Laboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Institute of Exact and Biological Sciences (ICEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael´s Hospital, Toronto, ON, Canada.
Exp Lung Res. 2020 Apr-May;46(3-4):64-74. doi: 10.1080/01902148.2020.1728595. Epub 2020 Feb 18.
Aluminum is the third most abundant metal in the earth's crust and is widely used in industry. Chronic contact with aluminum results in a reduction in the activity of electron transport chain complexes, leading to excessive production of reactive oxygen species (ROS) and oxidative stress. This study aimed to evaluate the effects of short-term exposure of aluminum hydroxide on oxidative stress and pulmonary inflammatory response. Male BALB/c mice were divided into three groups: control group (CG); phosphate buffered saline group (PBSG) and aluminum hydroxide group (AHG). CG was exposed to ambient air, while PBSG and AHG were exposed to PBS or aluminum hydroxide solutions via nebulization, three times per day for five consecutive days. Twenty-four hours after the last exposure, all animals were euthanized for subsequent analysis. Exposure to aluminum hydroxide in the blood resulted in lower platelet levels, higher neutrophils, and lower monocytes compared to CG and PBSG. Aluminum hydroxide promoted the recruitment of inflammatory cells to the lung. Macrophage, neutrophil and lymphocyte counts were higher in AHG compared to CG and PBSG. Protein oxidation and superoxide dismutase activity were higher, while catalase activity and reduced and oxidizes glutathione ratio in AHG were lower compared to CG and PBSG. Furthermore, there was an increase in the inflammatory markers CCL2 and IFN-γ in AHG compared to CG and PBSG. In conclusion, short-term nebulization with aluminum hydroxide induces the influx of inflammatory cells and oxidative stress in adult BALB/c mice.
铝是地壳中含量第三丰富的金属，广泛应用于工业。慢性接触铝会导致电子传递链复合物活性降低，从而导致活性氧（ROS）的过度产生和氧化应激。本研究旨在评估短期暴露于氢氧化铝对氧化应激和肺部炎症反应的影响。雄性 BALB/c 小鼠分为三组：对照组（CG）；磷酸盐缓冲盐水组（PBSG）和氢氧化铝组（AHG）。CG 暴露于环境空气中，而 PBSG 和 AHG 通过雾化暴露于 PBS 或氢氧化铝溶液中，每天三次，连续五天。最后一次暴露后 24 小时，所有动物均被安乐死以进行后续分析。与 CG 和 PBSG 相比，血液中暴露于氢氧化铝会导致血小板水平降低、中性粒细胞升高和单核细胞降低。氢氧化铝促进了炎症细胞向肺部的募集。与 CG 和 PBSG 相比，AHG 中的巨噬细胞、中性粒细胞和淋巴细胞计数更高。与 CG 和 PBSG 相比，AHG 中的蛋白氧化和超氧化物歧化酶活性更高，而过氧化氢酶活性和还原型/氧化型谷胱甘肽比值较低。此外，与 CG 和 PBSG 相比，AHG 中的炎症标志物 CCL2 和 IFN-γ 增加。总之，短期雾化吸入氢氧化铝会导致成年 BALB/c 小鼠炎症细胞浸润和氧化应激。
