Elucidating the underlying toxic mechanisms of nanoplastics on zebrafish hematological and circulatory systems

Abstract

Research on the impact of nanoplastics (NPs) on hematological and circulatory systems is currently limited. This study aimed to underscore the critical health risks associated with NPs in these systems by evaluating the toxicity of NPs in zebrafish and exploring the underlying mechanisms using a range of molecular biology techniques. Polystyrene nanoplastics (PS-NPs), which are 80 nm in size, were used in both acute and chronic exposure experiments with zebrafish. Zebrafish subjected to whole-mount in situ hybridization showed that acute exposure to PS-NPs resulted in abnormal development in primitive and definitive hematopoiesis, as well as in vascular and cardiac morphogenesis. Mechanistically, PS-NPs caused aberrant specification of early mesodermal hemangioblasts and cardiac progenitor cells, contributing to these defects. Transcriptome sequencing of adult zebrafish hearts following chronic exposure unveiled impaired mitochondrial function. Subsequent experiments demonstrated that PS-NPs induced mitochondrial dysfunction and inhibited the PINK1/Parkin-mediated mitophagy pathway. Our results highlight that PS-NPs impair the health of the hematological and circulatory systems by disrupting the specification of hemangioblasts and cardiac progenitor cells, as well as inhibiting mitochondrial function and the mitophagy pathway.