Impact of hydrogen peroxide-driven Fenton reaction on mouse oocyte quality

Faten Shaeib1, Jashoman Banerjee, Dhiman Maitra

  • 1Department of Obstetrics and Gynecology, The C.S. Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI 48201, USA.

Insights

Hydroxyl radical ((•)OH) generated by Fenton reaction damages mouse oocyte microtubules and chromosomal alignment. This damage, particularly from combined hydrogen peroxide and iron treatments, suggests a cause for poor oocyte quality.

Area of Science:

  • Reproductive Biology
  • Oxidative Stress Research
  • Cell Biology

Background:

  • Metaphase-II mouse oocytes are crucial for fertilization.
  • Microtubules (MT) and chromosomal alignment (CH) are vital for successful meiosis.
  • Oxidative stress, including hydroxyl radical ((•)OH) generation, can impact cellular structures.

Purpose of the Study:

  • To investigate the effect of hydroxyl radical ((•)OH) on metaphase-II mouse oocyte MT and CH.
  • To determine the role of the Fenton reaction in mediating this damage.
  • To explore potential therapeutic targets for mitigating oxidative stress-induced oocyte damage.

Main Methods:

  • Metaphase-II mouse oocytes were treated with hydrogen peroxide (H2O2) and/or iron (Fe(II)).
  • Oocytes were fixed, stained, and evaluated for MT and CH integrity by blinded observers.
  • Statistical analyses (Pearson χ(2) and Fisher exact tests) were used for outcome comparison.

Main Results:

  • Combined H2O2 and Fe(II) treatment significantly increased poor MT and CH scores (p<0.001).
  • H2O2 or Fe(II) alone showed minimal impact compared to controls.
  • Increasing H2O2 concentrations with fixed Fe(II) led to 70-100% poor MT and CH scores.

Conclusions:

  • Hydroxyl radical ((•)OH) generated via the Fenton reaction significantly deteriorates metaphase-II mouse oocyte spindle and chromosomal alignment.
  • This damage is a potential cause of poor oocyte quality.
  • Free iron and reactive oxygen species (ROS) scavengers may offer a therapeutic strategy against (•)OH-mediated oocyte damage.