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Neuro- and nephrotoxicity of subchronic cadmium chloride exposure and the potential chemoprotective effects of selenium nanoparticles

机译:亚铬镉氯化镉暴露的神经和肾毒性及硒纳米粒子的潜在化学防护作用

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Cadmium (Cd) exposure leads to production of reactive oxygen species (ROS), which are associated with Cd-induced neurotoxicity and nephrotoxicity. Selenium nanoparticles (Se-NPs) have high bioavailability and antioxidant activities so it attracted wide spread attention. The present study examined the possible ameliorative effect of Se-NPs with diameters of 3-5 nm and 10-20 nm against cadmium chloride (CdCl2)-induced neuro- and nephrotoxicity in rats. Rats were treated with Se-NPs (0 or 0.5 mg/kg BW, s.c.) one hour prior to the CdCl2 (0 or 5 mg/kg BW, p.o.). Pretreatment with Se-NPs significantly decreased CdCl2-induced elevation of serum kidney and brain damage biomarkers; lipid peroxidation; the percent of DNA fragmentation and nearly normalized the activity of acetylcholinesterase (AchE) and significantly increased the activity and expression of antioxidant biomarkers in the RNA and protein levels. Se-NPs also attenuated CdCl2-induced upregulation of kidney and brain pro-apoptotic B-cell CLL/lymphoma 2 associated X (Bax) RNA and protein levels with preventing the increased body burden of Cd and the altered Fe and Cu homeostasis. Histopathological analysis confirmed the biochemical and molecular outcomes. Our data stated that Se-NPs appear to be effective in ameliorating the adverse neurological and nephrotoxic effects induced by CdCl2 partially through the scavenging of free radicals, metal ion chelation, averting apoptosis and altering the cell-protective pathways. The results indicated that Se-NPs could potentially included as an additive to Cd-based industries to control Cd-induced brain and renal injury.
机译:镉(CD)暴露导致活性氧物质(ROS)的产生,其与CD诱导的神经毒性和肾毒性相关。硒纳米粒子(SE-NPS)具有高生物利用度和抗氧化活性,因此它吸引了广泛的关注。本研究检测了SE-NPS与直径为3-5nm和10-20nm对氯化镉(CDCl2)的可能改善作用,诱导大鼠的神经和肾毒性。在CDCl 2(0或5mg / kg BW,P.O.)之前,用Se-NPS(0或0.5mg / kg Bw,S.C.)用Se-NPS(0或0.5mg / kg Bw。)处理大鼠。使用SE-NPS的预处理显着降低了CDCL2诱导的血清肾和脑损伤生物标志物的升高;脂质过氧化; DNA片段化的百分比和几乎标准化乙酰胆碱酯酶(ACHE)的活性并显着增加RNA和蛋白质水平抗氧化生物标志物的活性和表达。 SE-NPS还减毒了CDCL2诱导的肾癌和脑促凋亡B细胞CLL /淋巴瘤2相关X(BAX)RNA和蛋白质水平,并通过防止增加CD的体重和改变的Fe和Cu稳态。组织病理学分析证实了生物化学和分子结果。我们的数据表示,SE-NPS似乎有效地改善了CDCL2的不良神经系统和肾毒性效果部分通过自由基,金属离子螯合,避免细胞凋亡和改变细胞保护途径。结果表明,SE-NPS可能包含作为对基于CD的行业的添加剂,以控制CD诱导的脑和肾损伤。

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