Graphene Oxide Nanosheets Induce Mitochondrial Toxicity in Human Ovarian Granulosa Cells: Implications for Female

Min Li1, Hedong Lu1, Chunya Ye1

  • 1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, People's Republic of China.

Abstract

Insights

Graphene oxide (GO) causes short-term mitochondrial damage in human ovarian cells, impacting viability and function. Recovery was observed after GO removal, but potential effects on ovarian reserve warrant further investigation.

Area of Science:

  • Biomedical Nanotechnology
  • Cell Biology
  • Reproductive Toxicology

Background:

  • Graphene oxide (GO) shows promise for biomedical uses.
  • Its effects on the female reproductive system, especially ovarian cells, are not well understood.
  • Investigating GO's impact on ovarian granulosa cells is crucial for assessing reproductive safety.

Purpose of the Study:

  • To evaluate the short-term toxicity of graphene oxide (GO) on human ovarian granulosa cells (KGN).
  • To specifically examine the effects of GO on mitochondrial structure and function.
  • To determine the dose-dependent cytotoxicity and recovery patterns of GO exposure.

Main Methods:

  • Cell viability (CCK-8) and apoptosis (flow cytometry) assays were performed.
  • Mitochondrial function was assessed via reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP), and morphology (confocal microscopy).
  • Transmission electron microscopy (TEM), ATP assays, mitochondrial complex I activity, and autophagy analysis were utilized to evaluate mitochondrial toxicity.

Main Results:

  • The 72-hour EC50 for GO was 29.73 μg/mL, with effects on viability observed even at 1 μg/mL.
  • Low GO concentrations induced mitochondrial damage, including morphological changes, reduced ATP production, decreased MMP, and impaired complex I activity.
  • Mitochondrial function and cell health recovered within 7 days after GO exposure ceased.

Conclusions:

  • Short-term, low-dose GO exposure induces transient mitochondrial damage in human ovarian granulosa cells.
  • This damage highlights potential risks to reproductive health, necessitating further safety research.
  • The impact on ovarian reserve function requires verification in animal models.