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This research explored the ameliorative effects of coriander (Coriandrum sativum) seed extract supplementation in mitigating nickel (Ni) toxicity in fish. For this purpose, Ctenopharyngodon idella fingerlings (average weight: 12.35 ± 0.04 g/fish) were randomly assigned to 18 tanks, divided into six groups with three replicates each. The six treatments were categorized as follows: the negative control group (NC) received no supplement and no Ni exposure, while the positive control group (PC) was exposed to 3.6 mg/L Ni without supplementation. The remaining four groups were fed dietary supplements with 1%, 2%, 3%, and 4% C. sativum, respectively, and were exposed to 3.6 mg/L Ni. Over the next 60 days, the trial continued. Waterborne Ni negatively impacted fish growth performance, blood profile, body composition, and antioxidant activity of C. idella. On the other hand, dietary C. sativum improved fish health and successfully reduced Ni toxic potential. Notably, 1% C. sativum supplementation enhanced growth performance (weight gain: 22.82 g; weight gain percentage: 185.74%) and improved carcass quality (protein: 14.65%; fat: 4.15%; ash: 2.74%; moisture: 74.84%). Additionally, it improved blood indices (RBCs: 2.45 × 10 mm; WBCs: 14.21 × 10 mm) and antioxidant activity (SOD: 30.26 U/mg; CAT: 3.66 U/mg; GST: 48.35 U/mg), significantly improving serum biochemical indices and mitigating Ni toxicity. In summary, the results suggest that dietary supplementation with 1% C. sativum effectively reduces Ni toxicity in C. idella.
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http://dx.doi.org/10.1038/s41598-025-13985-2 | DOI Listing |
Infect Dis Ther
September 2025
School of Biomedical Sciences, The Chinese University of Hong Kong (CUHK), Hong Kong SAR, China.
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Departamento de Química, Universidad Autónoma Metropolitana-Iztapalapa, Ave. Ferrocarril San Rafael Atlixco 186, Col. Leyes de Reforma 1A sección, Alcaldía Iztapalapa, 09310 Mexico City, Mexico.
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Department of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
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View Article and Find Full Text PDFFree Radic Biol Med
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Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China. Electronic address:
Metabolic dysfunction-associated steatotic liver disease (MASLD), a leading cause of chronic liver pathology, lacks effective therapies. This study identifies ferroptosis-a lipid peroxidation-driven, iron-dependent form of cell death-as a central pathogenic mechanism in MASLD. Integrative proteomic and histopathological analyses of human and murine MASLD livers revealed marked ferroptosis activation, characterized by dysregulated iron metabolism (reduced FTH1 and GPX4; elevated ACSL4) and oxidative stress.
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