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The joint effects of nanoplastics and TBBPA on neurodevelopmental toxicity in<i>Caenorhabditis elegans</i>
Summary
Researchers used the model organism C. elegans to study the combined neurodevelopmental effects of polystyrene nanoplastics and the flame retardant TBBPA. The study found that combined exposure produced synergistic harmful effects including reduced survival, impaired movement, oxidative stress, and dopaminergic neuron loss, with specific genes related to neurodegenerative pathways playing key roles in the observed toxicity.
Both of nanoplastics (NPs) and Tetrabromobisphenol A (TBBPA) are organic pollutants widely detected in the environment and organisms. The large specific surface area of NPs makes them ideal vectors for carrying various toxicants, such as organic pollutants, metals, or other nanomaterials, posing potential threats to human health. This study used <i>Caenorhabditis elegans</i> (<i>C. elegans</i>) to investigate the neurodevelopmental toxicity induced by combined exposure of TBBPA and polystyrene NPs. Our results showed that combined exposure caused synergistic inhibitory effects on the survival rate, body length/width, and locomotor ability. Furthermore, the overproduction of reactive oxygen species (ROS), lipofuscin accumulation, and dopaminergic neuronal loss suggested that oxidative stress was involved in induction of neurodevelopmental toxicity in <i>C. elegans</i>. The expressions of Parkinson's disease related gene (<i>pink-1</i>) and Alzheimer's disease related gene (<i>hop-1)</i> were significantly increased after combined exposure of TBBPA and polystyrene NPs. Knock out of <i>pink-1</i> and <i>hop-1</i> genes alleviated the adverse effects such as growth retardation, locomotion deficits, dopaminergic loss, and oxidative stress induction, indicating that <i>pink-1</i> and <i>hop-1</i> genes play an important role in neurodevelopmental toxicity induced by TBBPA and polystyrene NPs. In conclusion, TBBPA and polystyrene NPs had synergistic effect on oxidative stress induction and neurodevelopmental toxicity in <i>C. elegans</i>, which was mediated through increased expressions of <i>pink-1</i> and <i>hop-1</i>.
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