文献类型： 外文期刊

作者： Talukder, Milton ¹ ; Bi, Shao-Shuai ¹ ; Jin, Hai-Tao ³ ; Ge, Jing ¹ ; Zhang, Cong ¹ ; Lv, Mei-Wei ¹ ; Li, Jin-Long ¹ ;

作者机构： 1.Northeast Agr Univ, Coll Vet Med, 600 Changjiang St, Harbin 150030, Heilongjiang, Peoples R China

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

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

4.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou 450046, Henan, Peoples R China

5.Northeast Agr Univ, Key Lab Prov Educ Dept Heilongjiang Common Anim D, Harbin 150030, Peoples R China

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

关键词： Cadmium; Metal transporters; Oxidative stress; MTF1; Cerebral damage

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：8.071； 五年影响因子：8.35 ）

ISSN： 0269-7491

年卷期： 2021 年 285 卷

页码：

收录情况： SCI

摘要： Metal-responsive transcription factor 1 (MTF1) participates in redox homeostasis and heavy metals detoxification via regulating the expression of metal responsive genes. However, the exact role of MTF1 in Cd-induced cerebral toxicity remains unclear. Herein, we explored the mechanism of Cd-elicited cerebral toxicity through modulating MTF1/MTs pathway in chicken cerebrum exposed to different concentrations of Cd (35 mg, 70 mg, and 140 mg/kg CdCl2) via diet. Notably, cerebral tissues showed varying degrees of microstructural changes under Cd exposure. Cd exposure significantly up-regulated the expression of metal transporters (DMT1, ZIP8, and ZIP10) with concomitant elevated Cd level, as determined by ICP-MS. Cd significantly altered other cerebral biometals concentrations (particularly, Zn, Fe, Se, Cr, Mo, and Pb) and redox balance, resulting in increased cerebral oxidative stress. More importantly, Cd exposure suppressed MTF1 mRNA and nuclear protein levels and its target metal-responsive genes, notably metallothioneins (MT1 and MT2), and Fe and Cu transporter genes (FPN1, ATOX1, and XIAP). Moreover, Cd disrupted the regulation of expression of selenoproteome (particularly, GPxs and SelW), and cerebral Se level. Overall, our data revealed that molecular mechanisms associated with Cdinduced cerebral damage might include over-expression of DMT1, ZIP8 and ZIP10, and suppression of MTF1 and its main target metal-responsive genes as well as several selenoproteins. (C) 2021 Elsevier Ltd. All rights reserved.