Cardiotoxicity and neurobehavioral effects induced by acrylamide in Daphnia magna.

Acrylamide has neurotoxic and/or cardiotoxic effects on humans however available information regarding the neuro- and cardiotoxicity currently is very limited for freshwater organism models. Using three distinct techniques, thus, we investigated the neuro- and cardiotoxic effects of acrylamide in the freshwater invertebrate model, Daphnia magna. We exposed D. magna to acrylamide at concentrations of 0.3, 2.7, and 11.1 mg/L for 48 h alongside a control group. We then conducted physiological (thoracic limb activity and heart rate) and behavioral tests (including distance moved, velocity, turn angle, moving duration, the distance between subjects, and body contact frequency), as well as gene transcription analyses (related to cardiomyopathy, the serotonergic synapse, neuroactive ligand-receptor interactions, the GABAergic synapse, and acetylcholine receptors). After acrylamide exposure, the thoracic limb activity and heart rates of D. magna showed time- and dose dependent inhibition. From low to high exposure concentrations, both heart rates and thoracic limb activity were decreased. Additionally, the distance between subjects and body contact frequencies was significantly reduced. At the gene transcription level, acrylamide significantly altered the transcription of five genes related to cardiomyopathy and eight genes related to the serotonergic synapse, neuroactive ligand-receptor interactions, and the GABAergic synapse. The signs of hindered neural and cardiac functions were shown in D. magna. This suggests that acrylamide exposure leads to cardiotoxicity and neurobehavior defects in D. magna. Because cardiotoxicity and neurobehavioral changes may cause an ecological imbalance via predation of D. magna, acrylamide may also be considered a threat to freshwater ecosystem.

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