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Suppressive effects of subchronic aluminum overload on the splenic immune function may be related to oxidative stress in mice

机译:亚慢性铝超负荷对脾脏免疫功能的抑制作用可能与小鼠的氧化应激有关

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摘要

Aluminum (Al) is widely used in daily life and was recently recognized as a possible source of human intoxication because of its ability to accumulate in organs. The objective of the present study was to investigate the effects of subchronic Al overload on splenic immune function in mice. Furthermore, we have preliminarily explored its mechanism. The Al overload model was established via intragastric administration of Al once a day for 60 days. The body weight, spleen weight, and splenic coefficient were determined. The concentration of Al in the spleen was detected by inductively coupled plasma-mass spectrometry. The cytokine mRNA expression of spleen tissues was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Biochemical methods were used to detect superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) contents in spleen tissue. Body weight, spleen weight, and cytokine mRNA expression of spleen tissues were significantly reduced by Al overload. SOD and GSH-Px activities were also decreased, while the MDA content was increased in subchronic Al overload mice. The results indicate that subchronic exposure to aluminum trichloride (AlCl3) would result in Al accumulation, which suppressed spleen immune function through a mechanism related to oxidative stress.
机译:铝(Al)在日常生活中被广泛使用,由于其在器官中蓄积的能力,最近被公认为可能引起人体中毒。本研究的目的是研究亚慢性铝超负荷对小鼠脾脏免疫功能的影响。此外,我们已经初步探索了其机制。通过每天一次胃内给药60天来建立Al超负荷模型。确定体重,脾脏重量和脾脏系数。脾脏中的铝浓度通过电感耦合等离子体质谱法检测。逆转录定量聚合酶链反应(RT-qPCR)检测脾脏细胞因子的mRNA表达。生化方法用于检测脾脏组织中的超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)含量。铝超载显着降低了体重,脾脏重量和脾组织细胞因子mRNA的表达。亚慢性铝超负荷小鼠中SOD和GSH-Px活性也降低,而MDA含量增加。结果表明,亚慢性暴露于三氯化铝(AlCl3)将导致Al积累,这通过与氧化应激相关的机制抑制了脾脏的免疫功能。

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