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Unraveling the mechanisms of perfluorooctanesulfonic acid-induced dopaminergic neurotoxicity and microglial activation in developing zebrafish. | LitMetric

AI Article Synopsis

  • PFOS is a common environmental pollutant linked to neurotoxicity, but its specific effects on the nervous system are not fully understood.
  • This study on zebrafish found that exposure to PFOS resulted in various developmental issues, including increased mortality, deformities, and changes in movement behavior.
  • The research suggests that PFOS causes neuroinflammation and neuronal damage through the activation of microglia, impacting neurotransmitter systems and potentially contributing to neurological disorders.

Article Abstract

Perfluorooctanesulfonic acid (PFOS) is a prevalent, persistent organic pollutant in environmental matrices, yet its precise mechanism of neurotoxicity remains unclear. This study investigated the developmental and neurobehavioral effects of PFOS exposure (0, 100, 500, and 1000 μg/L) on zebrafish. The findings indicated that PFOS exposure caused various developmental abnormalities, including increased mortality, delayed hatching, shortened body length, bent spine, and edema in the pericardial and yolk sac regions. Subsequently, larvae exhibited a significant decrease in spontaneous movement frequency, altered touch-evoked response, and locomotor behavior. In fact, aberrant cellular responses in the brain and cardiac regions were observed. Microglial activation is a critical component of the inflammatory immune responses related to neurotoxicity. Likewise, our findings indicated that PFOS-induced microglial activation might be responsible for neuronal inflammation and apoptosis. Furthermore, AChE activity and dopamine content at the neurotransmitter level were also disrupted after PFOS exposure. The gene expression of dopamine signaling pathways and neuroinflammation were also altered. Collectively, our findings highlight that PFOS exposure can induce dopaminergic neurotoxicity and neuroinflammation through microglial activation, thus ultimately affecting behavior. Taken together, this study will provide mechanistic effects underlying the pathophysiology of neurological disorders.

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Source
http://dx.doi.org/10.1016/j.scitotenv.2023.164030DOI Listing

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