Toxic Effects of Povidone-Iodine on <i>Macrobrachium rosenbergii</i>: Concentration-Dependent Responses in Oxidative Stress, Immunosuppression, and Recovery Potential
2025
Tianhui Jiao | Yakun Wang | Jie Wei | Sikai Xu | Qiaoyan Zhou | Xidong Mu | Lingyun Yu
Povidone-iodine (PVP-I), a widely used aquaculture disinfectant, remains poorly understood in terms of sublethal toxicity and damage reversibility. This study employed <i>Macrobrachium rosenbergii</i> as the model organism to evaluate the acute toxicity and sublethal effects of PVP-I through a 4-day exposure experiment followed by a 7-day depuration period. Acute toxicity tests enabled the determination of 24–96 h median lethal concentrations (LC<sub>50</sub>), with the 96 h LC<sub>50</sub> being 5.67 mg/L and the safe concentration (SC) being 1.37 mg/L. Based on this, three sublethal concentrations (1.14, 1.89, and 2.84 mg/L) were tested over a 4-day exposure followed by a 7-day depuration period. Investigated endpoints included gill ultrastructure, apoptosis, and antioxidant and immune-related gene expression. Subacute exposure at 1.89 and 2.84 mg/L induced mitochondrial vacuolization, upregulated apoptosis-related genes (<i>Cyt-c</i>, <i>Caspase-3</i>, <i>Bok</i>), and downregulated antioxidant gene expression (<i>SOD</i>, <i>CAT</i>, <i>GSH-Px</i>). The high-concentration group also showed sustained Toll-like receptor (<i>Toll</i>) gene overexpression and acid phosphatase (<i>ACP</i>) gene suppression. After depuration, antioxidant gene expression normalized; however, apoptotic markers in gill tissue remained impaired. Overall, high PVP-I concentrations cause irreversible gill damage via mitochondrial-mediated apoptosis, whereas lower concentrations (≤1.14 mg/L) allow for greater recovery. These results offer crucial toxicodynamic insights for safer PVP-I use and risk assessment in <i>M. rosenbergii</i> aquaculture.
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