Frontiers in immunology · 2026
Benzo[a]pyrene-induced immunotoxicity, neurotoxicity, and cardiotoxicity in grass carp (Ctenopharyngodon idella).
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Hamed Mohamed, Naguib Mervat, Mohammed Elsayed S I, Hamada Alhosein, Alqahtani Abdulaziz R, Abdel-Tawab Hanem S, Sayed Alaa El-Din H
Аннотация
INTRODUCTION: Benzo[a]pyrene (B[a]P), a widespread polycyclic aromatic hydrocarbon (PAH), is a major aquatic pollutant with known toxic effects. However, its immunotoxicity during early fish development remains poorly understood. This study investigated the immunotoxic, neurotoxic, and cardiotoxic effects of B[a]P in grass carp (Ctenopharyngodon idella) Juvenile and evaluated associated neurotoxic and cardiotoxic alterations.
METHODS: Grass carp Juvenile were exposed to 1, 10, and 100 μM B[a]P for 14 days. Immune responses were assessed by measuring myeloperoxidase (MPO), nitric oxide (NO), nitroblue tetrazolium (NBT), and immunoglobulin M (IgM). Acetylcholinesterase (AChE) activity was determined as a neurotoxicity marker. Histopathological and histochemical analyses of brain and heart tissues were performed to evaluate tissue damage.
RESULTS: B[a]P exposure significantly increased MPO and NO levels, indicating activation of inflammatory and oxidative responses. In contrast, NBT activity and IgM concentrations were significantly reduced, suggesting suppression of innate and adaptive immunity. AChE activity was markedly inhibited, demonstrating neurotoxicity. Histopathological examination revealed dose-dependent degeneration, necrosis, vascular congestion, and tissue disorganization in cerebellar and cardiac tissues. Histochemical analyses showed alterations in neuronal RNA distribution and changes in cardiac polysaccharide and glycoprotein contents.
CONCLUSION: B[a]P induces significant immune dysfunction in grass carp Juvenile, characterized by inflammatory activation and suppression of immune defenses. These effects are accompanied by neurotoxic and cardiotoxic damage, highlighting the potential ecological risks of B[a]P contamination in aquatic environments.
METHODS: Grass carp Juvenile were exposed to 1, 10, and 100 μM B[a]P for 14 days. Immune responses were assessed by measuring myeloperoxidase (MPO), nitric oxide (NO), nitroblue tetrazolium (NBT), and immunoglobulin M (IgM). Acetylcholinesterase (AChE) activity was determined as a neurotoxicity marker. Histopathological and histochemical analyses of brain and heart tissues were performed to evaluate tissue damage.
RESULTS: B[a]P exposure significantly increased MPO and NO levels, indicating activation of inflammatory and oxidative responses. In contrast, NBT activity and IgM concentrations were significantly reduced, suggesting suppression of innate and adaptive immunity. AChE activity was markedly inhibited, demonstrating neurotoxicity. Histopathological examination revealed dose-dependent degeneration, necrosis, vascular congestion, and tissue disorganization in cerebellar and cardiac tissues. Histochemical analyses showed alterations in neuronal RNA distribution and changes in cardiac polysaccharide and glycoprotein contents.
CONCLUSION: B[a]P induces significant immune dysfunction in grass carp Juvenile, characterized by inflammatory activation and suppression of immune defenses. These effects are accompanied by neurotoxic and cardiotoxic damage, highlighting the potential ecological risks of B[a]P contamination in aquatic environments.