It is demonstrated that polystyrene exacerbates TPHP-induced gill toxicity through disruption of metabolism, barrier integrity, and apoptosis, underscoring the need to consider combined effects in aquatic risk assessment.
Abstract
The combined toxicity of microplastics (MPs) and co-occurring organic pollutants is a critical concern in environmental pollution risk assessment. Triphenyl phosphate (TPHP), a widely used flame retardant, frequently coexists with microplastics in aquatic environments. However, research on the impact of MPs on the toxicity of TPHP remains limited. This study integrated physiological, biochemical, and transcriptomic approaches to investigate the individual and combined effects of polystyrene (PS) MPs and TPHP on common carp (Cyprinus carpio) gills and the underlying mechanisms following 3 and 7 days of exposure. The results showed that PS and TPHP compromised the integrity of the gill epithelium, disrupted osmotic regulation, suppressed aerobic energy metabolism, and induced oxidative stress, inflammatory cascades, barrier protein depletion, and apoptosis. Crucially, formal interaction analysis using the interaction effect index (dI) revealed distinct combined toxicity patterns. Furthermore, transcriptomic profiling showed that combined exposure elicited the most extensive transcriptional suppression (1790 differentially expressed genes), uniquely enriching extracellular matrix (ECM) degradation and lipid metabolic disorders. Notably, although PS reduced TPHP accumulation in gills, co-exposure triggered the most severe molecular disturbances, indicating combined effects arise from intracellular pathway crosstalk rather than enhanced uptake. Our findings demonstrate that PS exacerbates TPHP-induced gill toxicity through disruption of metabolism, barrier integrity, and apoptosis, underscoring the need to consider combined effects in aquatic risk assessment.
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