The Link Between Paraquat and Demyelination: A Review of Current Evidence

Abstract

Paraquat (1,1′-dimethyl-4,4′-bipyridilium dichloride), a widely used bipyridinium herbicide, is known for inducing oxidative stress, leading to extensive cellular toxicity, particularly in the lungs, liver, kidneys, and central nervous system (CNS), and is implicated in fatal poisonings. Due to its biochemical similarities with the neurotoxin 1-methyl-4-phenylpyridinium (MPP+), paraquat has been used as a Parkinson’s disease model, although its broader neurotoxic effects suggest the participation of multiple mechanisms. Demyelinating diseases are conditions characterized by damage to the myelin sheath of neurons. They affect the CNS and peripheral nervous system (PNS), resulting in diverse clinical manifestations. In recent years, growing concerns have emerged about the impact of chronic, low-level exposure to herbicides on human health, particularly due to agricultural runoff contaminating drinking water sources and their presence in food. Studies indicate that paraquat may significantly impact myelinating cells, myelin-related gene expression, myelin structure, and cause neuroinflammation, potentially contributing to demyelination. Therefore, demyelination may represent another mechanism of neurotoxicity associated with paraquat, which requires further investigation. This manuscript reviews the potential association between paraquat and demyelination. Understanding this link is crucial for enhancing strategies to minimize exposure and preserve public health.