Mechanistic insights into phenanthrene-triggered oxidative stress-associated neurotoxicity, genotoxicity, and behavioral disturbances toward the brandling worm (Eisenia fetida) brain: The need for an ecotoxicological evaluation

Abstract

In this study, earthworm (Eisenia fetida) brain was chosen as targeted receptors to probe the mechanisms of oxidative stress-related neurotoxicity, genotoxicity, and behavioral disturbances triggered by PHE. Results showed that PHE stress can initiate significant amounts of ROS, thus triggering oxidative stress in E. fetida brain. These effects were accompanied by a significant increase of damage to macromolecules DNA and lipids, resulting in severe oxidative effects. PHE exposure can induce AChE inhibition by ROS-induced injury and the accumulation of excess ACh at the nicotinic post-synaptic membrane, thus inducing aggravated neurological dysfunction and neurotoxicity of E. fetida through an oxidative stress pathway. Moreover, the burrowing behavior of earthworms was disturbed by oxidative stress-induced neurotoxicity after exposure to PHE. Furthermore, the abnormal mRNA expression profiles of oxidative stress- and neurotoxicity-related genes in worm brain were induced by PHE stress. The IBR results suggested that E. fetida brain was suffered more serious damage caused by PHE under higher doses and long-term exposure. Taken together, PHE exposure can trigger oxidative stress-mediated neurotoxicity and genotoxicity in worm brain and behavioral disorder through ROS-induced damage. This study is of great significance to evaluate the harmful effects of PHE and its mechanisms on soil ecological health.