Linking oxidative stress and lipid remodeling in Palaemon adspersus exposed to barium chloride: Evidence from EC50, BMD and PLS-PM modeling

Barium (Ba) is a non-essential trace element increasingly detected in coastal ecosystems, yet its sublethal effects on marine invertebrates remain poorly characterized. This study investigated the biochemical and mechanistic responses of the shrimp Palaemon adspersus to barium chloride (BaCl₂) using an integrated dose-response and modeling framework. Shrimps were exposed for five days (0, 20, 40 and 80 mg/L), and hepatopancreas biomarkers were quantified: oxidative stress (H₂O₂, LOOH, MDA), protein oxidation (PCO, AOPP), antioxidant defenses (SOD, CAT, GPx, GST, GSH, MTs, Vit C, FRAP), neurotoxicity (AChE), and fatty acid composition (SFA, MUFA, PUFA; n-3/n-6). Ba bioaccumulated dose-dependently and was associated with increased oxidative and lipid peroxidation damage, coordinated but ultimately insufficient antioxidant activation, AChE inhibition, and shifts in fatty acids consistent with peroxidation-driven membrane remodeling. Benchmark Dose (BMD) modeling identified LOOH and AChE as the most sensitive endpoints (BMDL = 1.49 and 1.73 mg/L), while higher BMDL values for antioxidant enzymes indicated later compensatory responses. EC₅₀ analysis corroborated this ranking, confirming oxidative stress and cholinergic disruption as early biomarkers of Ba toxicity. Partial Least Squares Path Modeling (PLS-PM) showed that oxidative damage is the central driver linking antioxidant activation, fatty-acid remodeling, and AChE inhibition (GoF = 0.92), supporting a mechanistic cascade from mitochondrial ROS overproduction to membrane damage and neurofunctional impairment. Altogether, this work establishes oxidative stress-mediated toxicity as the primary pathway of Ba in P. adspersus, highlights fatty-acid composition as an integrative endpoint, and validates this species as a sensitive sentinel for biomonitoring trace-metal impacts in coastal and lagoon systems.