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K. Kiuchi, M. Kondo, S. Ueno, K. Moriguchi, K. Yoshizawa, A. Tsubura, M. Matsumura; Nicotinamide Functionally Rescues N-Methyl-N-Nitrosourea-Induced Retinopathy in Rats . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2842.
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Purpose: In our previous study, Nicotinamide (NAM) suppressed MNU-induced photoreceptor cell loss in rats when administered immediately after MNU treatment; a dose of 1000 mg/kg NAM completely suppressed photoreceptor cell loss, and a lower dose partially suppressed photoreceptor cell loss, as determined morphologically. In the present study, we evaluated functional rescue of MNU-induced retinopathy by NAM in Sprague-Dawley rats, comparing findings of ERG with those of retinal histology. Method: Rats were devided to 5 age-matched controls (group 1), and MNU treatment rats following immediately by injection of 1000 (group 3) or 50 mg/kg NAM (group 4) or vehicle (group 2) 5 rats per group. Animals were examined 7 days after the treatment, and the 3 groups of MNU-treated rats were compared with the MNU-untreated controls. Result: ERG findings correlated well with retinal histology. The outer nuclear layer and photoreceptor layer of MNU-untreated animals (group 1) was 67 um , while MNU-treated animals(group 4) showed thinning (3u m), while NAM treatment following MNU injection resulted in greater survival of photoreceptor cells (group 2, 70 and group 3, 47u m, respectively). Scotopic and photopic ERG results showed that both rod and cone photoreceptor cell functions, respectively, were comparable to controls by 1000 mg/kg NAM, whereas 50 mg/kg NAM treatment conferred less protection. Conclusion: NAM rescue photoreceptor cells from MNU-induced retinal damage both functionally and structurally. NAM at a dose of 1000 mg/kg caused no abnormality in blood chemistry. The results indicate that NAM has potential as a therapeutic agent for treatment of MNU induced retinal degeneration.
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