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Updated: Nov 5, 2025

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage
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Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage

Published on: February 15, 2020

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p53 and clock genes play an important role in memory and learning ability depression due to long-term ultraviolet A

Keiichi Hiramoto1, Y Yamate2, E F Sato2

  • 1Department of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie, Japan. hiramoto@suzuka-u.ac.jp.

Photochemical & Photobiological Sciences : Official Journal of the European Photochemistry Association and the European Society for Photobiology
|May 19, 2021
PubMed
Abstract

Insights

Long-term UVA eye irradiation impairs memory and learning by increasing p53 and reducing clock gene and Sirt1 levels. Inhibiting p53 can restore cognitive function, suggesting a novel therapeutic target.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Molecular Biology

Background:

  • Long-term exposure to ultraviolet A (UVA) radiation is known to impair cognitive functions like memory and learning in mice.
  • The precise molecular mechanisms underlying UVA-induced cognitive decline remain largely unelucidated.

Purpose of the Study:

  • To investigate the effects of chronic UVA eye irradiation on cognitive function and related molecular pathways in ICR mice.
  • To identify key molecular changes associated with UVA-induced memory and learning deficits.

Main Methods:

  • Mice eyes were subjected to UVA irradiation three times weekly for one year.
  • Cognitive performance was assessed using water maze and step-through passive avoidance tests.
  • Brain levels of p53, clock genes (Period2, Clock, Bmal1), NAD+ metabolizing enzymes (NMNAT, NAMPT), NAD+, and Sirt1 were quantified.

Main Results:

  • UVA irradiation significantly elevated p53 levels in the brain.
  • A significant decrease was observed in Period2, Bmal1, Clock, NMNAT and NAMPT activities, NAD+, and Sirt1 levels.
  • Inhibition of p53 activity ameliorated the cognitive deficits induced by UVA exposure.

Conclusions:

  • Chronic UVA eye irradiation disrupts the circadian clock gene expression and NAD+ metabolism.
  • Elevated p53 and reduced Sirt1 are implicated in UVA-induced memory and learning impairment.
  • Targeting p53 may offer a therapeutic strategy to mitigate cognitive decline from UVA exposure.
Keywords:
Brain and muscle arnt-like protein 1ClockNicotinamide adenine dinucleotideP53Sirtuin 1

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