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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.
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Wang et al. (2016) studied this question.
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