Reaction of the marine flatworm Macrostomum lignano exposed to xenobiotics
Xenobiotics are substances of various origins that accumulate in the environment and can have a negative impact on parts of the ecosystem. Marine coastal regions, especially river estuaries, play a prominent role in this context. The marine flatworm Macrostomum lignano is a perfect model organism for this purpose. A key mechanism of xenobiotic-induced toxicity is the formation of reactive oxygen species, which can result in cell death. This was observed in the Macrostomum model. ROS induction was also observed at sublethal doses of various xenobiotics. At higher concentrations of xenobiotics, the number of cell deaths increased significantly compared to unexposed animals. In the present study, the worms were more susceptible to fipronil than to imidacloprid. Various antioxidant enzymes of the host were downregulated in response to exposure to the xenobiotics, including Prdx1, Sod2, and Mdr5. Of the ROS-detoxifying enzymes, only Gstp1 showed significant upregulation. Xenobiotics also disrupt nervous system function by restricting movement and delaying regeneration. Even at low concentrations (10 µM), fipronil and imidacloprid reduce peripheral nerve function. I demonstrated that these xenobiotics have a significant impact on the morphology of the peripheral nerves of Macrostomum. After 15 days at the same concentration, fipronil reduced more peripheral nerves than imidacloprid. The study also revealed impaired myofibril organisation. Fifteen days after exposure to the xenobiotics, significant changes were observed in the ventral longitudinal body wall muscles of Macrostomum. Fipronil caused a greater decline in these muscles than imidacloprid did. This study clearly shows that even low, sublethal concentrations of these xenobiotics can severely impair Macrostomum biology. This could significantly impact its fitness and thus impair its role and importance in the ecosystem.
Xenobiotics, Oxidative stress, Regeneration
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