College of Animal Science and Technology, Zhejiang A and F University, Linan 311300, People's Republic of China.
Feed Science Institute, College of Animal Science, Zhejiang University, No.866, Yuhangtang Road, Hangzhou 310058, People's Republic of China.
Poult Sci. 2018 Sep 1;97(9):3207-3217. doi: 10.3382/ps/pey192.
Fluorosis can induce oxidative stress through leading to reactive oxygen species (ROS) generation. Selenium (Se) can eliminate ROS by direct and indirect manners. In this study, therefore, we investigated the possible protective effects of sodium selenite (SS) and selenomethionine (Se-Met) on fluorine (F)-induced oxidative stress in broilers. A total of 720 1-day-old Lingnan Yellow broilers were allotted to 4 groups (6 replicates of 30 birds each group) and fed with basal diet (control group), 800 mg/kg F (high F group), 800 mg/kg F+0.15 mg Se/kg as SS (SS group), or Se-Met (Se-Met group), respectively. The experiment lasted 50 d. High F group significantly decreased (P < 0.05) the average daily gain (ADG) and feed efficiency (FE) in comparison with control group. The contents of ROS, malondialdehyde, 8-hydroxydeoxyguanosine, protein carbonyl, and cysteinyl aspartate specific proteinases 3 in serum, liver, and kidney were higher (P < 0.05) in high F group than those in control group. Compared with control group, the decreased (P < 0.05) activities of glutathione peroxidase (GSH-Px) and cytoplasmic thioredoxin reductase (TrxR1) as well as contents of selenoprotein P (SelP), total protein (TP), and B-cell lymphoma-2 in serum and tissues were observed in high F group. Moreover, the pathological lesions of liver and kidney in high F group were more than those in control group. However, supplementation with SS and Se-Met could improve ADG and FE, increase SelP and TP concentrations, elevate GSH-Px and TrxR1 activities, minimize the changes of oxidative stress and apoptosis parameters as well as ultrastructure of liver and kidney, whereas the effects of Se-Met were better than those of SS. The results indicated that excess F could result in growth inhibition of broilers through inducing oxidative stress and subsequently caused oxidative damage to biological macromolecules and soft tissues as well as apoptosis, whereas dietary SS and Se-Met supplementation could antagonize high F induced growth retardation by inhibiting oxidative stress and a mechanism of apoptosis regulation and the impact was more with Se-Met.
氟中毒可通过产生活性氧（ROS）诱导氧化应激。硒（Se）可以通过直接和间接的方式消除 ROS。因此，在这项研究中，我们研究了亚硒酸钠（SS）和硒代蛋氨酸（Se-Met）对肉鸡氟（F）诱导的氧化应激的可能保护作用。总共 720 只 1 日龄岭南黄肉鸡被分为 4 组（每组 6 个重复，每个重复 30 只鸡），并分别用基础日粮（对照组）、800mg/kg F（高 F 组）、800mg/kg F+0.15mg Se/kg SS（SS 组）或 Se-Met（Se-Met 组）喂养。实验持续 50 天。与对照组相比，高 F 组的平均日增重（ADG）和饲料效率（FE）显著降低（P < 0.05）。与对照组相比，高 F 组血清、肝脏和肾脏中 ROS、丙二醛、8-羟基脱氧鸟苷、蛋白质羰基和半胱氨酸天冬氨酸特异性蛋白酶 3 的含量较高（P < 0.05）。与对照组相比，高 F 组血清和组织中谷胱甘肽过氧化物酶（GSH-Px）和细胞质硫氧还蛋白还原酶（TrxR1）的活性以及硒蛋白 P（SelP）、总蛋白（TP）和 B 细胞淋巴瘤-2 的含量均降低（P < 0.05）。此外，高 F 组的肝脏和肾脏的病理损伤比对照组更严重。然而，补充 SS 和 Se-Met 可以提高 ADG 和 FE，增加 SelP 和 TP 浓度，提高 GSH-Px 和 TrxR1 的活性，最小化肝脏和肾脏的氧化应激和细胞凋亡参数以及超微结构的变化，而 Se-Met 的效果优于 SS。结果表明，过量的 F 可通过诱导氧化应激导致肉鸡生长抑制，进而导致生物大分子和软组织氧化损伤和细胞凋亡，而日粮中补充 SS 和 Se-Met 可通过抑制氧化应激和细胞凋亡调节机制来拮抗高 F 诱导的生长迟缓，且 Se-Met 的影响更大。
