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| Main Authors: | , , , , , , , , , , |
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| Format: | Artículo Open Access |
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Wiley
2025
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| Online Access: | https://onlinelibrary.wiley.com/doi/10.1111/php.70059 |
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| author | Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan |
| author_facet | Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan |
| collection | Wiley Open Access |
| contents | Transcriptional benchmark dose modeling of ultraviolet radiation‐induced genomic activation in mouse skin Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan Photochemistry and Photobiology Abstract The in vivo transcriptional response of mouse skin to ultraviolet radiation (UV‐R) exposure reveals key genomic alterations associated with UV‐R‐induced damage but it does not provide precise dose thresholds for these effects. These initial findings provided the impetus to advance dose–response characterization by integrating benchmark dose (BMD) modeling with transcriptomic data, aiming to identify biologically relevant points of departure for gene and pathway activation. To accomplish this, mice were exposed to five erythemally weighted UV‐R doses (0–40 mJ/cm 2 ) emitted from a UV‐emitting tanning device, across six post‐exposure timepoints (0–96 h). Four analytical methods were used to estimate BMDs, with the lowest consistent response dose (LCRD) approach yielding the most sensitive estimates (1.21–3.44 mJ/cm 2 ). Transcriptomic responses revealed activation of shared pathways related to DNA damage and cancer, oxidative stress and metabolism, inflammation and immunity, and hormonal disruption. Notably, the majority of LCRD BMD estimates (1.21–3.44 mJ/cm 2 ) were lower than the International Electrotechnical Commission standard actinic exposure limit (3 mJ/cm 2 (erythemally weighted)) for broadband UV‐R (200–400 nm) for unprotected skin and the eye for an 8 h period. These findings suggest that transcriptomic BMD modeling can detect early biological responses to UV‐R at doses lower than current exposure limits. 10.1111/php.70059 http://creativecommons.org/licenses/by/4.0/ |
| doi_str_mv | 10.1111/php.70059 |
| format | Artículo Open Access |
| id | wiley_oa_10_1111_php_70059 |
| institution | Wiley Open Access |
| license_str_mv | http://creativecommons.org/licenses/by/4.0/ |
| publishDate | 2025 |
| publisher | Wiley |
| record_format | wiley_oa |
| spellingShingle | Transcriptional benchmark dose modeling of ultraviolet radiation‐induced genomic activation in mouse skin Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan Photochemistry and Photobiology Transcriptional benchmark dose modeling of ultraviolet radiation‐induced genomic activation in mouse skin Sami S. Qutob Samantha P. M. Roesch Sandy Smiley Pascale V. Bellier Andrew Williams Kate B. Cook Matthew J. Meier Andrea Rowan‐Carroll Carole L. Yauk James P. McNamee Vinita Chauhan Photochemistry and Photobiology Abstract The in vivo transcriptional response of mouse skin to ultraviolet radiation (UV‐R) exposure reveals key genomic alterations associated with UV‐R‐induced damage but it does not provide precise dose thresholds for these effects. These initial findings provided the impetus to advance dose–response characterization by integrating benchmark dose (BMD) modeling with transcriptomic data, aiming to identify biologically relevant points of departure for gene and pathway activation. To accomplish this, mice were exposed to five erythemally weighted UV‐R doses (0–40 mJ/cm 2 ) emitted from a UV‐emitting tanning device, across six post‐exposure timepoints (0–96 h). Four analytical methods were used to estimate BMDs, with the lowest consistent response dose (LCRD) approach yielding the most sensitive estimates (1.21–3.44 mJ/cm 2 ). Transcriptomic responses revealed activation of shared pathways related to DNA damage and cancer, oxidative stress and metabolism, inflammation and immunity, and hormonal disruption. Notably, the majority of LCRD BMD estimates (1.21–3.44 mJ/cm 2 ) were lower than the International Electrotechnical Commission standard actinic exposure limit (3 mJ/cm 2 (erythemally weighted)) for broadband UV‐R (200–400 nm) for unprotected skin and the eye for an 8 h period. These findings suggest that transcriptomic BMD modeling can detect early biological responses to UV‐R at doses lower than current exposure limits. 10.1111/php.70059 http://creativecommons.org/licenses/by/4.0/ |
| title | Transcriptional benchmark dose modeling of ultraviolet radiation‐induced genomic activation in mouse skin |
| topic | Photochemistry and Photobiology |
| url | https://onlinelibrary.wiley.com/doi/10.1111/php.70059 |