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Related Concept Videos

Oogenesis02:07

Oogenesis

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In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
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Related Experiment Video

Updated: Jun 12, 2025

A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust
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Silica nanoparticles cause ovarian dysfunction and fertility decrease in mice via oxidative stress-activated

Wenpeng Liu1, Hui Liu1, Shumin Zhang1

  • 1School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.

Ecotoxicology and Environmental Safety
|September 20, 2024
PubMed
Summary

Silica nanoparticles (SiNPs) damage ovarian function, reduce fertility by causing oxidative stress and mitochondrial dysfunction. N-acetylcysteine (NAC) supplementation helped restore reproductive health in mice exposed to SiNPs.

Keywords:
ApoptosisAutophagyFemale reproductive toxicityFolliculogenesisOxidative StressSilica nanoparticles

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Area of Science:

  • Toxicology
  • Reproductive Biology
  • Nanotechnology

Background:

  • Silica nanoparticles (SiNPs) are prevalent in commercial products, raising concerns about human exposure.
  • Existing research suggests SiNPs may negatively impact fertility, but the precise mechanisms of female reproductive toxicity are unclear.

Purpose of the Study:

  • To elucidate the mechanisms underlying female reproductive toxicity induced by silica nanoparticles (SiNPs).
  • To investigate the protective effects of N-acetylcysteine (NAC) against SiNP-induced reproductive damage.

Main Methods:

  • Female C57BL/6 mice were orally administered SiNPs (0, 3, 10 mg/kg bw) daily for eight weeks, with or without NAC.
  • Assessed ovarian damage, follicle count, sex hormone levels, estrous cyclicity, and fertility.
  • Analyzed oxidative stress markers (ROS, MDA, SOD), Nrf2/HO-1 pathway, mitochondrial function, autophagy (PI3K/AKT/mTOR, PINK1/Parkin), and apoptosis (ATM/p53).

Main Results:

  • SiNPs caused ovarian damage, reduced ovarian follicles, disrupted sex hormones, altered estrous cycles, and decreased female fertility.
  • SiNPs induced ovarian oxidative stress, mitochondrial dysfunction, and promoted autophagy and apoptosis via specific signaling pathways.
  • NAC supplementation largely reversed the adverse reproductive effects of SiNPs.

Conclusions:

  • SiNPs induce female subfertility by damaging ovaries through oxidative stress and mitochondrial dysfunction, leading to autophagy and apoptosis.
  • The Nrf2/HO-1, PI3K/AKT/mTOR, PINK1/Parkin, and ATM/p53 pathways are critically involved in SiNP-induced reproductive toxicity.
  • NAC demonstrates a protective role against SiNP-induced female reproductive toxicity.