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<p>Exposure to food-borne toxins, such as aflatoxin B<sub>1</sub> (AFB), is one of the largest issues challenging the aquaculture sustainability worldwide. The objective of the current investigation was to determine whether hesperidin, HES (150&#xa0;mg/kg diet), could protect African catfish (<i>Clarias gariepinus</i>) from food-borne AFB (19.7&#xa0;µg/kg diet). For 60&#xa0;days, 160 fish (58.34 ± 0.39&#xa0;g) were assigned to four treatments, each with four replications (40 fish per treatment; 10 fish per replicate). Group 1 (control) and Group 2 were fed on basal diets fortified with 0 and 150&#xa0;mg/kg HES, respectively, without AFB exposure. Group 3 and Group 4 were fed basal diets fortified with AFB and AFB + HES, respectively. We evaluated survival, oxidative/antioxidant status, hepatic and renal function, brain neurotransmitters, neuronal damage markers, and tissue histopathology. The findings showed that an AFB-contaminated diet induced oxidative stress by increasing the lipid peroxidation product (MDA) and reducing total antioxidant capacity and catalase activity. A reduction in the survivability (77.5%) and an elevation in the hepatic (alanine aminotransferase and aspartate aminotransferase) and renal (creatinine) markers were noticed in the AFB-intoxicated group. AFB exposure lowered the total protein, albumin, and globulin levels. Furthermore, the brain level of acetyl choline esterase was reduced, while the damage marker (8-hydroxy-2′-deoxyguanosine) level was increased by AFB intoxication. Various pathological alterations were shown in the liver, kidney, brain, and gills of the AFB-intoxicated groups. Dietary HES ameliorated the bad effects of AFB intoxication by increasing the fish survivability (90%), reducing the oxidative stress, and boosting the antioxidant status. Furthermore, the protein profile and brain neurotransmitter were improved with a reduction of the DNA damage marker. Dietary HES restored the tissue histomorphology of the AFB-intoxicated group. We can conclude that the dietary fortification of HES at a level of 150&#xa0;mg/kg could mitigate the physiological and pathological disorders induced by the widely present toxin (AFB) in African catfish, which results in improvement of the sustainability of this species culture.</p>

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Hesperidin flavonoid protects African catfish from aflatoxin B1-induced oxidative stress, hepato-renal dysfunction, neurotransmitter disorders, and histological changes

  • 期刊论文

  • 发表日期：

    2026年3月26日

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  • Rowida E. Ibrahim,
  • Gehad E. Elshopakey,
  • Ahmed S. AlSaqufi,
  • Abdallah Tageldein Mansour,
  • Yousef Alkhamis,
  • Hesham A. Hassanien,
  • Mohamed Ashour,
  • Mohamed Y. M. Aly,
  • Afaf N. Abdel Rahman,
  • Mohamed Fouad Mansour

摘要

Exposure to food-borne toxins, such as aflatoxin B1 (AFB), is one of the largest issues challenging the aquaculture sustainability worldwide. The objective of the current investigation was to determine whether hesperidin, HES (150 mg/kg diet), could protect African catfish (Clarias gariepinus) from food-borne AFB (19.7 µg/kg diet). For 60 days, 160 fish (58.34 ± 0.39 g) were assigned to four treatments, each with four replications (40 fish per treatment; 10 fish per replicate). Group 1 (control) and Group 2 were fed on basal diets fortified with 0 and 150 mg/kg HES, respectively, without AFB exposure. Group 3 and Group 4 were fed basal diets fortified with AFB and AFB + HES, respectively. We evaluated survival, oxidative/antioxidant status, hepatic and renal function, brain neurotransmitters, neuronal damage markers, and tissue histopathology. The findings showed that an AFB-contaminated diet induced oxidative stress by increasing the lipid peroxidation product (MDA) and reducing total antioxidant capacity and catalase activity. A reduction in the survivability (77.5%) and an elevation in the hepatic (alanine aminotransferase and aspartate aminotransferase) and renal (creatinine) markers were noticed in the AFB-intoxicated group. AFB exposure lowered the total protein, albumin, and globulin levels. Furthermore, the brain level of acetyl choline esterase was reduced, while the damage marker (8-hydroxy-2′-deoxyguanosine) level was increased by AFB intoxication. Various pathological alterations were shown in the liver, kidney, brain, and gills of the AFB-intoxicated groups. Dietary HES ameliorated the bad effects of AFB intoxication by increasing the fish survivability (90%), reducing the oxidative stress, and boosting the antioxidant status. Furthermore, the protein profile and brain neurotransmitter were improved with a reduction of the DNA damage marker. Dietary HES restored the tissue histomorphology of the AFB-intoxicated group. We can conclude that the dietary fortification of HES at a level of 150 mg/kg could mitigate the physiological and pathological disorders induced by the widely present toxin (AFB) in African catfish, which results in improvement of the sustainability of this species culture.