1. Variation in ultraviolet-B (UV-B)-induced DNA damage repair mechanisms in plants and humans: an avenue for developing protection against skin photoaging.
- Author
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Mmbando, Gideon Sadikiel
- Subjects
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EFFECT of radiation on plants , *DNA repair , *TUMOR suppressor proteins , *P53 antioncogene , *EXCISION repair , *SKIN aging - Abstract
Purpose: The increasing amounts of ultraviolet-B (UV-B) light in our surroundings have sparked worries about the possible effects on humans and plants. The detrimental effects of heightened UV-B exposure on these two vital elements of terrestrial life are different due to their unique and concurrent nature. Understanding common vulnerabilities and distinctive adaptations of UV-B radiation by exploring the physiological and biochemical responses of plants and the effects on human health is of huge importance. The comparative effects of UV-B radiation on plants and animals, however, are poorly studied. This review sheds light on the sophisticated web of UV-B radiation effects by navigating the complex interaction between botanical and medical perspectives, drawing upon current findings. Conclusion: By providing a comprehensive understanding of the complex effects of heightened UV-B radiation on plants and humans, this study summarizes relevant adaptation strategies to the heightened UV-B radiation stress, which offer new approaches for improving human cellular resilience to environmental stressors. UV-B: Ultraviolet-B radiation CPD: Cyclobutane pyrimidine dimer UVR8: UV RESISTANCE LOCUS8 (UVR8) COP1: CONSTITUTIVELY PHOTOMORPHOGENIC1 ATM/ATR: Ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia and Rad3-related XPA: Xeroderma pigmentosum complementation group A XPC: Xeroderma pigmentosum complementation group C XPD: xeroderma pigmentosum D helicase P53: Tumor suppressor protein 'guardian of the genome' In plants, high doses of UV-B radiation activate the UV RESISTANCE LOCUS8 (UVR8) signaling pathway, which results in increased production of flavonoids and enhanced activity of DNA damage-repairing enzymes. In humans, the high UV-B radiation leads to the activation of genes for protection in different pathways, such as tumor suppressor gene p53 and nucleotide excision repair proteins, including xeroderma pigmentosum complementation group A (XPA), xeroderma pigmentosum complementation group C (XPC), and xeroderma pigmentosum D helicase (XPD). The cellular response to UV-induced DNA damage is largely controlled by the activation of the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia and Rad3-related (ATR) protein kinases. Since humans lack cyclobutane pyrimidine dimer (CPD) photolyase, photolyase from UV-B-tolerant plants could be added to sunscreen extract and dermatological cream to increase their effectiveness in shielding human cells from UV-B damage. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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