In vivo effects on the immune function of fathead minnow (Pimephales promelas) following ingestion and intraperitoneal injection of polystyrene nanoplastics.

Nanoplastics (1-100 nm) are potentially the most hazardous litter in the environment. Recent scientific studies have documented their toxic effects at the cellular and molecular levels, but knowledge underlying mechanisms of their toxicity is still scarce. Nanoplastics are known for their ability to induce immune and inflammatory responses as well as generating reactive oxygen species. While some studies have addressed the immunotoxicity of nanoplastics in vitro and on in vivo in fish after intraperitoneal injection, no information is available on adult fish after ingestion of a contaminated prey. The present study is the first to attempt to address the immunotoxicity of nanoplastics in adult fish after trophic transfer. Pimephales promelas is a well-established bioindicator species to study the immunotoxicity of nanoparticles and the innate immune responses of fish. This study aims to assess the in vivo innate immune response of adult P. promelas following exposure to polystyrene nanoplastics by measuring the gene expression of ncf, nox2, mst1 and c3; these genes are related with the immune function of neutrophils, macrophages and complement in fish. Two target organs (liver and head kidney) and two routes of exposure (IP- injection and ingestion) were analyzed. After 48 h of exposure, polystyrene nanoplastics were encountered in the liver and kidney of both IP-injection and ingestion exposed fish, and significantly affected the innate immune system of P. promelas by downregulating the gene expression ncf, mst1, and c3 in liver and kidney. Significant difference between treatments was only observed for the gene expression of nfc in liver. Results of this study indicate that polystyrene nanoplastics can exhibit immunotoxicity in fish through an environmentally relevant route of exposure, interfering with the synthesis and function of neutrophils, macrophages, and complement of P. promelas in their principal hematopoietic tissues, which may potentially compromise its ability to survive in nature.