Di (2-ethyl hexyl) phthalate (DEHP)-induced spleen toxicity in quail (Coturnix japonica) via disturbing Nrf2-mediated defense response

文献类型: 外文期刊

第一作者: Yu, Lei

作者: Yu, Lei;Guo, Jian-Ying;Huang, Yue-Qiang;Wang, Hui;Talukder, Milton;Li, Jin-Long;Li, Hui-Xin;Talukder, Milton;Li, Jin-Long;Li, Jin-Long

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关键词: Di-(2-ethylhexyl) phthalate; Splenic toxicity; Oxidative stress; Nrf2 signaling pathway

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: 2019 年 251 卷

页码:

收录情况: SCI

摘要: Di(2-ethylhexyl) phthalate (DEHP), as a widely used plasticizer, is reported to have widespread environmental and global health hazards. Trace amounts of phthalates in the environment are sufficient to disrupt ecological balance and affect human health. However, DEHP-induced splenic toxicity remains in an unknown state. Therefore, to explore the mechanism of DEHP-induced splenic toxicity, male quail were employed with 0, 250, 500 and 750 mg/kg body weight DEHP by daily gastric perfusion for 45 days. Notably, splenic corpuscular border and cell gap enlargement were observed in the spleen tissue of DEHP-exposed quail under the histopathological analysis. Furthermore, DEHP induced dysregulation of oxidative stress markers by increasing malondialdehyde (MDA) content and decreasing superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities. Low concentration of DEHP (<= 250 mg/kg) exposure suppressed nuclear factor-E2-related factor 2 (Nrf2) signaling pathway, while high concentration of DEHP (>= 500 mg/kg) exposure activated Nrf2-mediated defense response. DEHP induced splenic oxidative stress via interfering Nrf2 signal pathway and altering the transcription of its downstream genes. In conclusion, this study suggested that DEHP induced splenic toxicity. (C) 2019 Elsevier Ltd. All rights reserved.

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