We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Unveil new insights into microplastic and benzo[a]pyrene toxicity in the seaworm Hediste diversicolor coelomic fluid: A transdisciplinary approach
Summary
Researchers studied how microplastics and the carcinogenic pollutant benzo[a]pyrene affect the internal body fluid of marine seaworms, both individually and in combination. They found that microplastics enhanced the accumulation of the pollutant in the worms' immune cells and that combined exposure caused more severe DNA damage and cell death than either contaminant alone. The study demonstrates that microplastics can amplify the harmful effects of chemical pollutants in marine invertebrates.
Microplastics (MPs) pollution presents a pressing concern for marine ecosystems, as their small size facilitates both ingestion and accumulation by organisms, as well as the transport of harmful pollutants. This dual threat complicates their ecological impact, especially concerning compartments like the coelomic fluid, crucial for marine invertebrate physiology. In this study, we investigated the toxicological effects of environmentally relevant concentrations of MPs (10 and 50 mg/kg sediment), both alone and in combination with benzo[a]pyrene (B[a]P, 1 µg/kg sediment), a carcinogenic polycyclic aromatic hydrocarbon known for its genotoxic and pro-apoptotic properties. The benthic polychaete Hediste diversicolor was exposed to these treatments for 7 days through spiked sediments, simulating realistic environmental conditions. The MPs used were particles smaller than 30 µm, composed of a mixture of polymers, including PE, PET, PP, LDPE, HDPE, and PEVA, with varied morphologies such as fragments, fibers, and films. Analyses revealed that both MPs and B[a]P were internalized by coelomocytes, with MPs enhancing B[a]P bioaccumulation. Combined exposures led to marked cytotoxic and genotoxic effects, evidenced by decreased lysosomal membrane stability (LMS), elevated micronuclei frequency (FMN), and increased DNA fragmentation, as assessed by terminal dUTP nick-end labeling (TUNEL) assay. Co-exposure also altered apoptotic and DNA repair pathways, as demonstrated by upregulation of P53, Bax, and Casp-3, alongside downregulation of the anti-apoptotic marker Bcl-2. These findings suggest that co-exposure intensifies cellular damage and apoptotic signaling. Overall, this study underscores the risks of MPs in marine ecosystems, particularly their role in accumulating and transferring harmful substances affecting biota health.
Sign in to start a discussion.