8-hydroxyguanine and isodialuric-acid

Oxidative stress and reactive oxygen species (ROS)-induced DNA base damage are thought to be central mediators of UV-induced carcinogenesis and skin aging. However, increased steady-state levels of ROS-induced DNA base damage have not been reported after chronic UV exposure. Accumulation of ROS-induced DNA base damage is governed by rates of lesion formation and repair. Repair is generally performed by Base Excision Repair (BER), which is initiated by DNA glycosylases, such as 8-oxoguanine glycosylase and Nei-Endonuclease VIII-Like 1 (NEIL1). In the current study, UV light (UVB) was used to elicit protracted low-level ROS challenge in wild-type (WT) and Neil1

Topics: Animals; Cytokines; DNA Damage; DNA Glycosylases; DNA Repair; Gene Expression Profiling; Gene Expression Regulation; Guanine; Inflammation; Mice; Mice, Knockout; Neutrophil Infiltration; Oxidative Stress; Pyrimidines; Reactive Oxygen Species; Skin; Thymine; Ultraviolet Rays; Uracil