Rapamycin inhibits acrolein-induced apoptosis by alleviating ROS-driven mitochondrial dysfunction in male germ cells

X He1, W Song, C Liu

  • 1College of Veterinary Medicine, Shaanxi Centre of Stem Cells Engineering & Technology, Key Lab for Animal Biotechnology of Agriculture Ministry of China, Northwest A&F University, Yangling, 712100, Shaanxi, China.

Cell Proliferation
|February 4, 2014
PubMed
Abstract

Insights

Acrolein exposure increases reactive oxygen species (ROS) and damages male germ cells. Rapamycin treatment alleviates this damage by reducing ROS and protecting mitochondria, suggesting a therapeutic potential for male reproductive toxicity.

Area of Science:

  • Toxicology
  • Reproductive Biology
  • Biochemistry

Background:

  • Acrolein (Acr) is a reactive aldehyde that generates reactive oxygen species (ROS).
  • Elevated Acr levels are linked to factors like smoking, aging, and environmental pollutants.
  • Acr-induced ROS may negatively impact sperm quality and male fertility.

Purpose of the Study:

  • To investigate the reproductive toxicity of Acr-induced ROS in male germ cells (MGCs) in vitro.
  • To explore Rapamycin as a potential agent to mitigate Acr-induced reproductive damage.

Main Methods:

  • Exposure of MGC-derived GC-1 cells to Acr in vitro.
  • Measurement of intracellular ROS using dihydroethidium and DCFH-DA fluorescent dyes.
  • Assessment of mitochondrial membrane potential and apoptosis markers (Bcl2/Bax ratio).

Main Results:

  • Acr exposure significantly increased ROS generation in MGCs.
  • Acr reduced the Bcl2/Bax ratio, decreased mitochondrial membrane potential, and induced apoptosis.
  • Rapamycin treatment effectively alleviated Acr-induced ROS and apoptosis, preserving mitochondrial function.

Conclusions:

  • Rapamycin mitigates Acr-induced apoptosis in MGCs.
  • The protective effect of Rapamycin involves alleviating ROS-driven mitochondrial dysfunction.
  • Rapamycin shows promise in counteracting Acr's negative impact on male reproductive cells.

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