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Nephrotoxicity and genotoxicity of silver nanoparticles in juvenile rats and possible mechanisms of action

Ye Liu

Ye Liu

  • Tianjin Medical University General Hospital, Ministry of Education and Tianjin City, Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Repair and Regeneration in Central Nervous SystemTianjin, China
  • Nankai University College of Medicine, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of EducationTianjin, China
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Liu, Ye
, 
Li Sun

Li Sun

Tianjin Medical University General Hospital, Ministry of Education and Tianjin City, Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Repair and Regeneration in Central Nervous SystemTianjin, China
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Sun, Li
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Guili Yang

Guili Yang

Tianjin Medical University General Hospital, Ministry of Education and Tianjin City, Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Repair and Regeneration in Central Nervous SystemTianjin, China
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Yang, Guili
 y 
Zhuo Yang

Zhuo Yang

Nankai University College of Medicine, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of EducationTianjin, China
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Yang, Zhuo
  
29 jun 2020
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Categoría del artículo: Original article
Publicado en línea: 29 jun 2020
Páginas: 121 - 129
Recibido: 01 nov 2019
Aceptado: 01 may 2020
DOI: https://doi.org/10.2478/aiht-2020-71-3364
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© 2020 Ye Liu et al., published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.

Figure 1

Transition electron microscopy of silver nanoparticles in suspension
Transition electron microscopy of silver nanoparticles in suspension

Figure 2

Experimental design of AgNP administration, sampling, and tissue collection; AgNP – silver nanoparticles; H&E – haematoxylin and eosin; ELISA – enzyme-linked immunosorbent assay
Experimental design of AgNP administration, sampling, and tissue collection; AgNP – silver nanoparticles; H&E – haematoxylin and eosin; ELISA – enzyme-linked immunosorbent assay

Figure 3

Mean (±SEM) body weight (A), urinary microalbumin (B), serum creatinine (C), tail intensity (comet assay) (D), the frequency of micronucleated PCEs in bone marrow (E), and the PCE to NCE ratio (F) in control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; AgNP – silver nanoparticles; NCE – normochromatic erythrocytes; PCE – polychromatic erythrocytes; SEM – standard error of the mean
Mean (±SEM) body weight (A), urinary microalbumin (B), serum creatinine (C), tail intensity (comet assay) (D), the frequency of micronucleated PCEs in bone marrow (E), and the PCE to NCE ratio (F) in control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; AgNP – silver nanoparticles; NCE – normochromatic erythrocytes; PCE – polychromatic erythrocytes; SEM – standard error of the mean

Figure 4

Mean (±SEM) ROS GSH, SOD IL-6, IL-1β, and TNF-α in kidney cells and tissue of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; GSH – glutathione; IL – interleukin; ROS – reactive oxygen species; SEM – standard error of the mean; SOD – superoxide dismutase; TNF – tumour necrosis factor
Mean (±SEM) ROS GSH, SOD IL-6, IL-1β, and TNF-α in kidney cells and tissue of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; GSH – glutathione; IL – interleukin; ROS – reactive oxygen species; SEM – standard error of the mean; SOD – superoxide dismutase; TNF – tumour necrosis factor

Figure 5

Mean (±SEM) NOX4 and TRPC6 in rat renal cortex (normalised to β-actin expression) of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; NOX – NADPH oxidase 4; SEM – standard error of the mean; TRPC6 – transient receptor potential cation channel subfamily C member 6
Mean (±SEM) NOX4 and TRPC6 in rat renal cortex (normalised to β-actin expression) of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; NOX – NADPH oxidase 4; SEM – standard error of the mean; TRPC6 – transient receptor potential cation channel subfamily C member 6

Figure 6

TRPC6 immunofluorescence staining of the renal cortex (50 μm scale bar) (A) and mean (±SEM) fluorescent intensity (B) in the glomeruli of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; SEM – standard error of the mean; TRPC6 – transient receptor potential cation channel subfamily C member 6
TRPC6 immunofluorescence staining of the renal cortex (50 μm scale bar) (A) and mean (±SEM) fluorescent intensity (B) in the glomeruli of control and juvenile rats treated with AgNPs for one, two, or three weeks (n=8 per group); *P<0.05; SEM – standard error of the mean; TRPC6 – transient receptor potential cation channel subfamily C member 6

Figure 7

Histological findings in the kidney of juvenile rats: (A) control group, (B) 1-wk-AgNP group (C) 2-wk- AgNP group; (D) 3-wk-AgNP group (100 μm scale bar; arrows indicate typically affected areas)
Histological findings in the kidney of juvenile rats: (A) control group, (B) 1-wk-AgNP group (C) 2-wk- AgNP group; (D) 3-wk-AgNP group (100 μm scale bar; arrows indicate typically affected areas)

Figure 8

Diagram of the main likely mechanisms of AgNP nephrotoxicity based on oxidative stress; AgNP – silver nanoparticles; H&E – haematoxylin and eosin; ELISA – enzyme-linked immunosorbent assay; GSH – glutathione; ROS – reactive oxygen species; SOD – superoxide dismutase; TRPC6– transient receptor potential cation channel subfamily C member 6
Diagram of the main likely mechanisms of AgNP nephrotoxicity based on oxidative stress; AgNP – silver nanoparticles; H&E – haematoxylin and eosin; ELISA – enzyme-linked immunosorbent assay; GSH – glutathione; ROS – reactive oxygen species; SOD – superoxide dismutase; TRPC6– transient receptor potential cation channel subfamily C member 6
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