Bi Shao-Shuai, Talukder Milton, Jin Hai-Tao, Lv Mei-Wei, Ge Jing, Zhang Cong, Li Jin-Long
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
College of Biotechnology and Pharmaceutical Engineering of West Anhui University, Lu'an 237012, China.
Anim Nutr. 2022 Aug 19;11:402-412. doi: 10.1016/j.aninu.2022.06.021. eCollection 2022 Dec.
This study aims to investigate the role of metal regulatory transcription factor 1 (MTF1)-mediated metal response in cadmium (Cd)-induced cerebellar injury, and to evaluate the antagonistic effects of nano-selenium (Nano-Se) against Cd toxicity. A total of 80 chicks (1 d old, male, Hy-Line Variety White) were randomly allocated to 4 treatment groups for 3 months: the control group (fed with a basic diet, = 20), the Nano-Se group (basic diet with 1 mg/kg nano-Se 1 mg/kg Nano-Se in basic diet, = 20), the Nano-Se + Cd group (basic diet with 1 mg/kg Nano-Se and 140 mg/kg CdCl, = 20) and the Cd group (basic diet with 140 mg/kg CdCl , = 20). The results of the experiment showed that the Purkinje cells were significantly decreased with their degradation and indistinct nucleoli after Cd exposure. Moreover, exposure to Cd caused a significant accumulation of Cd and cupper. However, the contents of Se, iron, and zinc were decreased, thereby disturbing the metal homeostasis in the cerebellum. The Cd exposure also resulted in high levels of malondialdehyde (MDA) and down regulation of selenoprotein transcriptome. Furthermore, the expressions of , metallothionein 1 (), , zinc transporter 3 (), , , zrt, irt-like protein 8 (), , transferrin (), ferroportin 1 (), ATPase copper transporting beta (), and copper uptake protein 1 () were inhibited by Cd exposure. However, all these changes were significantly alleviated by the supplementation of Nano-Se. This study proved that Cd could disorder metal homeostasis and induce oxidative stress, whereas Nano-Se could relieve all these negative effects caused by Cd via activating the MTF1-mediated metal response in the cerebellum of chicken.
本研究旨在探讨金属调节转录因子1（MTF1）介导的金属反应在镉（Cd）诱导的小脑损伤中的作用，并评估纳米硒（Nano-Se）对Cd毒性的拮抗作用。总共80只雏鸡（1日龄，雄性，海兰白鸡）被随机分为4个处理组，为期3个月：对照组（饲喂基础日粮，n = 20）、纳米硒组（基础日粮中添加1 mg/kg纳米硒，n = 20）、纳米硒+镉组（基础日粮中添加1 mg/kg纳米硒和140 mg/kg氯化镉，n = 20）和镉组（基础日粮中添加140 mg/kg氯化镉，n = 20）。实验结果表明，Cd暴露后浦肯野细胞显著减少，细胞降解，核仁模糊。此外，Cd暴露导致Cd和铜显著蓄积。然而，硒、铁和锌的含量降低，从而扰乱了小脑中的金属稳态。Cd暴露还导致丙二醛（MDA）水平升高和硒蛋白转录组下调。此外，Cd暴露抑制了金属硫蛋白1（MT1）、锌转运体3（ZnT3）、Zrt、Irt样蛋白8（ZIP8）、转铁蛋白（Tf）、铁转运蛋白1（Fpn1）、ATP酶铜转运β（ATP7B）和铜摄取蛋白1（CTR1）的表达。然而，补充纳米硒后，所有这些变化均得到显著缓解。本研究证明，Cd可扰乱金属稳态并诱导氧化应激，而纳米硒可通过激活鸡小脑中MTF1介导的金属反应来缓解Cd引起的所有这些负面影响。
