Functional rescue of N-methyl-N-nitrosourea-induced retinopathy by nicotinamide in Sprague-Dawley rats

被引：27
作者：
Kiuchi, K
Kondo, M
Ueno, S
Moriguchi, K
Yoshizawa, K
Miyake, Y
Matsumura, M
Tsubura, A [1 ]
机构：
[1] Kansai Med Univ, Dept Pathol, Osaka 5708506, Japan
[2] Kansai Med Univ, Dept Ophthalmol, Osaka 5708506, Japan
[3] Nagoya Univ, Sch Med, Dept Ophthalmol, Showa Ku, Nagoya, Aichi 466, Japan
[4] Fujisawa Pharmaceut Co Ltd, Toxicol Res Labs, Dept Toxicol Pathol, Yodogawa Ku, Osaka 532, Japan
来源：
CURRENT EYE RESEARCH | 2003年 / 26卷 / 06期
关键词：
electroretinogram; nicotinamide; N-methyl-N-nitrosourea; retinitis pigmentosa; retinopathy;
D O I：
10.1076/ceyr.26.5.355.15435
中图分类号：
R77 [眼科学];
学科分类号：
100212 ;
摘要：
Purpose. A single intraperitoneal injection of 60 mg/kg body weight of N-methyl-N-nitrosourea (MNU) into rats results in retinal degeneration over a 7-day period in all treated animals. The purpose of this study was to determine whether nicotinamide (NAM) can lead to a functional rescue of the MNU-induced retinopathy. Methods. NAM, a water-soluble B-group vitamin (vitamin BA was administered immediately after MNU injection, and retinas were examined morphologically and functionally. Results. Morphologically, 1000 mg/kg NAM completely suppressed and 50 mg/kg NAM partially suppressed the photoreceptor cell loss. Functionally, scotopic and photopic electroretinographic (ERG) recordings showed that both rod and cone photoreceptor cells were well protected from MNU damage by 1000 mg/kg NAM and partially protected by 50 mg/kg NAM. Conclusions. NAM can protect photoreceptor cells from MNU-induced retinopathy both structurally and functionally.
引用
收藏
页码：355 / 362
页数：8
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