4.1 Article

Neurotoxicity associated with oxidative stress and inflammasome gene expression induced by allethrin in SH-SY5Y cells

Journal

TOXICOLOGY AND INDUSTRIAL HEALTH
Volume 38, Issue 12, Pages 777-788

Publisher

SAGE PUBLICATIONS INC
DOI: 10.1177/07482337221089585

Keywords

SH-SY5Y cells; inflammasome; oxidative stress; allethrin; neurotoxicity

Funding

  1. Project Fisiopatologia neurodegenerativa in vitro por efecto de plaguicidas de uso veterinario, Universidad Nacional Mayor de San Marcos [PCONFIGI A19080231]
  2. Consiglio Nazionale delle Ricerche, Istituto di Genetica Molecolare Luca Cavalli-Sforza, Pavia (CNR-Pavia, Italy) [02-2021]
  3. National Council for Science-Technology and Technological Innovation (CONCYTEC-Peru) [02-2021-FONDECYT]

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Pyrethroids, including allethrin, have largely been used as commercial insecticides. The toxicity of allethrin is little known, but it is assumed that, as occurs with other pyrethroids, it could cause alterations of the nervous system and pose both occupational and non-occupational health hazards. To evaluate the neurotoxicity of allethrin we used the MTT assay of SH-SY5Y neuroblastoma cells to determine cell viability. Dose-dependent reductions of cell viability served to compare the vehicle-group and the IC50 for allethrin, which was 49.19 mu M. ROS production increased significantly at concentrations of 10-200 mu M of allethrin, and NO levels were significantly increased by the effect of allethrin at a minimum concentration of 50 mu M. Lipid peroxidation increased by the effect of allethrin at concentrations of 25, 50, 100, and 200 mu M. Caspase 3/7 activity was induced by allethrin concentrations of 50, 100, and 200 mu M. Here, we suggest that allethrin might affect the inflammasome complex (Caspase-1, NLRP3, and PYDC1) and apoptosis (Bax and Bcl-2) gene expression by mRNA fold change expression levels shown in Caspase-1 (2.46-fold), NLRP3 (1.57-fold), PYDC1 (1.48-fold), and Bax (2.1-fold). These results demonstrated that allethrin induced neurotoxicity effects on SH-SY5Y cells through activation of inflammasome pathways, cell death, and oxidative stress.

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