Andrew W Siu1, Chi-ho To. 1. Laboratory of Experimental Optometry, Department of Optometry and Radiography, The Hong Kong Polytechnic University, Hung Hom, Kowloon, China.
Abstract
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 mM iron (II) or sodium nitroprusside (SNP) solution for 60 minutes at 37 degrees C. The amounts of malondialdehyde (MDA) were measured and the concentrations per unit weight protein provided an index of LPO. RESULTS: After the iron (II) and SNP treatments, MDA levels were significantly different among the three tissues (p < 0.0001) in a dose-dependent manner (p < 0.0001). The retinal MDA level was significantly higher than those of the kidney (p < 0.001) and the liver (p < 0.001). For the iron (II)-treated homogenates, the differences in MDA were statistically significant in the retina (p = 0.0001) and the liver (p = 0.0004). For the SNP-treated homogenates, the differences in MDA were all statistically significant in the retina (p = 0.002), the 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 than liver and kidney tissue. The retinal responses to SNP and iron (II) treatments were comparable, suggesting that NO(*)- and (*)OH-induced LPO damage shared similar mechanism in vitro. Future work is required to identify the protective system in living retina.
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 mM iron (II) or sodium nitroprusside (SNP) solution for 60 minutes at 37 degrees C. The amounts of malondialdehyde (MDA) were measured and the concentrations per unit weight protein provided an index of LPO. RESULTS: After the iron (II) and SNP treatments, MDA levels were significantly different among the three tissues (p < 0.0001) in a dose-dependent manner (p < 0.0001). The retinal MDA level was significantly higher than those of the kidney (p < 0.001) and the liver (p < 0.001). For the iron (II)-treated homogenates, the differences in MDA were statistically significant in the retina (p = 0.0001) and the liver (p = 0.0004). For the SNP-treated homogenates, the differences in MDA were all statistically significant in the retina (p = 0.002), the 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 than liver and kidney tissue. The retinal responses to SNP and iron (II) treatments were comparable, suggesting that NO(*)- and (*)OH-induced LPO damage shared similar mechanism in vitro. Future work is required to identify the protective system in living retina.