Tissue-Specific Accumulation, Toxicological Effects, and Detoxification Strategies in the Mysid Neomysis awatschensis Exposed to Dissolved Paralytic Shellfish Toxins

The direct uptake of dissolved paralytic shellfish toxins (PSTs) from seawater by marine organisms and the consequent toxicological impacts remain poorly understood. This study investigated the accumulation, acute and sublethal toxicity, and molecular responses to dissolved PSTs in Neomysis awatschensis. Results demonstrate that N. awatschensis can take up the dissolved PSTs, exhibiting a triphasic kinetic profile: absorption, stabilization, and subsequent elimination. Notably, 83.9% of the accumulated PSTs were concentrated in the cephalothorax. Acute exposure to PSTs induced severe neurobehavioral impairments, including observed paralysis, convulsions, and mortality. Sublethal exposure to 0.5 μmol STX eq L–1 elicited multifaceted physiological disruptions, encompassing significant oxidative stress evidenced by the elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), complex dysregulation of neurotransmission characterized by the increased dopamine (DA) and γ-aminobutyric acid (GABA) concentrations concomitant with inhibited acetylcholinesterase (AChE) activity. The expressions of genes associated with ABC transporters, cytochrome P450, and phase II metabolic and antioxidant enzymes were significantly upregulated, while genes involved in governing synaptic function and neurotransmission showed notable dysregulation. The transcriptional response of N. awatschensis to PSTs reveals a multilevel defense strategy involving detoxification, oxidative stress mitigation, and neurobehavioral adaptation. This study highlights the substantial ecotoxicological hazard of dissolved PSTs to mysids.