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Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Pyrethrin II Impairs Mitochondrial Potential through ROS and MAPK Pathways in HT‑22 Cells.

Jiaojiao Gao1, Xinbi Zhang2, Qie Mu2

  • 1Department of Biological and Food Engineering, Lyuliang University, Lvliang, Shanxi 033001, China.

Neurotoxicology
|July 13, 2026
PubMed
Summary

Pyrethrin II causes neuronal injury by increasing reactive oxygen species (ROS) and disrupting the JNK/ERK balance, leading to cell death. This study reveals a key mechanism of its neurotoxicity in vitro.

Keywords:
MAPK signaling pathwayMitochondrial functionPyrethrin IIReactive oxygen species

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Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Pyrethrin II is a common insecticide component.
  • Its neurotoxic mechanisms, particularly in hippocampal neurons, require elucidation.

Purpose of the Study:

  • To investigate Pyrethrin II-induced hippocampal neuronal injury.
  • To explore the roles of reactive oxygen species (ROS) and the MAPK pathway in this injury.

Main Methods:

  • HT-22 cells were treated with Pyrethrin II.
  • Assays included CCK-8, transcriptomics, ROS measurement, Western blotting, JC-1 staining, TUNEL, cleaved caspase-3, EdU, and PCNA.

Main Results:

  • Pyrethrin II induced dose-dependent ROS production and MAPK pathway dysregulation (JNK/p38 activation, ERK suppression).
  • ROS overproduction led to decreased mitochondrial membrane potential and apoptosis.
  • ERK suppression impaired cell proliferation, while JNK activation promoted apoptosis.

Conclusions:

  • Pyrethrin II causes neurotoxicity via ROS-mediated disruption of the JNK/ERK axis, affecting the proliferation-apoptosis balance.
  • This mechanism involves mitochondrial dysfunction and cell death.
  • Targeting this pathway requires caution due to essential physiological roles of JNK and ERK.