Background: Free radicals can cause cellular oxidation and consequent membrane lipid peroxidation (LPO). The significance of these effects on retinal tissue is unclear. This study compared the retinal LPO products, after the incubation with nitric oxide or hydroxyl radical, with those of two commonly studied tissues–kidney and liver.

Methods: Retina, liver and kidney were obtained from Sprague‐Dawley rats. These samples were homogenised and incubated with variously 2, 20 or 200 uM iron (II) or sodium nitroprusside (SNP) solution for 60 minutes at 37d̀ C. The amounts of malondialdehyde (MDA) were measured and the concentrations per unit weight protein provided an index of LPO.

Results: After die iron (II) and SNP treatments, MDA levels were significandy different among die three tissues (p < 0.0001) in a dose‐dependent manner (p < 0.0001). The retinal MDA level was significandy higher dian diose of die kidney (p < 0.001) and the liver (p < 0.001). For die iron (II)‐treated homogenates, die differences in MDA were statistically significant in the retina (p = 0.0001) and die liver (p = 0.0004). For die SNP‐treated homogenates, die differences in MDA were all statistically significant in die retina (p = 0.002), die liver (p < 0.0001) and the kidney (p < 0.0001). There was no statistical difference in retinal MDA concentrations between iron (II) and SNP treatments (p = 0.41).

Discussion: Retinal tissue is several times more susceptible to free radical‐induced LPO dian liver and kidney tissue. The retinal responses to SNP and iron (II) treatments were comparable, suggesting diat NO*‐ and *OH‐induced LPO damage shared similar mechanism in vitro. Future work is required to identify the protective system in living retina.