Toxins, Vol. 17, Pages 568: Dose-Dependent but Non-Interactive Effects of Ochratoxin A and Selenomethionine on Hepatic Lipid Metabolism and Oxidative Stress in Broiler Chickens


Toxins, Vol. 17, Pages 568: Dose-Dependent but Non-Interactive Effects of Ochratoxin A and Selenomethionine on Hepatic Lipid Metabolism and Oxidative Stress in Broiler Chickens

Toxins doi: 10.3390/toxins17120568

Authors:
Szabina Kulcsár
Krisztián Balogh
Erika Zándoki
Edward Agyarko
Omeralfaroug Ali
Benjámin Kövesi
Ágnes Freiler-Nagy
András Szabó
Miklós Mézes

This study examined the effects of ochratoxin A (OTA) exposure and graded dietary selenium (Se) supplementation on fatty acid (FA) composition and oxidative stress markers in the liver of broiler chickens. OTA is known to generate oxidative stress, promote lipid peroxidation, and affect the antioxidant system. Se, an essential trace element with antioxidant properties, may help counteract OTA-induced toxicity. In this short-term (5-day) in vivo feeding experiment, 21-day-old broiler chickens were divided into six groups, each with six birds: Control (diet free from Se), 0.3 mg/kg Se, 0.5 mg/kg Se, 2 mg/kg OTA, 2 mg/kg OTA + 0.3 mg/kg Se, 2 mg/kg OTA + 0.5 mg/kg Se. Our findings show that supplementing 0.3 mg/kg (p < 0.01) or 0.5 mg/kg Se (p < 0.001) in OTA-exposed birds significantly reduced the early oxidative stress markers (conjugated dienes and trienes) and significantly increased (0.3 mg/kg p < 0.01; 0.5 mg/kg p < 0.001) glutathione levels, indicating enhanced glutathione-dependent antioxidant protection. The treatments also significantly altered the ratio of monounsaturated and n6/n3 polyunsaturated FAs. OTA with 0.3 mg/kg Se supplementation significantly (p ˂ 0.05) reduced total unsaturation and FA average chain length. At a dose of 0.3 mg/kg, the interaction of Se and OTA altered the PUFA composition, while 0.5 mg/kg Se supplementation enhanced antioxidant defense and reduced lipid peroxidation. These results highlight the dual but separate role of Se, where inadequate doses may enhance OTA toxicity, while optimal supplementation may have a protective effect on hepatic lipid homeostasis. These findings can be used in the future progress of the mitigation strategy against OTA exposure in poultry nutrition.



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