Study of Pathological Mechanism in Light Induced Retinal Damage using DNA Base Excision Repair Gene Knockout Mice

本研究旨在利用8-氧代鸟嘌呤-DNA糖基化酶（OGG 1）、人MutT同源物1（MTH 1）和MutY糖基化酶同源物（MUTYH）基因敲除小鼠阐明光诱导视网膜损伤的病理机制。将小鼠暴露于350-385 nm波长的光，并且视网膜辐射暴露为75 J/cm 2。MUTYH基因敲除小鼠视网膜光损伤减轻，提示MUTYH参与了光损伤的病理机制。我们的研究结果表明，通过控制MUTYH抑制神经变性可能有效地保护视网膜光损伤。

The present study aimed to elucidate the pathological mechanism in light induced retinal damage using 8-oxoguanine-DNA glycosylase (OGG1), human MutT Homolog 1 (MTH1) and MutY glycosylase homologue (MUTYH) knockout mice. Mice were exposed to 350-385 nm wavelengths light, and retinal radiant exposure was 75 J/cm2. Retinal light damage was reduced in MUTYH knockout mice, indicating that MUTYH involved in the pathological mechanism of light damage. Our results show the possibility that the suppression of neurodegeneration by control of MUTYH may effectively protect retinal light damage.