Attenuation of retinal photooxidative damage in thioredoxin transgenic mice

Neurosci Lett. 2002 Jun 28;326(2):142-6. doi: 10.1016/s0304-3940(02)00314-2.

Abstract

Thioredoxin (TRX) is an endogenous redox (reduction/oxidation) regulator that has cytoprotective effects against various types of oxidative stresses. Exposure to excessive levels of white light induces retinal photoreceptor damage. To test the cytoprotective effect of overexpressed TRX against retinal photooxidative damage, both TRX transgenic (trx-tg) mice and C57BL/6 (wild type) mice were exposed to intense white fluorescent light. The amounts of oxidized and tyrosine-phosphorylated proteins decreased in the neural retinas of the trx-tg mice compared to the wild type mice after light exposure. The electroretinographic amplitudes were higher and the formation of oxidized DNA was lower in trx-tg mice compared to wild type mice after light exposure. These results suggest that overexpression of TRX suppresses retinal photooxidative damage. TRX intensification may be a useful therapeutic strategy to prevent retinal photic injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytoprotection*
  • DNA Damage / drug effects
  • Electroretinography
  • Eye Proteins / metabolism
  • Humans
  • Light*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic / genetics
  • Oxidation-Reduction / drug effects
  • Oxidative Stress*
  • Phosphorylation
  • Reference Values
  • Retina / drug effects*
  • Retina / pathology
  • Retina / physiopathology
  • Retina / radiation effects*
  • Thioredoxins / genetics
  • Thioredoxins / pharmacology*
  • Tyrosine / metabolism

Substances

  • Eye Proteins
  • Tyrosine
  • Thioredoxins