NRF2 plays a significant role in the suppression of genotoxicity during aging whereas its protective role for acute UVB genotoxicity is limited to MIS response in mouse skin epidermis

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ID: 338265
2026
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Abstract
Our body is continuously exposed to endogenous and exogenous sources of oxidative stress arising from physiological metabolism and environmental factors such as ultraviolet (UV) radiation. These stresses generate reactive oxygen species (ROS) that can induce genotoxicity through oxidative DNA damage. To evaluate the contribution of NRF2, which is a master transcription factor regulating cellular antioxidant responses, to the suppression of oxidative stress-induced genotoxicity in the skin, we examined Nrf2-deficient mice regarding mutagenic responses to two separate biological situations: acute UVB exposures and the chronic process of aging. Analyses were performed using transgenic mice carrying the bacterial lacZ gene as a mutational reporter. No significant differences were detected between Nrf2-deficient and wild-type mice in mutagenicity, induced mutation spectrum, and mutation distribution within the reporter gene after acute UVB exposure, whereas the dose-response kinetics of UVB-induced mutation in the phase called "mutation induction suppression" (MIS) differed significantly between genotypes, with a more pronounced MIS response observed in the Nrf2-/- epidermis. Little contribution of ROS to genotoxicity was observed after the acute exposure. Notably, however, the age-dependent accumulation of mutations was significantly elevated in the Nrf2-deficient epidermis compared to the wild-type. These findings indicate that NRF2 plays a protective role for the skin, not by directly preventing genotoxicity, but by promoting tissue recovery after acute UVB damage and, more importantly, by suppressing the genotoxic effects of physiologically produced ROS in a chronic aging process.
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Authors Hironobu Ikehata, Masayuki P. Yamamoto
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Journal mutation research/genetic toxicology and environmental mutagenesis
Year 2026
DOI
10.1093/mutage/geag037
URL
https://doi.org/10.1093/mutage/geag037
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