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The common carp (Cyprinus carpio) kidney uniquely integrates excretory nephrons, renal hematopoietic tissue, and hormonally active thyroid follicles, positioning it as a candidate “multipurpose biomarker organ” for pollutants like perfluorooctanoic acid (PFOA), a prototype long-chain PFAS and persistent organic pollutant exhibiting nephrotoxic, immunotoxic, and thyroid-disrupting effects. Building on prior histological, ultrastructural, and morphometric analyses from carp exposed to waterborne PFOA (0, 200 ng L−1, 2 mg L−1 for 56 days), a hierarchical multipurpose index comprising nephrotoxic, immunotoxic, and thyrotoxic subindices was developed from z-scored light-, electron-microscopy, and morphometric features, enabling cross-scale integration; proximal tubule vesiculations and effete rodlet cells (RCs) were newly quantified from archival electron micrographs. The subindices captured PFOA-induced glomerular hyperfiltration with proximal protein reabsorption and collecting duct RCs recruitment (nephrotoxic); hematopoietic tissue RCs recruitment, clustering, and exocytosis (immunotoxic); and increased thyroid follicle abundance/vesiculation, cross-sectional area, and perimeter (thyrotoxic). Quantification of previously only qualitatively assessed features provided statistical validation, while radar plot integration rendered results more intuitively evident—particularly highlighting the non-monotonic thyroid response—condensing organ-level complexity into a coherent framework supporting carp kidney as a translational One Health model for multi-endpoint waterborne pollutant assessment.

Perfluorooctanoic acid (PFOA), a persistent per- and polyfluoroalkyl substance (PFAS), remains a global toxicological concern due to its ubiquity, bioaccumulation potential, and toxicity even at low concentrations. This study aimed to elucidate the ultrastructural effects of PFOA on the gills of Cyprinus carpio, a species of high ecological and trophic relevance. Gill samples from fish experimentally exposed to two PFOA concentrations (200 ng L−1 and 2 mg L−1), one of which was environmentally relevant, were examined by transmission electron microscopy. The results revealed cytotoxic changes primarily affecting mitochondria-rich (chloride) cells and, to a lesser extent, epithelial and mucous cells. The main alterations included mitochondrial degeneration, Golgi and endoplasmic reticulum stress, and autophagic activation, indicating a coordinated impairment of the endomembrane system. These findings suggest that PFOA induces a bioenergetic and proteo-synthetic imbalance compromising cellular homeostasis. Both direct cytotoxic and indirect endocrine-mediated mechanisms may contribute to the observed lesions. The pronounced sensitivity of mitochondria-rich cells supports their use as generalist biomarkers of PFOA exposure and effect. Within a One Health framework, these cells may also serve as translational models for elucidating conserved subcellular mechanisms of PFAS-induced cytotoxicity across vertebrates, with implications for environmental and human health risk assessment.