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Fumonisin B1 induces poly (ADP-ribose) (PAR) polymer-mediated cell death (parthanatos) in neuroblastoma
Souren Paul1, Rekha Jakhar2, Monika Bhardwaj2
1The Hormel Institute, University of Minnesota, 801 16th Ave NE, Austin, MN, 55912, USA; Department of Biotechnology, Daegu University, Kyoungsan, Kyoungbook, 38453, Republic of Korea.
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.
Insights
Fumonisin B1 (FB1), a mycotoxin, triggers neurotoxicity via parthanatos in neuroblastoma cells. This caspase-independent cell death involves DNA damage, PARP-1 overactivation, and ROS generation.
Area of Science:
- Toxicology
- Cell Biology
- Neuroscience
Background:
- Fumonisin B1 (FB1) is a mycotoxin from Fusarium species with known toxic effects.
- FB1 exhibits dose-dependent nephrotoxicity, hepatotoxicity, and neurotoxicity.
- Previous research suggests FB1 induces cell death through parthanatos.
Purpose of the Study:
- To elucidate the specific signaling pathway of FB1-induced parthanatos in neuroblastoma cells.
- To investigate the molecular mechanisms underlying FB1 neurotoxicity.
- To characterize the cell death pathway activated by FB1.
Main Methods:
- Utilized SH-SY5Y neuroblastoma cells treated with 50 μM FB1.
- Assessed cell death markers, including caspase-independent pathways.
- Monitored poly (ADP-ribose) polymerase-1 (PARP-1) activation, reactive oxygen species (ROS) generation, and intracellular calcium levels.
- Examined endoplasmic reticulum (ER) stress, DNA damage, and chromatin condensation.
Main Results:
- FB1 induced caspase-independent cell death.
- Observed rapid PARP-1 activation, c-Jun N-terminal kinase activation, ROS generation, and increased intracellular calcium.
- FB1 treatment led to increased ER stress, DNA damage, and chromatin decondensation.
- Apoptosis-inducing factor nuclear translocation and PAR accumulation were linked to necroptosis signaling.
Conclusions:
- FB1 neurotoxicity in SH-SY5Y cells occurs via parthanatos, a caspase-independent cell death pathway.
- The pathway involves excessive DNA damage, PARP-1 overactivation, ROS production, and ER stress.
- FB1-induced parthanatos shares signaling elements with necroptosis.
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