Triclocarban exposure affects mouse oocyte in vitro maturation through inducing mitochondrial dysfunction and

Zhi-Ming Ding1, Muhammad Jamil Ahmad1, Fei Meng1

  • 1Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Education Ministry of China, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.

Insights

Triclocarban (TCC) exposure impairs mouse oocyte maturation by disrupting cell cycles, mitochondria, and increasing oxidative stress and apoptosis. This antibacterial agent negatively impacts reproductive health.

Area of Science:

  • Reproductive toxicology
  • Cell biology
  • Environmental health

Background:

  • Triclocarban (TCC) is a widely used antibacterial agent in personal care products.
  • Environmental TCC contamination is linked to adverse reproductive effects in humans and animals.

Purpose of the Study:

  • To investigate the toxic effects of TCC on mouse oocyte maturation in vitro.
  • To elucidate the underlying mechanisms of TCC-induced oocyte developmental disruption.

Main Methods:

  • In vitro maturation of mouse oocytes exposed to TCC.
  • Assessment of polar body extrusion (PBE) rates.
  • Analysis of cell cycle progression, spindle assembly checkpoint (SAC) activity, and cytoskeletal dynamics.
  • Evaluation of mitochondrial function (ATP content, mitochondrial membrane potential - MMP).
  • Measurement of oxidative stress markers, apoptosis levels, and histone methylation (H3K27me2, H3K27me3).

Main Results:

  • TCC significantly reduced PBE rates in immature mouse oocytes.
  • TCC exposure disrupted cell cycle progression and cytoskeletal dynamics, leading to sustained SAC activation.
  • Mitochondrial damage, reduced ATP, and decreased MMP were observed in TCC-treated oocytes.
  • TCC induced oxidative stress, triggered early apoptosis, and altered histone methylation patterns (increased H3K27me2 and H3K27me3).

Conclusions:

  • TCC exposure in vitro disrupts mouse oocyte maturation.
  • Mechanisms include impaired cell cycle control, compromised cytoskeletal organization, mitochondrial dysfunction, oxidative stress, apoptosis, and epigenetic alterations.
  • These findings highlight the potential reproductive risks associated with TCC environmental exposure.