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Oxidative damage of DNA induced by X-irradiation decreases the uterine endometrial receptivity which involves

Wei Gao1, Jin-Xiao Liang2, Shuai Liu1

  • 1Department of Biochemistry and Molecular Biology, Dalian Medical University, Liaoning Provincial Core Lab of Glycobiology and Glycoengineering Dalian, PRC.

International Journal of Clinical and Experimental Medicine
|June 12, 2015
PubMed

Insights

X irradiation causes female infertility by damaging endometrial cells, leading to mitochondrial and lysosomal dysfunction. Protective agents like NAC may help improve uterine receptivity after radiation exposure.

Area of Science:

  • Reproductive biology
  • Cellular biology
  • Radiation oncology

Background:

  • X irradiation is a known risk factor for female infertility.
  • The precise mechanisms underlying radiation-induced endometrial damage remain unclear.
  • Endometrial epithelial cells play a crucial role in uterine receptivity.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms of X irradiation-induced endometrial dysfunction.
  • To identify potential protective strategies against radiation-induced infertility.

Main Methods:

  • Exposure of endometrial cells to X irradiation.
  • Assessment of morphological and functional changes in endometrial epithelial cells.
  • Evaluation of mitochondrial and lysosomal function.
  • Measurement of oxidative DNA damage.
  • Testing the efficacy of N-acetylcysteine (NAC), ammonium chloride (NH4Cl), and pepstatin A (Pep A) as protective agents.

Main Results:

  • X irradiation induced significant morphological and functional impairments in endometrial epithelial cells.
  • Mitochondrial and lysosomal dysfunction, along with oxidative DNA damage, were observed post-irradiation.
  • Pretreatment with NAC, NH4Cl, or Pep A mitigated the X irradiation-induced cellular damages.
  • These findings highlight the role of oxidative stress and organelle dysfunction in radiation-induced endometrial damage.

Conclusions:

  • X irradiation impairs uterine receptivity through oxidative DNA damage, mitochondrial dysfunction, and lysosomal dysfunction.
  • Targeting these pathways with protective agents like NAC shows promise for preserving endometrial function and fertility after radiation exposure.
Keywords:
DNA damageX irradiationendometrial receptivitylysosomal membrane instabilitymitochondrial dysfunctionoxidative stress

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