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

Genhong Yao, Lingsong Yang, Yali Hu, Jun Liang, Junfeng Liang, Yayi Hou

Research output: Contribution to journalArticlepeer-review

60 Scopus citations

Abstract

Although the effect of 4-nonylphenol on cells of immune system have long been recognized, little is known about the effect of 4-nonylphenol on the induction of apoptosis and related signaling events in the lymphoid cells. In the present study, we used cultured thymocytes of mice to investigate the ability of 4-nonylphenol to induce the apoptosis of thymocytes and to explore the role of signal transduction pathway leading to apoptosis. The results showed that the cytotoxic effects of 4-nonyphenol involved DNA fragmentation (DNA ladder), characteristic of apoptosis. Staining of 4-nonyphenol-treated thymocytes with DNA-binding fluorochrome Hoechst 33258 showed the typical apoptotic nuclei condensation and fragmentation of chromatin. The rates of apoptosis of the 4-nonylphenol-treated thymocytes increased significantly at 4 and 6 h, which were determined by analysis of hypodiploid cells and FITC-Annexin V and PI double staining. Flow cytometer analysis also revealed that the loss of mitochondrial membrane potential and increased activity of caspase-3 occurred concomitantly with the onset of 4-nonyphenol-induced apoptosis. Furthermore, a caspase-3 inhibitor, z-DEVD-fmk protected thymocytes from apoptosis induced by 4-nonyphenol. These results suggest that 4-nonylphenol induces thymocyte apoptosis via caspase-3 activation and mitochondrial depolarization.

Original languageEnglish
Pages (from-to)915-926
Number of pages12
JournalMolecular Immunology
Volume43
Issue number7
DOIs
StatePublished - Mar 2006

Keywords

  • Apoptosis
  • Caspase-3
  • Mitochondrial depolarization
  • Nonylphenol
  • Thymocytes

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