College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; Beijing General Station of Animal Husbandry, Beijing 100107, China.
Ecotoxicol Environ Saf. 2024 Nov 1;286:117169. doi: 10.1016/j.ecoenv.2024.117169. Epub 2024 Oct 12.
T-2 toxin (T-2) is a highly toxic mycotoxin that threatens organism health, yet its hepatoxicity on ducks remains unknown. The present study aimed to assess the hepatoxicity and redox reactions induced by T-2 in ducks. Sixty 7-day-old ducklings were divided into 4 groups and exposed to 0, 200, 400 and 800 μg/kg bodyweight of T-2 through oral gavage for 2 weeks. The growth performance, liver histopathology, biochemical indicators, antioxidant capacity and hepatic damage-related genes of ducks were analyzed. The results revealed that 800 µg/kg T-2 inhibited the growth and feed intake of ducks, whereas liver index increased with the elevation of T-2 concentration. Histological examinations exhibited that T-2 caused hepatic cord disappeared and severe steatosis. Moreover, serum AST, ALT and TG were substantially higher in 400 μg/kg group, while γ-GT and ALB were reduced under 800 μg/kg T-2 exposure. In addition, significant increase of malondialdehyde (MDA) in liver, decrease of hepatic total antioxidant capacity (T-AOC) and serum glutathione peroxidase (GPx) were observed in all T-2 groups. Furthermore, T-2 disrupted lipid metabolism and oxidative stress-related genes expression in liver. The transcript level of fatty acid binding protein 1 (FABP1) was markedly raised in all T-2 groups, and hepatic acyl-CoA oxidase 1 (ACOX1) was significantly raised in 200 and 400 μg/kg T-2 groups. Under 800 μg/kg T-2, significant induction of hypoxia inducible factor-1 alpha (HIF-1α), and downregulated peroxisome proliferator-activated receptor (PPAR)-alpha, carnitine palmitoyl transferase 1A (CPT1A), peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1α), GPx1, catalase (CAT) mRNA levels were observed. Therefore, we conclude that T-2 caused liver injury through lipid metabolism disruption and oxidative stress in ducks, which reinforces understanding about the hepatoxicity mechanisms of T-2 and provides new targets for detoxication and prevention.
T-2 毒素（T-2）是一种具有高度毒性的真菌毒素，会对生物体健康造成威胁，但它对鸭子的肝毒性仍不清楚。本研究旨在评估 T-2 对鸭子的肝毒性和氧化还原反应。将 60 只 7 日龄的雏鸭分为 4 组，通过口服灌胃分别暴露于 0、200、400 和 800μg/kg 体重的 T-2 毒素，为期 2 周。分析了鸭子的生长性能、肝组织病理学、生化指标、抗氧化能力和肝损伤相关基因。结果表明，800μg/kg 的 T-2 抑制了鸭子的生长和采食量，而肝指数随着 T-2 浓度的升高而增加。组织学检查显示 T-2 导致肝索消失和严重的脂肪变性。此外，血清 AST、ALT 和 TG 在 400μg/kg 组显著升高，而γ-GT 和 ALB 在 800μg/kg T-2 暴露组中降低。此外，在所有 T-2 组中均观察到肝中丙二醛（MDA）显著增加，肝总抗氧化能力（T-AOC）和血清谷胱甘肽过氧化物酶（GPx）减少。此外，T-2 破坏了肝中脂质代谢和氧化应激相关基因的表达。所有 T-2 组的脂肪酸结合蛋白 1（FABP1）转录水平显著升高，200 和 400μg/kg T-2 组的酰基辅酶 A 氧化酶 1（ACOX1）显著升高。在 800μg/kg T-2 下，缺氧诱导因子 1 阿尔法（HIF-1α）显著诱导，过氧化物酶体增殖物激活受体（PPAR）-α、肉碱棕榈酰转移酶 1A（CPT1A）、过氧化物酶体增殖物激活受体γ共激活因子 1α（PGC-1α）、GPx1、过氧化氢酶（CAT）mRNA 水平下调。因此，我们得出结论，T-2 通过破坏脂质代谢和氧化应激导致鸭子肝损伤，这加强了对 T-2 肝毒性机制的理解，并为解毒和预防提供了新的靶点。
