Prothioconazole exposure disrupts oocyte maturation and fertilization by inducing mitochondrial dysfunction and apoptosis in mice

Free Radic Biol Med. 2024 Mar:213:274-284. doi: 10.1016/j.freeradbiomed.2024.01.027. Epub 2024 Jan 18.

Abstract

Prothioconazole (PTC), a novel broad-spectrum triazole fungicide, has attracted widespread concern due to its wide use and toxicological effects on non-target organisms. However, little is known about the impact of PTC on oocyte quality and female fertility, especially on oocyte maturation and fertilization. In the present study, we reported that PTC exposure affects the oocyte developmental competence and oocyte fertilization ability to weaken female fertility. Firstly, PTC compromises oocyte development ability by disrupting spindle morphology and chromosome alignment, as well as decreasing acetylation level of α-tubulin and disrupting kinetochore-microtubule attachments. In addition, PTC compromises oocyte fertilization ability by weakening the sperm binding ability and impairing the dynamics of Juno, Cortical granule and Ovastacin. Finally, single-cell transcriptome analysis revealed that PTC exposure has potentially toxic effects on oocyte development and fertilization, which is caused by the mitochondrial dysfunction and the occurrence of oxidative stress and apoptosis. In summary, our results indicated that PTC exposure had potentially toxic effects on female fertility and led to poor oocyte quality in female mice.

Keywords: Apoptosis; Fertilization; Mitochondria; Oocyte maturation; Oxidative stress; Prothioconazole.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Female
  • Fertilization
  • Male
  • Mice
  • Mitochondrial Diseases* / metabolism
  • Oocytes / metabolism
  • Oxidative Stress
  • Semen*
  • Triazoles

Substances

  • prothioconazole
  • Triazoles