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Prolonged exposure to the herbicide atrazine suppresses immune cell functions by inducing spleen cell apoptosis in rats
Ecotoxicology and Environmental Safety ( IF 6.8 ) Pub Date : 2021-06-02 , DOI: 10.1016/j.ecoenv.2021.112386
Jingyan Ge 1 , Jian Liu 2 , Taiwei Wang 3 , Di Huang 4 , Junwei Li 4 , Shuang Zhang 3 , Mengqi Wang 5 , Wei Liu 6 , Lijing Zhao 3
Affiliation  

Atrazine (ATR) is a herbicide used widely worldwide. Because of its prolonged persistence in the environment and accumulation in the body, ATR exposure is a potential threat to human health. Our previous study showed that subacute exposure to ATR suppresses cellular immune function in mice. In this study, the effects of long-term exposure to ATR on rat immunological system function were measured. Four-week-old female Sprague-Dawley (SD) rats were treated with 0.4 μmol/L, 2 μmol/L and 10 μmol/L ATR for 24 weeks. The results showed that the spleen index increased, white blood cells decreased, and monocytes and eosinophils increased. No obvious changes were detected in the numbers of neutrophils and lymphocytes. Th1, Th2, and Th17 cells decreased significantly, while Treg cells increased after long-term ATR exposure. Moreover, serum levels of cytokines, including TNF-α, INF-γ, IL-6, and IL-12, decreased, while IL-1, IL-4, and IL-5 increased. Degenerative changes and cell apoptosis were found in the spleen; Caspase-3 and Caspase-9 were upregulated, and Bcl-2 was downregulated. These results suggested that long-term ATR exposure may inhibit immune system function.



中文翻译:

长期暴露于除草剂阿特拉津通过诱导大鼠脾细胞凋亡抑制免疫细胞功能

阿特拉津 (ATR) 是一种在世界范围内广泛使用的除草剂。由于其在环境中的长期持久性和体内积累,ATR 暴露是对人类健康的潜在威胁。我们之前的研究表明,亚急性暴露于 ATR 会抑制小鼠的细胞免疫功能。在这项研究中,测量了长期暴露于 ATR 对大鼠免疫系统功能的影响。4 周龄雌性 Sprague-Dawley (SD) 大鼠分别用 0.4 μmol/L、2 μmol/L 和 10 μmol/L ATR 治疗 24 周。结果显示脾脏指数升高,白细胞减少,单核细胞和嗜酸性粒细胞增多。中性粒细胞和淋巴细胞数量未见明显变化。Th1、Th2 和 Th17 细胞显着减少,而 Treg 细胞在长期 ATR 暴露后增加。而且,TNF-α、INF-γ、IL-6 和 IL-12 等细胞因子的血清水平降低,而 IL-1、IL-4 和 IL-5 升高。脾脏出现退行性改变和细胞凋亡;Caspase-3 和 Caspase-9 上调,Bcl-2 下调。这些结果表明长期 ATR 暴露可能会抑制免疫系统功能。

更新日期:2021-06-02
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