Mitigation of mycotoxin residues and activation of endogenous stem cells in broiler chickens using a toxin binder: Implications for meat safety and performance enhancement.

IF 2 Q2 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Veterinary World Pub Date : 2025-07-01 Epub Date: 2025-07-08 DOI:10.14202/vetworld.2025.1850-1862
Erma Safitri, Hery Purnobasuki, Tita Damayanti Lestari, Suzanita Utama, Rimayanti Rimayanti, Mirni Lamid, Mutmainah Wardatul Jannah, Siti Darodjah, Goo Jang, Mitsuhiro Takagi
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引用次数: 0

Abstract

Background and aim: Mycotoxin contamination in poultry feed, particularly with aflatoxin B1 (AFB1) and ochratoxin A (OTA), poses significant threats to broiler health, meat quality, and consumer safety. Toxin binders are commonly used to mitigate these effects; however, their impact on endogenous stem cell activity and overall broiler performance remains underexplored. This study aimed to evaluate the efficacy of a commercial toxin binder in reducing AFB1 and OTA residues in broiler meat, inducing endogenous stem cell production, and improving growth and feed performance indices.

Materials and methods: Twenty Cobb broilers were randomly assigned to four groups: Negative control (C-), positive control with mycotoxin-contaminated feed (C+), treatment 1 (T1: 1.1 g/kg binder), and treatment 2 (T2: 1.6 g/kg binder). Broilers were fed for 35 days. AFB1 and OTA levels in pectoral muscles were quantified using high-performance liquid chromatography, while endogenous stem cell markers (CD34+, CD45+, CD105-) in spleen tissue were assessed through flow cytometry. Growth parameters, feed conversion ratio (FCR), and performance index were also evaluated.

Results: AFB1 and OTA residues were significantly reduced in T1 and T2 compared to C+ (p < 0.05), with T2 showing the lowest levels (0.0023 μg/mL and 0.073 μg/mL, respectively). Flow cytometry revealed that T2 significantly induced endogenous stem cells (35.62% ± 2.16) compared to all other groups. The highest average daily growth occurred in T1 (68.78 ± 4.78 g/day), while the best FCR (1.38 ± 0.079) and performance index (386.2 ± 14.34) were also recorded in T1. No mortality occurred in any group.

Conclusion: Administering a toxin binder at 1.6 g/kg effectively reduced AFB1 and OTA residues and significantly activated endogenous stem cells, suggesting a protective and regenerative effect. Meanwhile, a dose of 1.1 g/kg yielded optimal growth performance and feed efficiency. These findings support the dual functional role of toxin binders in enhancing broiler meat safety and physiological resilience.

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使用毒素粘合剂减轻肉鸡霉菌毒素残留和激活内源性干细胞:对肉类安全和提高生产性能的影响
背景与目的:家禽饲料中的霉菌毒素污染,特别是黄曲霉毒素B1 (AFB1)和赭曲霉毒素A (OTA),对肉鸡的健康、肉质量和消费者安全构成重大威胁。毒素粘合剂通常用于减轻这些影响;然而,它们对内源干细胞活性和肉鸡整体生产性能的影响仍未得到充分研究。本研究旨在评价一种商业毒素粘合剂在减少肉仔鸡肉中AFB1和OTA残留、诱导内源干细胞产生以及改善生长和饲料性能指标方面的效果。材料与方法:将20只科布肉鸡随机分为4组:阴性对照(C-)、霉菌毒素污染饲料阳性对照(C+)、处理1 (T1: 1.1 g/kg黏合剂)和处理2 (T2: 1.6 g/kg黏合剂)。饲喂35 d。采用高效液相色谱法定量测定胸肌组织中AFB1和OTA水平,采用流式细胞术测定脾脏组织中内源性干细胞标志物(CD34+、CD45+、CD105-)水平。并对生长参数、饲料系数(FCR)和性能指标进行评价。结果:与C+相比,T1和T2的AFB1和OTA残留量显著减少(p < 0.05),其中T2最低(分别为0.0023 μg/mL和0.073 μg/mL)。流式细胞术显示,与其他各组相比,T2显著诱导内源性干细胞(35.62%±2.16)。平均日生长量最高的是T1(68.78±4.78 g/d),最佳的是FCR(1.38±0.079)和性能指数(386.2±14.34)。两组均无死亡发生。结论:1.6 g/kg剂量的毒素结合剂能有效减少AFB1和OTA残留,显著激活内源性干细胞,具有保护和再生作用。同时,1.1 g/kg的添加量获得了最佳的生长性能和饲料效率。这些发现支持了毒素结合剂在提高肉鸡肉品安全性和生理弹性方面的双重功能作用。
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来源期刊
Veterinary World
Veterinary World Multiple-
CiteScore
3.60
自引率
12.50%
发文量
317
审稿时长
16 weeks
期刊介绍: Veterinary World publishes high quality papers focusing on Veterinary and Animal Science. The fields of study are bacteriology, parasitology, pathology, virology, immunology, mycology, public health, biotechnology, meat science, fish diseases, nutrition, gynecology, genetics, wildlife, laboratory animals, animal models of human infections, prion diseases and epidemiology. Studies on zoonotic and emerging infections are highly appreciated. Review articles are highly appreciated. All articles published by Veterinary World are made freely and permanently accessible online. All articles to Veterinary World are posted online immediately as they are ready for publication.
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