Protozoan-mediated long-term trophic transfer of combined pollutants: Implications for organ development in higher-trophic-level predator

Pollutants in aquatic ecosystems, originating from industrial and human activities, interact and propagate through the food chain, exerting synergistic impact on higher trophic levels. However, the long-term combined effects of trophically transferred pollutants on the development of higher-trophic-level predator remains insufficiently understood. To address this knowledge gap, the zebrafish model was utilized to investigate the transfer effects of microplastics and cadmium via protozoan primary consumers. Prolonged exposure to these combined pollutants resulted in morphological abnormalities and developmental delays in the heart, liver, and gonads of zebrafish. Physiological and biochemical analyses revealed significant alterations in growth hormone levels in these organs, accompanied by increased levels of insulin, estrogen, and testosterone. Transcriptome sequencing identified numerous differentially expressed genes under co-exposure conditions. Pathway analysis indicated disruptions in key signaling pathways related to growth and development such as Wnt/β-catenin, growth hormone, estrogen, and androgen signaling, highlighting a central mechanism through which long-term combined pollutant exposure induces organ developmental disorders. This study provides critical insights into the cumulative transfer of pollutants through the food chain, offering valuable perspectives on their potential ecological impacts and food safety implications. • Long-term co-pollutant transfer increased developmental abnormalities in zebrafish. • Key hormones GH, insulin, estrogen, and testosterone are significantly altered. • Three core signaling pathways regulating growth and development were disrupted. • Functional genes in key growth-regulating pathways were mostly downregulated by >50 %.