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.

中文翻译：

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阐明纳米塑料对斑马鱼血液和循环系统的潜在毒性机制


目前关于纳米塑料（NP）对血液和循环系统影响的研究还很有限。本研究旨在通过评估斑马鱼中纳米颗粒的毒性并利用一系列分子生物学技术探索其潜在机制，强调与这些系统中的纳米颗粒相关的关键健康风险。尺寸为 80 nm 的聚苯乙烯纳米塑料 (PS-NP) 用于斑马鱼的急性和慢性暴露实验。对斑马鱼进行整体原位杂交表明，急性暴露于 PS-NP 会导致原始和最终造血功能以及血管和心脏形态发生的异常发育。从机制上讲，PS-NPs 引起早期中胚层成血管细胞和心脏祖细胞的异常规范，从而导致这些缺陷。慢性暴露后成年斑马鱼心脏的转录组测序揭示了线粒体功能受损。随后的实验表明，PS-NPs 诱导线粒体功能障碍并抑制 PINK1/Parkin 介导的线粒体自噬途径。我们的研究结果强调，PS-NP 通过破坏成血管细胞和心脏祖细胞的规格，以及抑制线粒体功能和线粒体自噬途径，损害血液和循环系统的健康。