Analysis of retinal degeneration in vitamin C knockout mice

(1)维生素C敲除小鼠（SMP30敲除小鼠）给予0.0375 g/L维生素C水溶液后，眼内维生素C水平降至野生型小鼠的1/3左右。维生素C敲除小鼠给予1.5 g/L的维生素C水溶液后，其眼内维生素C水平与野生型小鼠相近。因此，在维生素C敲除小鼠的眼睛中，2v维生素C剂量可被视为分别实现V维生素C缺乏和充足的适当剂量。(2) UVR-B致SMP30基因敲除小鼠（维生素C缺乏）组视网膜损伤和晶状体混浊明显大于SMP30基因敲除小鼠（维生素C充足）组和野生型小鼠组。提示维生素C缺乏增加小鼠视网膜和晶状体对UVR-B诱导的氧化应激的易感性。

(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.