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 Ali

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

BACKGROUND/AIMS: Cerium oxide nanoparticles (CeO₂ 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 CeO₂ NPs. We have recently demonstrated that pulmonary exposure to CeO₂ 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 CeO₂ 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 CeO₂ 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 CeO₂ NPs. Histopathological changes in lungs of CeO₂ NPs-treated rats included marked interstitial cell infiltration and congestion. These were aggravated by the combination of CP + CeO₂ 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 CeO₂ 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 : international journal of experimental cellular physiology, biochemistry, and pharmacology
Volume52
Issue number3
DOIs
Publication statusPublished - Jan 1 2019

Fingerprint

Acute Kidney Injury
Nanoparticles
Kidney
Lung
Comet Assay
DNA Damage
Interleukin-6
Creatinine
Tumor Necrosis Factor-alpha
Cerium
Vehicle Emissions
Inhalation Exposure
ceric oxide
Air Pollution
Intraperitoneal Injections
Catalase
Cisplatin
Drinking
Glutathione
Urea

Keywords

  • Acute renal failure
  • Cerium oxide nanoparticles
  • Lung inflammation

ASJC Scopus subject areas

  • Physiology

Cite this

Impact of Pulmonary Exposure to Cerium Oxide Nanoparticles on Experimental Acute Kidney Injury. / Nemmar, Abderrahim; Al-Salam, Suhail; Al Ansari, Zinab; Alkharas, Zainab A.; Al Ahbabi, Rauda M.; Beegam, Sumaya; Yuvaraju, Priya; Yasin, Javed; Ali, Badreldin.

In: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, Vol. 52, No. 3, 01.01.2019, p. 439-454.

Research output: Contribution to journalArticle

Nemmar, Abderrahim ; Al-Salam, Suhail ; Al Ansari, Zinab ; Alkharas, Zainab A. ; Al Ahbabi, Rauda M. ; Beegam, Sumaya ; Yuvaraju, Priya ; Yasin, Javed ; Ali, Badreldin. / Impact of Pulmonary Exposure to Cerium Oxide Nanoparticles on Experimental Acute Kidney Injury. In: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2019 ; Vol. 52, No. 3. pp. 439-454.
@article{bc0e241f45dc4810ae056953a2246069,
title = "Impact of Pulmonary Exposure to Cerium Oxide Nanoparticles on Experimental Acute Kidney Injury",
abstract = "BACKGROUND/AIMS: Cerium oxide nanoparticles (CeO₂ 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 CeO₂ NPs. We have recently demonstrated that pulmonary exposure to CeO₂ 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 CeO₂ 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 CeO₂ 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 CeO₂ NPs. Histopathological changes in lungs of CeO₂ NPs-treated rats included marked interstitial cell infiltration and congestion. These were aggravated by the combination of CP + CeO₂ 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 CeO₂ NPs in the lung exacerbated the renal and lung effects of CP-induced AKI.",
keywords = "Acute renal failure, Cerium oxide nanoparticles, Lung inflammation",
author = "Abderrahim Nemmar and Suhail Al-Salam and {Al Ansari}, Zinab and Alkharas, {Zainab A.} and {Al Ahbabi}, {Rauda M.} and Sumaya Beegam and Priya Yuvaraju and Javed Yasin and Badreldin Ali",
year = "2019",
month = "1",
day = "1",
doi = "10.33594/000000032",
language = "English",
volume = "52",
pages = "439--454",
journal = "Cellular Physiology and Biochemistry",
issn = "1015-8987",
publisher = "S. Karger AG",
number = "3",

}

TY - JOUR

T1 - Impact of Pulmonary Exposure to Cerium Oxide Nanoparticles on Experimental Acute Kidney Injury

AU - Nemmar, Abderrahim

AU - Al-Salam, Suhail

AU - Al Ansari, Zinab

AU - Alkharas, Zainab A.

AU - Al Ahbabi, Rauda M.

AU - Beegam, Sumaya

AU - Yuvaraju, Priya

AU - Yasin, Javed

AU - Ali, Badreldin

PY - 2019/1/1

Y1 - 2019/1/1

N2 - BACKGROUND/AIMS: Cerium oxide nanoparticles (CeO₂ 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 CeO₂ NPs. We have recently demonstrated that pulmonary exposure to CeO₂ 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 CeO₂ 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 CeO₂ 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 CeO₂ NPs. Histopathological changes in lungs of CeO₂ NPs-treated rats included marked interstitial cell infiltration and congestion. These were aggravated by the combination of CP + CeO₂ 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 CeO₂ NPs in the lung exacerbated the renal and lung effects of CP-induced AKI.

AB - BACKGROUND/AIMS: Cerium oxide nanoparticles (CeO₂ 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 CeO₂ NPs. We have recently demonstrated that pulmonary exposure to CeO₂ 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 CeO₂ 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 CeO₂ 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 CeO₂ NPs. Histopathological changes in lungs of CeO₂ NPs-treated rats included marked interstitial cell infiltration and congestion. These were aggravated by the combination of CP + CeO₂ 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 CeO₂ NPs in the lung exacerbated the renal and lung effects of CP-induced AKI.

KW - Acute renal failure

KW - Cerium oxide nanoparticles

KW - Lung inflammation

UR - http://www.scopus.com/inward/record.url?scp=85062967511&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85062967511&partnerID=8YFLogxK

U2 - 10.33594/000000032

DO - 10.33594/000000032

M3 - Article

VL - 52

SP - 439

EP - 454

JO - Cellular Physiology and Biochemistry

JF - Cellular Physiology and Biochemistry

SN - 1015-8987

IS - 3

ER -