Further studies needed for topical DNA repair effects after ultraviolet light skin damage
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Key takeaways:
- Eight of the 18 tested genes underwent significant changes 24 hours after UVB exposure.
- While the skin was naturally able to recover, DNA repair enzymes, T4N5 and photolyase did not show any added benefit.
Topical DNA repair enzymes did not participate in the recovery of damaged skin, characterized by altered genes, following ultraviolet light exposure, according to a study.
It is known that deoxynucleic acid (DNA) damage to the skin is caused by ultraviolet (UV) light. Although this damage is well documented, there are challenges that practitioners continue to face, according to the study.
“The ability to treat DNA damage and restore skin to the original state before it is grossly damaged remains a clinical challenge,” Jane M. Anderson, BSA, of the research department at Moy-Fincher-Chipps Facial Plastics & Dermatology in Beverly Hills, California, and colleagues wrote.
In this study, the researchers determined the 24-hour changes in gene expression among certain gene families following UV B-ray (UVB) exposure to assess the natural recovery mechanisms of skin. The authors also evaluated the restoration of damaged skin after 2 weeks of topical DNA repair enzymes treatment.
Researchers took samples of the right and left post-auricular areas of the skin of 48 patients before and 24 hours after UVB exposure using noninvasive, adhesive patch collection kits. After patients applied topical DNA repair enzymes to the right post-auricular area once daily for 2 weeks, the skin was reassessed for damage.
Results showed that eight of the 18 tested genes underwent significant changes 24 hours after UVB exposure. The gene families that experienced downregulation compared with baseline included vitamin A, mucin, programmed cell death protein, small proline-rich protein, cystatin and keratinocyte (P < .01 for all). In contrast, interleukin experienced significant upregulation (P < .01).
The DNA repair enzymes used in this study, T4N5 and photolyase, did not show any effect on the expression of the studied genes. Nevertheless, the authors found that the skin was naturally able to recover from DNA damage over the course of 2 weeks with five of the seven genes tested exhibiting a reversal toward baseline.
The authors, however, do not rule out that additional repair may be needed to fully return to baseline.
“Other gene families that may not fully recover from UVB exposure should be investigated to better understand UV events that lead to skin cancers,” Anderson and colleagues wrote.
The authors concluded that certain genes are altered by UV exposure and may play a role in skin cancer growth, specifically genes in the mucin and cystatin families for squamous cell carcinoma and genes in the vitamin A family for melanoma.
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