The ubiquitous co-existence of triphenyl phosphate (TPhP) and heavy metals in sediments raises significant biotoxicity concerns. However, uncertainty still exists regarding their combined toxicity to benthic organisms. Therefore, this research was conducted to elucidate the influences of cadmium (Cd) on TPhP toxicity to Corbicula fluminea (C. fluminea) in sediments. As a result, Cd promoted the accumulation of TPhP in C. fluminea and enhanced TPhP toxicity, manifested by damaged cell membranes and pronounced histological alterations. Molecular docking revealed that TPhP-Cd complexes exhibit greater binding affinity to cytochrome P4501A1 (CYP1A1) compared to TPhP alone. With the activity of CYP1A1 increasing, the biotransformation of TPhP was promoted in low-TPhP+Cd treatments (T5C0/T5C5/T5C35). Additionally, metabolites related to antioxidant defence and repair processes were reinforced to alleviate the toxicity of TPhP and Cd. However, excessive oxidative stress impaired the CYP1A1 activity in high-TPhP+Cd treatments (T35C0/T35C5/T35C35). Furthermore, metabolic pathway analysis revealed significant perturbations in the citrate cycle, alanine, aspartate and glutamate metabolism, purine metabolism, and pyrimidine metabolism. These disruptions weakened the repair capacity and aggravated apoptosis in digestive glands, potentially contributing to the synergistic toxicity of TPhP and Cd. The results highlight the ecological risks posed by TPhP in combination with heavy metals to benthic organisms.
Read full abstract