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伏马菌素B1对草鱼幼鱼生长性能和肠道结构完整性的作用机制()。 (注:括号内原文似乎不完整)

Mechanism of fumonisin B1 on growth performance and intestinal structural integrity of juvenile grass carp ().

作者信息

Chen Daiyu, Jiang Weidan, Wu Pei, Liu Yang, Ren Hongmei, Jin Xiaowan, Zhou Xiaoqiu, Feng Lin

机构信息

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China.

Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, China.

出版信息

Anim Nutr. 2025 Jan 25;21:193-206. doi: 10.1016/j.aninu.2024.11.023. eCollection 2025 Jun.

DOI:10.1016/j.aninu.2024.11.023
PMID:40487097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12143613/
Abstract

Fumonisin B1 (FB1) is a prevalent mycotoxin found in plant-based feed ingredients, and it negatively impacts the performance of aquatic animals. However, the mechanism of this toxicity remains unclear. This study aims to investigate the effect and underlying mechanism of dietary FB1 on the growth performance of juvenile grass carp (). A total of 720 juvenile grass carp (10.92 ± 0.02 g) were fed with four different levels of FB1 diets (0, 2.06, 3.94, and 8.05 mg/kg) for 30 d and each group had 3 replicates of 60 fish. Our data indicated that when the FB1 concentration in the diet exceeded 3.94 mg/kg, there was a significant decline in growth performance (e.g., final body weight, percent weight gain, and body length) ( < 0.05), as well as reductions in the activities of digestive enzymes (e.g., chymotrypsin and trypsin), alkaline phosphatase, and creatine kinase in juvenile grass carp ( < 0.05). Furthermore, increased levels of intestinal sphinganine (Sa), sphingosine (So), and FB1 residues were observed, along with disruptions in intestinal tissue structure and elevated serum D-lactic acid levels ( < 0.05). Additionally, FB1 inhibited the Kelch-like ECH-associated protein 1a/NF-E2-related factor-2 signaling pathway, resulting in decreased gene expression of intestinal copper-zinc superoxide dismutase, glutathione peroxidase 4b, and glutathione peroxidase 1a ( < 0.05). These alterations were accompanied by a reduction in glutathione levels, total superoxide dismutase activity, and total antioxidant capacity ( < 0.05), as well as an increase in levels of reactive oxygen species and malondialdehyde in the intestine ( < 0.05). FB1 induced intestinal apoptosis by downregulating the gene expression of B-cell lymphoma 2 ( = 0.009), while simultaneously upregulating the expression of Bcl-2-associated X protein, apoptotic protease activating factor-1, caspase-9, and caspase-3 ( < 0.05). Additionally, FB1 decreased the gene expression of apical junction complex-related molecules (e.g., zonula occluden-1, occludin, and nectin) ( < 0.05), while increasing the expression of claudin-15b, myosin light chain kinase, Rho family GTPases, and Rho-associated protein kinase ( < 0.05). These findings indicated that dietary FB1 negatively impacts the growth performance of juvenile grass carp, likely due to reduced digestive and absorptive capacities, elevated intestinal Sa and So levels, and disruption of intestinal structure integrity. This study filled the study gap on the toxicity of FB1 to the intestines of aquatic animals.

摘要

伏马菌素B1(FB1)是一种在植物性饲料原料中普遍存在的霉菌毒素,它会对水生动物的生长性能产生负面影响。然而,这种毒性的机制仍不清楚。本研究旨在探讨日粮中FB1对草鱼幼鱼生长性能的影响及潜在机制。总共720尾草鱼幼鱼(10.92±0.02克)被投喂四种不同水平FB1的日粮(0、2.06、3.94和8.05毫克/千克),为期30天,每组有3个重复,每个重复60尾鱼。我们的数据表明,当日粮中FB1浓度超过3.94毫克/千克时,生长性能(如终末体重、增重百分比和体长)显著下降(P<0.05),草鱼幼鱼的消化酶(如胰凝乳蛋白酶和胰蛋白酶)、碱性磷酸酶和肌酸激酶活性也降低(P<0.05)。此外,观察到肠道鞘氨醇(Sa)、鞘氨醇(So)水平和FB1残留量增加,同时肠道组织结构受到破坏,血清D-乳酸水平升高(P<0.05)。此外,FB1抑制了类Kelch样ECH相关蛋白1a/核因子E2相关因子2信号通路,导致肠道铜锌超氧化物歧化酶、谷胱甘肽过氧化物酶4b和谷胱甘肽过氧化物酶1a的基因表达下降(P<0.05)。这些变化伴随着谷胱甘肽水平、总超氧化物歧化酶活性和总抗氧化能力的降低(P<0.05),以及肠道中活性氧物种和丙二醛水平的升高(P<0.05)。FB1通过下调B细胞淋巴瘤2的基因表达诱导肠道细胞凋亡(P=0.009),同时上调Bcl-2相关X蛋白、凋亡蛋白酶激活因子-1、半胱天冬酶-9和半胱天冬酶-3的表达(P<0.05)。此外,FB1降低了顶端连接复合体相关分子(如闭合蛋白-1、闭合蛋白和连接黏附分子)的基因表达(P<0.05),同时增加了紧密连接蛋白-15b、肌球蛋白轻链激酶、Rho家族GTP酶和Rho相关蛋白激酶的表达(P<0.05)。这些发现表明日粮中FB1对草鱼幼鱼的生长性能产生负面影响,可能是由于消化和吸收能力降低、肠道Sa和So水平升高以及肠道结构完整性受到破坏。本研究填补了FB1对水生动物肠道毒性研究的空白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/c8588d03a148/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/c89acf314438/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/23e9146b702f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/8d54863493bb/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/3a5252057f9b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/c8588d03a148/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/c89acf314438/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/23e9146b702f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/8d54863493bb/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/3a5252057f9b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd1/12143613/c8588d03a148/gr5.jpg

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