Analysis of retinal degeneration in vitamin C knockout mice

维生素C敲除小鼠视网膜变性分析

• 批准号: 22791681
• 负责人: HASHIZUME Kohei
• 金额: $ 2.58万
• 依托单位: Iwate Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22791681/
• 关键词: ビタミンC; 網膜変性; 加齢性眼疾患; 酸化ストレス; 遺伝子

(1) In vitamin C knockout mice(SMP30 knockout mice) given the 0.0375 g/L aqueous solution of vitamin C, the eye vitamin C level decreased to approximately 1/3 of that in wild type mice. In vitamin C knockout mice given the 1.5 g/L aqueous solution of vitamin C, the eye vitamin C level was similar to that in wild type mice. Thus, the 2 V vitamin C doses can be viewed as appropriate for achieving V vitamin C deficiency and sufficiency, respectively, in the vitamin C knockout mouse eye.(2) In SMP30 knockout mice(vitamin C deficiency) group retina damage and lens opacities induced by UVR-B were significantly larger than in SMP30 knockout mice(vitamin C sufficiency) group or in wild type mice group. It was suggested that vitamin C deficiency increases retina and lens susceptibility to UVR-B induced oxidative stress in mice.

(1)在给予0.0375 g/L维生素C水溶液的维生素C敲除小鼠（SMP 30敲除小鼠）中，眼睛维生素C水平降低至野生型小鼠的约1/3。在给予1.5 g/L维生素C水溶液的维生素C敲除小鼠中，眼睛维生素C水平与野生型小鼠相似。因此，2 V维生素C剂量可被视为分别适合于在维生素C敲除小鼠眼中实现V维生素C缺乏和充足。(2)在SMP 30基因敲除小鼠（维生素C缺乏）组中，UVR-B诱导的视网膜损伤和透镜混浊显著大于SMP 30基因敲除小鼠（维生素C充足）组或野生型小鼠组。提示维生素C缺乏增加了小鼠视网膜和透镜对UVR-B诱导的氧化应激的敏感性。