Advertisement

Archives of Toxicology

, Volume 81, Issue 4, pp 279–282 | Cite as

Apoptosis induced by acrylamide in SH-SY5Y cells

  • Tomoyuki SumizawaEmail author
  • Hideki Igisu
Molecular Toxicology

Abstract

Acrylamide (1–5 mM) dose-dependently decreased cell viability in human neuroblastoma cells (SH-SY5Y). The caspase-3 activity and cell population in sub-G1 phase were elevated and peaked on exposure to 3 mM acrylamide, while both were less so at higher dose (4 and 5 mM). Z-VAD-fmk, a pan-caspase inhibitor, lowered the apparent cytotoxicity of acrylamide. U0126, a specific inhibitor of extracellular signal-regulated protein kinase (ERK) kinase, suppressed the elevation of caspase-3 activities as well as that of sub-G1 population. Thus, although mechanisms other than caspase-dependent apoptosis may be involved, apoptotic process seems to take place in the genesis of toxicity of acrylamide in SH-SY5Y cells through ERK pathway and activation of caspase-3.

Keywords

Acrylamide SH-SY5Y cells Caspase-3 Apoptosis ERK 

Notes

Acknowledgments

We thank Dr. Tsutomu Sugiura (Department of Immunology) for his help. This work was supported in part by Grant-in Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan.

References

  1. DeJongh J, Nordin-Andersson M, Ploeger BA, Forsby A (1999) Estimation of systemic toxicity of acrylamide by integration of in vitro toxicity data with kinetic simulations. Toxicol Appl Pharmacol 158:261–268PubMedCrossRefGoogle Scholar
  2. Gold BG, Schaumburg HH (2000) Acrylamide. In: Spencer PS, Schaumburg HH (eds) Experimental and clinical neurotoxicology, 2nd edn. Oxford University Press, New York pp 124–132Google Scholar
  3. Hartley CL, Anderson VE, Anderton BH, Robertson J (1997) Acrylamide and 2,5-hexanedione induce collapse of neurofilaments in SH-SY5Y human neuroblastoma cells to form perikaryal inclusion bodies. Neuropathol Appl Neurobiol 23:364–372PubMedCrossRefGoogle Scholar
  4. Johnson GL, Lapadat R (2002) Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 298:1911–1912PubMedCrossRefGoogle Scholar
  5. Li SX, Cui N, Zhang CL, Zhao XL, Yu SF, Xie KQ (2006) Effect of subchronic exposure to acrylamide induced on the expression of bcl-2, bax and caspase-3 in the rat nervous system. Toxicology 217:46–53PubMedCrossRefGoogle Scholar
  6. Morrison RS, Kinoshita Y, Johnson MD, Guo W, Garden GA (2003) p53-Dependent cell death signaling in neurons. Neurochem Res 28:15–27PubMedCrossRefGoogle Scholar
  7. Okuno T, Matsuoka M, Sumizawa T, Igisu H (2006) Involvement of the extracellular signal-regulated protein kinase pathway in phosphorylation of p53 protein and exerting cytotoxicity in human neuroblastoma cells (SH-SY5Y) exposed to acrylamide. Arch Toxicol 80:146–153PubMedCrossRefGoogle Scholar
  8. Stanciu M, Wang Y, Kentor R, Burke N, Watkins S, Kress G, Reynolds I, Klann E, Angiolieri MR, Johnson JW, DeFranco DB (2000) Persistent activation of ERK contributes to glutamate-induced oxidative toxicity in a neuronal cell line and primary cortical neuron cultures. J Biol Chem 275:12200–12206PubMedCrossRefGoogle Scholar
  9. Subramaniam S, Zirrgiebel U, von Bohlen Und Halbach O, Strelau J, Laliberte C, Kaplan DR, Unsicker K (2004) ERK activation promotes neuronal degeneration predominantly through plasma membrane damage and independently of caspase-3. J Cell Biol 165:357–369PubMedCrossRefGoogle Scholar
  10. Vousden KH (2000) p53: death star. Cell 103:691–694PubMedCrossRefGoogle Scholar
  11. Xia Z, Dickens M, Raingeaud J, Davis RJ, Greenberg ME (1995) Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis. Science 270:1326–1331PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  1. 1.Department of Environmental Toxicology, Institute of Industrial Ecological SciencesUniversity of Occupational and Environmental HealthKitakyushuJapan

Personalised recommendations