What question did this study set out to answer?

This research aims to characterize the effects of barium chloride on oxidative stress and lipid remodeling in the shrimp Palaemon adspersus.

March 5, 2026Open Access

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

Key Points

This research aims to characterize the effects of barium chloride on oxidative stress and lipid remodeling in the shrimp Palaemon adspersus.
Shrimp were exposed to varying concentrations of barium chloride for five days.
Biochemical markers of oxidative stress, antioxidant defenses, and fatty acid composition were quantified.
Dose-response relationships were analyzed using EC50 and Benchmark Dose modeling.
Partial Least Squares Path Modeling (PLS-PM) was used to elucidate mechanistic pathways.
Barium bioaccumulation was dose-dependent with significant oxidative stress observed.
Antioxidant activation was insufficient, leading to increased oxidative damage and lipid peroxidation.
AChE inhibition was identified as a sensitive marker of neurotoxicity related to barium exposure.
PLS-PM indicated that oxidative damage drives the relationship between antioxidant response and neurofunctional impairment.

Abstract

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 (BaCl 2 ) 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 (H 2 O 2 , 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. EC 50 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. • BaCl 2 exposure induces strong mitochondrial-ROS responses in Palaemon adspersus . • Oxidative damage and antioxidant imbalance increase in a clear dose-response. • Fatty-acid remodeling reveals membrane vulnerability under Ba exposure. • AChE inhibition shows high sensitivity to Ba-driven neurotoxicity. • EC 50 , BMD and PLS-PM identify mechanistic pathways and toxicity thresholds.

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Khila et al. (Tue,) studied this question.

synapsesocial.com/papers/69a91e4cd6127c7a504c223e https://doi.org/https://doi.org/10.1016/j.marpolbul.2026.119475

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