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Nephrotoxicity and possible mechanisms of decabrominated diphenyl ethers (BDE-209) exposure to kidney in broilers
Ecotoxicology and Environmental Safety ( IF 6.2 ) Pub Date : 2020-11-16 , DOI: 10.1016/j.ecoenv.2020.111638
Shiyao Sun , Yuhong Jin , Junhua Yang , Zhihui Zhao , Qinxiong Rao

The flame retardant decabrominated diphenyl ether (BDE-209) is a widely used chemical in a variety of products and exists extensively in the environment. BDE-209 has been reported to induce kidney injury and dysfunction. However, the causes and mechanisms of its nephrotoxicity are still under investigation. In this study, 150 male broilers were exposed to BDE-209 concentrations of 0, 0.004, 0.04, 0.4, 4.0 g/kg for 42 days. The relative kidney weight, histopathology, markers of renal injury, oxidative stress, inflammation, apoptosis and the expression of MAPK signaling pathways-related proteins were assessed. The results showed that the concentrations of blood urea nitrogen (BUN), creatinine (CRE) and the neutrophil gelatinase-associated lipocalin (NGAL), significantly increased after exposure to BDE-209 with the doses more than 0.04 g/kg. Similarly, severe damage of renal morphology was observed, including atrophy and necrosis of glomeruli, and swelling and granular degeneration of the renal tubular epithelium. In the renal homogenates, the oxidative stress was evidenced by the elevated concentrations of MDA and NO, and decreased levels of GSH-Px, GSH and SOD. Due to the inflammatory response, the level of NF-κB and the pro-inflammatory cytokines TNF-α, IL-1β, IL-18 were remarkably upregulated, while the content of the anti-inflammatory cytokine IL-10 decreased. Additionally, the apoptotic analysis showed notable upregulations of Bax/Bcl-2 ratio, the relative expression of p-ERK1/2 and p-JNK1/2, and the expression of Bax, cytochrome c and caspase 3. The present study indicates that BDE-209 exposure can cause nephrotoxicity in broilers through oxidative stress and inflammation, which activate the phosphorylation of key proteins of the MAPK signaling pathways, and subsequently induce mitochondria-mediated kidney apoptosis.



中文翻译:

十溴二苯醚(BDE-209)暴露于肉鸡肾脏中的肾毒性及其可能机制

阻燃剂十溴化二苯醚(BDE-209)是多种产品中广泛使用的化学品,并且广泛存在于环境中。据报道,BDE-209可引起肾脏损伤和功能障碍。然而,其肾毒性的原因和机制仍在研究中。在这项研究中,将150只雄性肉鸡暴露于BDE-209浓度为0、0.004、0.04、0.4、4.0 g / kg的环境中42天。评估了相对肾脏重量,组织病理学,肾脏损伤标志物,氧化应激,炎症,细胞凋亡以及MAPK信号通路相关蛋白的表达。结果表明,当剂量超过0.04 g / kg的BDE-209暴露后,血尿素氮(BUN),肌酐(CRE)和中性粒细胞明胶酶相关脂质钙蛋白(NGAL)的浓度显着增加。同样,观察到严重的肾脏形态损害,包括肾小球萎缩和坏死,以及肾小管上皮肿胀和颗粒变性。在肾脏匀浆中,MDA和NO浓度升高,GSH-Px,GSH和SOD含量降低证明了氧化应激。由于炎症反应,NF-κB和促炎细胞因子TNF-α,IL-1β,IL-18的水平显着上调,而抗炎细胞因子IL-10的含量降低。此外,细胞凋亡分析表明Bax / Bcl-2比明显上调,p-ERK1 / 2和p-JNK1 / 2的相对表达,以及Bax,细胞色素c和caspase 3的表达。本研究表明BDE -209暴露可通过氧化应激和炎症在肉鸡中引起肾毒性,

更新日期:2020-11-16
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