Inhaled silica nanoparticles cause chronic kidney disease in rats.

Inhaled silica nanoparticles cause chronic kidney disease in rats.
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吸入二氧化硅纳米粒子会导致大鼠慢性肾病。

DOI:
10.1152/ajprenal.00021.2022
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发表时间:
2022
期刊:
American journal of physiology. Renal physiology
影响因子:
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通讯作者:
Venugopal,Vidh
Venugopal,Vidh
中科院分区:
--
文献类型:
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作者:
Sasai,Fumihiko;Rogers,KeeganL;Orlicky,DavidJ;Stem,Arthur;Schaeffer,Joshua;Garcia,Gabriela;Fox,Jacob;Ray,MatthewS;Butler-Dawson,Jaime;Gonzalez-Quiroz,Marvin;Leiva,Ricardo;Taduri,Gangadhar;Anutrakululchai,Sirirat;Venugopal,Vidh

文献摘要

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在甘蔗燃烧过程中释放的二氧化硅纳米颗粒(SiNPs)被认为在病因不明的慢性肾脏疾病中发挥作用。我们测试了甘蔗中存在的大小的原始SiNP在通过大鼠的肺施用时可能引起慢性肾损伤的假设。我们每周两次(4 mg/剂)通过口咽抽吸向大鼠施用200-或300-nm无定形SiNP或媒介物13周,随后在另外13周后安乐死(总共26周)。评价组织中SiNP的存在和组织学损伤的证据。两种尺寸的SiNP均引起肾损伤,早期肾小管损伤和炎症(第13周),尽管停止SiNP给药,但在第26周继续炎症和慢性纤维化。两种尺寸的SiNPs都引起了肺和肾的局部炎症,并在第13周的血清和尿液中检测到,200 nm的颗粒也定位于肾脏,没有证据表明300 nm的颗粒保留。在第26周,200 nm二氧化硅从肾脏中有一定程度的清除,SiNP的尿水平降低,但在200 nm和300 nm暴露的大鼠中仍然显著。总之,吸入的SiNP引起慢性肾损伤,尽管停止SiNP施用,该慢性肾损伤仍在发展。这些发现支持了这一假设,即人类暴露于燃烧甘蔗田中发现的无定形二氧化硅纳米颗粒可能在病因不明的慢性肾脏病中起着参与性作用。新&值得注意的是,在甘蔗燃烧过程中释放的二氧化硅纳米颗粒(SiNPs)的吸入被假定在病因不明的慢性肾脏病(CKDu)中起着作用。我们通过抽吸向大鼠施用200-和300-nm的无定形SiNP,并观察到肾损伤,即使在停止SiNP暴露后仍持续存在肾小管损伤和炎症。这些发现支持了这样的假设,即人类暴露于甘蔗灰中发现的SiNPs可能具有参与性作用CKDu。
Silica nanoparticles (SiNPs) released during the burning of sugarcane have been postulated to have a role in chronic kidney disease of unknown etiology. We tested the hypothesis that pristine SiNPs of the size present in sugarcane might cause chronic kidney injury when administered through the lung in rats. We administered 200- or 300-nm amorphous SiNPs twice weekly (4 mg/dose), or vehicle by oropharyngeal aspiration for 13 wk to rats followed by euthanasia after an additional 13 wk (26 wk total). Tissues were evaluated for the presence of SiNPs and evidence of histological injury. Both sizes of SiNPs caused kidney damage, with early tubular injury and inflammation (atweek 13) that continued to inflammation and chronic fibrosis atweek 26despite discontinuation of the SiNP administration. Both sizes of SiNPs caused local inflammation in the lung and kidney and were detected in the serum and urine atweek 13, and the 200-nm particles were also localized to the kidney with no evidence of retention of the 300-nm particles. Atweek 26, there was some clearance of the 200-nm silica from the kidneys, and urinary levels of SiNPs were reduced but still significant in both 200- and 300 nm-exposed rats. In conclusion, inhaled SiNPs cause chronic kidney injury that progresses despite stopping the SiNP administration. These findings support the hypothesis that human exposure to amorphous silica nanoparticles found in burned sugarcane fields could have a participatory role in chronic kidney disease of unknown etiology.NEW & NOTEWORTHYInhalation of silica nanoparticles (SiNPs) released during the burning of sugarcane has been postulated to have a role in chronic kidney disease of unknown etiology (CKDu). We administered 200- and 300-nm amorphous SiNPs to rats by aspiration and observed kidney damage with tubular injury and inflammation that persisted even after stopping the SiNP exposure. These findings support the hypothesis that human exposure to SiNPs found in sugarcane ash could have a participatory role CKDu.