Paraquat modulates immunological function in bone marrow-derived macrophages

Piyarat Srinontong1,2, Jaroon Wandee1,2, Worapol Aengwanich1,3

  • 11 Faculty of Veterinary Sciences, Mahasarakham University, Maha Sarakham, Thailand.

Insights

The herbicide paraquat (PQ) induces oxidative stress and apoptosis in immune cells by increasing reactive oxygen species (ROS). This study reveals PQ elevates pro-inflammatory gene expression, impacting macrophage function.

Area of Science:

  • Immunology
  • Toxicology
  • Cell Biology

Background:

  • Paraquat (PQ) is a herbicide known to affect the immune system.
  • The precise mechanisms by which PQ impacts immune cell viability and function remain unclear.

Purpose of the Study:

  • To investigate the effects of PQ on free radical production, oxidative stress, cell death, and pro-inflammatory gene expression in murine bone marrow-derived macrophages (BMDMs) in vitro.
  • To elucidate the cellular and molecular mechanisms underlying PQ-induced immunotoxicity.

Main Methods:

  • Murine BMDMs were exposed to PQ at concentrations of 0, 200, and 400 µM for 24 hours.
  • Assessed intracellular reactive oxygen species (ROS) production, apoptosis, cell viability, nitric oxide (NO) production, and the expression of inducible nitric oxide synthase (iNOS) and IL-6.

Main Results:

  • PQ treatment decreased cell viability and induced apoptosis in a dose-dependent manner.
  • PQ exposure elevated ROS generation and increased mRNA levels of pro-inflammatory mediators iNOS and IL-6.
  • Nitric oxide production decreased, while lipid peroxide levels remained unchanged.

Conclusions:

  • Increased cellular ROS production by PQ triggers apoptosis in BMDMs.
  • The herbicide paraquat stimulates the production of iNOS and IL-6, indicating a pro-inflammatory response in macrophages.