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<p>Polystyrene micro- and nanoplastics (MNPs) have emerged as pervasive environmental pollutants posing significant risks to mammalian health. This study investigated the systemic impacts of co-exposure to Cr(VI), microplastics (MP), and nanoplastics (NP) on the hematological profiles and hepatic integrity of Wistar rats. Utilizing advanced microscopic and morphometric techniques, we evaluated the histoarchitectural alterations in peripheral blood, hematopoietic progenitor cells, and hepatocytes. Results indicated that Cr(VI) (8&#xa0;µg/mL) induced substantial pathological changes, including erythrocytic microcytosis and stomatocytosis, reactive lymphocytosis, and marked platelet aggregation. While isolated MNP exposure (1.14&#xa0;µg/day) exerted negligible effects on erythrocytes and lymphocytes, it triggered severe thrombocytic disruptions, characterized by morphological aberrations, thrombocytosis, and extensive platelet agglutination. These platelet disorders correlated strongly with impaired megakaryocyte maturation and a high incidence of bone marrow emperipolesis. Furthermore, nuclear fragmentation was observed within hepatocytes across treatment groups. Crucially, the co-administration of Cr(VI) and MNPs appeared to attenuate individual hematotoxic effects, suggesting a complex interaction where MNPs may modulate free metal availability, thereby reducing immediate biological damage. This study provides essential baseline data on the toxicological dynamics of combined plastic and heavy metal exposure in mammals. Our findings underscore the necessity of considering multi-pollutant interactions to achieve more reliable health risk assessments and to elucidate the cellular dynamics underlying environmental co-exposure.</p>

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Beyond Hepatotoxicity: Chronic Cr(VI) and PS-MNPs Co-Exposure Disrupts Megakaryopoiesis and Induces Cytomorphological Alterations in Wistar Rats

  • 期刊论文

  • 发表日期：

    2026年7月7日

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  • Damir Suljević,
  • Maja Mitrašinović-Brulić

摘要

Polystyrene micro- and nanoplastics (MNPs) have emerged as pervasive environmental pollutants posing significant risks to mammalian health. This study investigated the systemic impacts of co-exposure to Cr(VI), microplastics (MP), and nanoplastics (NP) on the hematological profiles and hepatic integrity of Wistar rats. Utilizing advanced microscopic and morphometric techniques, we evaluated the histoarchitectural alterations in peripheral blood, hematopoietic progenitor cells, and hepatocytes. Results indicated that Cr(VI) (8 µg/mL) induced substantial pathological changes, including erythrocytic microcytosis and stomatocytosis, reactive lymphocytosis, and marked platelet aggregation. While isolated MNP exposure (1.14 µg/day) exerted negligible effects on erythrocytes and lymphocytes, it triggered severe thrombocytic disruptions, characterized by morphological aberrations, thrombocytosis, and extensive platelet agglutination. These platelet disorders correlated strongly with impaired megakaryocyte maturation and a high incidence of bone marrow emperipolesis. Furthermore, nuclear fragmentation was observed within hepatocytes across treatment groups. Crucially, the co-administration of Cr(VI) and MNPs appeared to attenuate individual hematotoxic effects, suggesting a complex interaction where MNPs may modulate free metal availability, thereby reducing immediate biological damage. This study provides essential baseline data on the toxicological dynamics of combined plastic and heavy metal exposure in mammals. Our findings underscore the necessity of considering multi-pollutant interactions to achieve more reliable health risk assessments and to elucidate the cellular dynamics underlying environmental co-exposure.