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Nonylphenol-induced thymocyte apoptosis involved caspase-3 activation and mitochondrial depolarization

Genhong Yao1, Lingsong Yang, Yali Hu

  • 1Jiangsu Province Key Lab of Reproductive Medicine, Nanjing Medical University, Nanjing 210029, China.

Molecular Immunology
|July 28, 2005
PubMed

Insights

4-nonylphenol induces apoptosis in mouse thymocytes, a type of immune cell. This process involves DNA fragmentation, chromatin condensation, and caspase-3 activation, indicating a specific cell death pathway.

Area of Science:

  • Immunotoxicology
  • Cell Biology
  • Molecular Toxicology

Background:

  • The impact of 4-nonylphenol on immune cells is known, but its specific role in inducing apoptosis in lymphoid cells remains unclear.
  • Investigating the signaling pathways involved in 4-nonylphenol-induced apoptosis is crucial for understanding its immunotoxic effects.

Purpose of the Study:

  • To determine if 4-nonylphenol induces apoptosis in mouse thymocytes.
  • To elucidate the signaling mechanisms, including caspase activation and mitochondrial changes, underlying 4-nonylphenol-induced thymocyte apoptosis.

Main Methods:

  • Cultured mouse thymocytes were treated with 4-nonylphenol.
  • Apoptosis was assessed via DNA fragmentation (DNA ladder), nuclear morphology (Hoechst 33258 staining), hypodiploid cell analysis, and Annexin V/PI staining.
  • Mitochondrial membrane potential and caspase-3 activity were measured using flow cytometry.
  • The effect of a caspase-3 inhibitor (z-DEVD-fmk) was evaluated.

Main Results:

  • 4-nonylphenol induced characteristic apoptotic features, including DNA fragmentation and nuclear condensation.
  • Apoptosis rates significantly increased at 4 and 6 hours post-treatment.
  • Loss of mitochondrial membrane potential and increased caspase-3 activity were observed.
  • Caspase-3 inhibition protected thymocytes from 4-nonylphenol-induced apoptosis.

Conclusions:

  • 4-nonylphenol triggers apoptosis in mouse thymocytes.
  • The process is mediated by caspase-3 activation and mitochondrial depolarization.
  • These findings highlight a specific mechanism of 4-nonylphenol immunotoxicity.

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