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Protective Effects of Natural Compounds Against Paraquat-Induced Pulmonary Toxicity: The Role of the Nrf2/Are Signaling Pathway Publisher Pubmed



Badibostan H1 ; Eizadimood N1 ; Hayes AW2, 3 ; Karimi G4, 5
Authors
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Authors Affiliations
  1. 1. Isfahan Clinical Toxicology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Center for Environmental Occupational Risk Analysis and Management, College of Public Health, University of South Florida, Tampa, FL, United States
  3. 3. Institute for Integrative Toxicology, Michigan State University, East Lansing, MI, United States
  4. 4. Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
  5. 5. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Source: International Journal of Environmental Health Research Published:2024


Abstract

Paraquat (PQ) is a toxic herbicide to humans. Once absorbed, it accumulates in the lungs. PQ has been well documented that the generation of reactive oxygen species (ROS) is the main mechanism of its toxicity. Oxidative damage of PQ in lungs is represented as generation of cytotoxic and fibrotic mediators, interruption of epithelial and endothelial barriers, and inflammatory cell infiltration. No effective treatment for PQ toxicity is currently available. Several studies have shown that natural compounds (NCs) have the potential to alleviate PQ-induced pulmonary toxicity, due to their antioxidant and anti-inflammatory effects. NCs function as protective agents through stimulation of nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathways. Elevation of Nrf2 levels leads to the expression of its downstream enzymes such as SOD, CAT, and HO-1. The hypothesized role of the Nrf2/ARE signaling pathway as the protective mechanism of NCs against PQ-induced pulmonary toxicity is reviewed. © 2023 Informa UK Limited, trading as Taylor & Francis Group.
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