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<p>This study investigated the toxicological effects of chronic cadmium (Cd) exposure (0, 100, 300, and 500 μg/L for 28 days) on juvenile crucian carp (<i>Carassius auratus</i>), assessing impacts on gill tissue and gut microbiota using a multi-faceted approach. Histological analysis revealed concentration-dependent gill damage, including severe lamellar fusion and desquamation, with a parallel increase in apoptotic cells confirmed by TUNEL staining. Biochemically, Cd induced significant oxidative stress, as shown by decreased superoxide dismutase (SOD) activity, lowered levels of reduced glutathione (GSH) and total antioxidant capacity (T-AOC), and elevated malondialdehyde (MDA), a marker of lipid peroxidation. Gene expression analysis confirmed the activation of endoplasmic reticulum (ER) stress and pro-apoptotic pathways, with upregulation of <i>chop</i> and <i>bax</i> and downregulation of <i>bcl2</i>. Furthermore, Cd exposure profoundly restructured the gut microbiota, leading to pronounced dysbiosis and loss of microbial homeostasis. Collectively, these findings demonstrate that chronic Cd exposure induces gill damage in juvenile<i> C. auratus</i> through interconnected oxidative stress, ER stress, and apoptosis, while concurrently causing significant disruption to the intestinal microbial ecosystem.</p>

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Chronic cadmium exposure disrupts the gill–gut axis via oxidative and endoplasmic reticulum stress in juvenile Carassius auratus

  • 期刊论文

  • 发表日期：

    2026年1月16日

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  • Haitang Wang,
  • Shanya Cai,
  • Xingxing Fang

摘要

This study investigated the toxicological effects of chronic cadmium (Cd) exposure (0, 100, 300, and 500 μg/L for 28 days) on juvenile crucian carp (Carassius auratus), assessing impacts on gill tissue and gut microbiota using a multi-faceted approach. Histological analysis revealed concentration-dependent gill damage, including severe lamellar fusion and desquamation, with a parallel increase in apoptotic cells confirmed by TUNEL staining. Biochemically, Cd induced significant oxidative stress, as shown by decreased superoxide dismutase (SOD) activity, lowered levels of reduced glutathione (GSH) and total antioxidant capacity (T-AOC), and elevated malondialdehyde (MDA), a marker of lipid peroxidation. Gene expression analysis confirmed the activation of endoplasmic reticulum (ER) stress and pro-apoptotic pathways, with upregulation of chop and bax and downregulation of bcl2. Furthermore, Cd exposure profoundly restructured the gut microbiota, leading to pronounced dysbiosis and loss of microbial homeostasis. Collectively, these findings demonstrate that chronic Cd exposure induces gill damage in juvenile C. auratus through interconnected oxidative stress, ER stress, and apoptosis, while concurrently causing significant disruption to the intestinal microbial ecosystem.