文献类型： 外文期刊

作者： Bi, Shao-Shuai ¹ ; Talukder, Milton ¹ ; Jin, Hai-Tao ⁴ ; Lv, Mei-Wei ¹ ; Ge, Jing ¹ ; Zhang, Cong ¹ ; Li, Jin-Long ¹ ;

作者机构： 1.Northeast Agr Univ, Coll Vet Med, Harbin 150030, Peoples R China

2.West Anhui Univ, Coll Biol & Pharmaceut Engn, Luan 237012, Peoples R China

3.Patuakhali Sci & Technol Univ, Fac Anim Sci & Vet Med, Dept Physiol & Pharmacol, Barishal 8210, Bangladesh

4.Heilongjiang Acad Agr Sci, Qual & Safety Inst Agr Prod, Harbin 150010, Peoples R China

5.Henan Agr Univ, Coll Vet Med, Zhengzhou 450046, Peoples R China

6.Northeast Agr Univ, Dept Heilongjiang Common Anim Dis Prevent & Treat, Key Lab Prov Educ, Harbin 150030, Peoples R China

7.Northeast Agr Univ, Heilongjiang Key Lab, Lab Anim & Comparat Med, Harbin 150030, Peoples R China

关键词： Cadmium; Selenoprotein transcriptome; MTF1-mediated metal response; Chicken; Cerebellar injury

期刊名称：NEUROTOXICITY RESEARCH （ 影响因子：3.978； 五年影响因子：3.821 ）

ISSN： 1029-8428

年卷期：

页码：

收录情况： SCI

摘要： Cadmium (Cd) is a toxic environmental contaminant, which bio-accumulate in animals through the food chain. Cerebellum is one of the primary target organs for Cd exposure. In this study, we established a chronic Cd exposure model; 60 chickens were treated with Cd (0 mg/kg, 35 mg/kg, 70 mg/kg) for 90 days. Clinical manifestations indicated that the chicken was depressed and has unstable gait under Cd exposure. Histopathological results indicated that Cd induced neuronal shrunken and indistinct nucleoli, and the number of Purkinje cells decreased significantly. Cerebellar metal contents were analyzed by ICP-MS. We found that Cd caused Cd and Cu accumulation and decreased the content of Se, Fe, and Zn, suggesting that Cd disturbed metal homeostasis. Besides, Cd treatment group also showed high levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) content and inhibited selenoprotein transcriptome, suggesting that Cd exposure resulted in oxidative stress. Notably, low-dose Cd exposure activated MTF1 mRNA and protein expression and its target metal-responsive genes, including MT1, MT2, DMT1, ZIP8, ZIP10, TF, and ATP7B which indicate cellular adaptive response against Cd-induced damage. On the other hand, 70 mg/kg Cd downregulated MTF1-mediated metal response, which was involved in Cd-induced cerebellar injury in chicken. In conclusion, our data demonstrated that molecular mechanisms are associated with Cd-induced cerebellar injury due to disturbing MTF1-mediated metal response.