Fumonisin B1 induces poly (ADP-ribose) (PAR) polymer-mediated cell death (parthanatos) in neuroblastoma

Souren Paul, Rekha Jakhar, Monika Bhardwaj, Anil Kumar Chauhan, Sun Chul Kang

Research output: Contribution to journalArticlepeer-review

Abstract

Fumonisin B1 (FB1) is a well-known mycotoxin produced by Fusarium spp. and has a wide range of dose-dependent toxic effects, including nephrotoxicity, hepatotoxicity, and neurotoxicity. This research illustrated that FB1 exerts its toxicity in the neuroblastoma cell line through a distinct cell-death pathway called parthanatos. FB1 can cause excessive DNA strand breaks, leading to poly (ADP-ribose) polymerase-1 (PARP-1) overactivation and cell death. In this study, we used 50 μM FB1-treated SH-SY5Y neuroblastoma cells to elucidate the signaling pathway of FB1-induced parthanatos. We observed that FB1-induced cell death is caspase-independent and accompanied by rapid activation of PARP-1, c-Jun N-terminal kinase activation, reactive oxygen species (ROS) generation, and intracellular calcium increase. FB1 treatment also increased endoplasmic reticulum stress due to the rapid increase of calcium ions and ROS levels. In addition, FB1 induced massive DNA damage and chromatin decondensation. We also observed that apoptosis-inducing factor nuclear translocation and PAR accumulation were associated with the necroptosis signal.

Original languageEnglish (US)
Article number112326
JournalFood and Chemical Toxicology
Volume154
DOIs
StatePublished - Aug 2021

Bibliographical note

Publisher Copyright:
© 2021 Elsevier Ltd

Keywords

  • Endoplasmic reticulum stress
  • Fumonisin B1
  • Neurodegeneration
  • Parthanatos
  • Poly (ADP-Ribose) polymerase-1

PubMed: MeSH publication types

  • Journal Article

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