Stress Signaling in Paraquat-Induced Target Organ Toxicity

  • Shuyi Wang Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA
  • Wei Guo Center for Cardiovascular Research and Alternative Medicine, and Department of Animal Sciences, University of Wyoming, Laramie, WY 82071, USA
  • Jun Ren Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA
Keywords: Antioxidants, Cardiac function, Inflammation, Mitochondrial injury, Oxidative stress, Paraquat, Reactive oxygen species, Stress signaling, Target organ toxicity

Abstract

Paraquat is a rather toxic pro-oxidant herbicide, prompting multi-organ failure, including the heart, brain, and lung injuries, although the precise underlying mechanism(s) remains poorly understood. Up-to-date, a number of signaling machineries have been postulated for paraquat toxicity, such as accumulation of free radical species and development of oxidative stress. Paraquat is believed to serve as a potent ROS generator, resulting in detrimental biological effects through oxidative stress injury and mitochondrial dysfunction. In this mini-review we will recapitulate some aspects of paraquat toxicity in main body organs, including the lungs, brain, and heart. Cellular mechanisms behind paraquat toxicity will be discussed with a focus on oxidative stress, mitochondrial injury, and autophagy. Special attention will be given to the direct stress signaling and pro-inflammatory signaling cascades triggered by paraquat exposure in the herbicide-induced organ damage.

Published
2016-03-01
How to Cite
Wang, S., Guo, W., & Ren, J. (2016). Stress Signaling in Paraquat-Induced Target Organ Toxicity. Reactive Oxygen Species, 1(2), 131‒140. Retrieved from https://aimsci.com/ros/index.php/ros/article/view/26
Section
Review Articles