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.