animals. Vitamin E treatment of DM rats inhibited theses diabetes–induced changes in peak OP2 latency and summed OP1–4 by 44±32% (p=0.025) and 36±41% (p=0.046), respectively as compared to DM control. ERG amplitude was reduced (p<0.05) in DM for a–wave, OP1–3, b–wave, and summed OP1–4 compared to NDM. Diabetes–induced alterations in amplitudes for OP1, OP2, & b–wave were inhibited 85±77% (p=0.006), 40±45% (p=0.041), and 57±50% (p=0.036) respectively, by Vitamin E treatment as compared to DM control. Retinal vascular leakage was increased by 94±61% (n=4) in DM compared to NDM animals, an effect abolished by Vitamin E treatment as compared to untreated DM (n=4, 6.3±2.1 vs 22.7±7.2, p=0.006). Conclusions: Treatment with d–α–tocopherol ameliorates diabetes–induced ERG and RVP in abnormalities. Thus, high dose Vitamin E may have therapeutic role in the treatment of diabetic ocular disease.

Keywords: antioxidants • diabetes • electrophysiology: non–clinical 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×