Wei Shi,Shuge Sun,Yu Han,Yu Tang,Weishang Zhou,Xueying Du,Guangxu Liu
Recently, the ubiquitous presence of microplastics (MPs) has drawn worldwide concern over its potential threat to aquatic organisms. However, the effects of MPs on the olfactory ability of fish and the subsequent odorant evoked behaviors remain elusive. In the present study, we analyzed the potential olfactory toxicity of polystyrene (PS) MPs by assessing olfactory-driven behaviors of goldfish in response to odorants. Our results showed that the olfactory-driven behavioral responses of goldfish to L -cysteine and taurocholic acid were significantly hampered by a 28-day MP exposure. Further analysis demonstrated that exposure to MPs may suppress the expression of genes encoding olfactory G protein-coupled receptors, inhibit the enzyme activities of cation transport ATPases crucial for action potential generation, alter the in vivo contents of neurotransmitters as well as metabolites involved in the transduction of electrical signals, and cause olfactory bulb injury and neurotoxicity closely related to the processing of electrical signals. In conclusion, the results obtained in the present study suggest that MPs at environmentally relevant concentrations could impair the olfactory-mediated behavioral responses of goldfish, probably through hampering odorant identification, action potential generation, olfactory neural signal transduction, and olfactory information processing.
Tetrabromobisphenol A (TBBPA) is one of the most extensively used brominated flame retardants and its increasing use in consumer products has raised concerns about its ecotoxicity. Given the ubiquity of TBBPA in aquatic environments, it is inevitable that these chemicals will enter the olfactory chambers of fish via water currents. Nevertheless, the olfactory toxicity of TBBPA to aquatic organisms and the underlying toxic mechanisms have yet to be elucidated. Therefore, we investigated the olfactory toxicity of TBBPA in the goldfish Carassius auratus , a model organism widely used in sensory biology. Results showed that exposure to TBBPA resulted in abnormal olfactory-mediated behaviors and diminished electro-olfactogram (EOG) responses, indicating reduced olfactory acuity. To uncover the underlying mechanisms of action, we examined the structural integrity of the olfactory epithelium (OE), expression levels of olfactory G protein-coupled receptors (GPCRs), enzymatic activities of ion transporters, and fluctuations in neurotransmitters. Additionally, comparative transcriptomic analysis was employed to investigate the molecular mechanisms further. Our study demonstrates for the first time that TBBPA at environmentally relevant levels can adversely affect the olfactory sensitivity of aquatic organisms by interfering with the transmission of aqueous stimuli to olfactory receptors, impeding the binding of odorants to their receptors, disrupting the olfactory signal transduction pathway, and ultimately affecting the generation of action potentials.
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