ArticleVeterinary research communications2026
Chronic cadmium exposure disrupts the gill-gut axis via oxidative and endoplasmic reticulum stress in juvenile Carassius auratus.
Article in Veterinary research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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