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Imidacloprid affects human cells through mitochondrial dysfunction and oxidative stress.

Fenghua Wei1, Fei Cheng2, Huizhen Li3

  • 1School of Chemistry and Environment, Jiaying University, Meizhou 514015, China; Guangdong Provincial Key Laboratory of Environmental Pollution and Health, College of Environment and Climate, Jinan University, Guangzhou 510632, China.

The Science of the Total Environment
|August 11, 2024
PubMed
Summary

Neonicotinoid pesticide imidacloprid disrupts human cell mitochondria, causing oxidative stress, DNA damage, and apoptosis. This highlights potential human health risks beyond neurotoxicity, emphasizing mitochondrial toxicity concerns.

Keywords:
Human health thresholdImidaclopridMitochondrial dysfunctionNeonicotinoids insecticidesSH-SY5Y cells

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Area of Science:

  • Environmental toxicology
  • Cellular toxicology
  • Human health risk assessment

Background:

  • Neonicotinoid pesticides are widely used globally.
  • Concerns exist regarding non-target organism toxicity beyond neurotoxicity.
  • Potential human health risks via additional toxicity pathways are emerging.

Purpose of the Study:

  • To investigate the effects of imidacloprid on human neuroblastoma SH-SY5Y cells.
  • To examine mitochondrial function, oxidative stress, DNA damage, and gene transcription.
  • To assess potential human health risks associated with imidacloprid exposure.

Main Methods:

  • Exposure of SH-SY5Y cells to varying concentrations of imidacloprid (0.05–200 μmol/L) for 48 hours.
  • Assay of mitochondrial function, including adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP).
  • Measurement of reactive oxygen species (ROS), hydrogen peroxide (H2O2), calcium ion levels, DNA damage, and gene transcription.

Main Results:

  • Imidacloprid induced mitochondrial dysfunction, decreasing ATP and MMP levels.
  • Oxidative stress was observed, with increased ROS and H2O2 generation.
  • DNA damage and apoptosis occurred at concentrations above 47.6 μmol/L.
  • ATP degradation was the most sensitive endpoint (EC50 = 0.74 μmol/L).

Conclusions:

  • Imidacloprid exposure leads to mitochondrial dysfunction and oxidative stress in human neuroblastoma cells.
  • These effects can result in DNA damage and apoptosis, indicating potential human health risks.
  • The study supports further research into neonicotinoid-induced mitochondrial toxicity in humans.