Impact of pulmonary exposure to cerium oxide nanoparticles on experimental acute kidney injury

Abderrahim Nemmar*, Suhail Al-Salam, Zinab Al Ansari, Zainab A. Alkharas, Rauda M. Al Ahbabi, Sumaya Beegam, Priya Yuvaraju, Javed Yasin, Badreldin H. Ali

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Background/Aims: Cerium oxide nanoparticles (CeO 2 NPs) are released from diesel engines that use cerium compounds as a catalytic agent to decrease the diesel exhaust particles, leading to human exposure by inhalation to CeO 2 NPs. We have recently demonstrated that pulmonary exposure to CeO 2 NPs induces lung inflammation, thrombosis, and oxidative stress in various organs including kidneys. It is well known that particulate air pollution effects are greater in patients with renal diseases. The aim of this study is to investigate the effects of pulmonary exposure to CeO 2 NPs in a rat model of acute kidney injury (AKI). Methods: AKI was induced in rats by a single intraperitoneal injection of cisplatin (CP, 6 mg/kg). Six days later, the rats were intratracheally (i.t.) instilled with either CeO 2 NPs (1 mg/kg) or saline (control), and various renal and pulmonary endpoints were assessed 24 h afterward using histological, colorimetric assay, enzyme-linked immunosorbent assay and Comet assay techniques. Results: CP alone decreased body weight, and increased water intake, urine volume and relative kidney weight. CP also increased the plasma concentrations urea and creatinine, and decreased creatinine clearance. In the kidneys, CP significantly increased renal injury molecule-1, interleukin-6 (IL-6), tumor necrosis factor α (TNFα) and glutathione concentrations, and caused renal tubular necrosis, and DNA injury assessed by Comet assay. All these actions were significantly aggravated in rats given both CP and CeO 2 NPs. Histopathological changes in lungs of CeO 2 NPs-treated rats included marked interstitial cell infiltration and congestion. These were aggravated by the combination of CP + CeO 2 NPs. Moreover, this combination exacerbated the increase in the concentrations of TNFα and IL-6, and the decrease in the activity of pulmonary catalase and total nitric oxide concentration, and lung DNA damage. Conclusion: We conclude that the presence of CeO 2 NPs in the lung exacerbated the renal and lung effects of CP-induced AKI.

Original languageEnglish
Pages (from-to)439-454
Number of pages16
JournalCellular Physiology and Biochemistry
Issue number3
Publication statusPublished - 2019
Externally publishedYes


  • Acute renal failure
  • Cerium oxide nanoparticles
  • Lung inflammation

ASJC Scopus subject areas

  • Physiology


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