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. 2022 Nov 14;12(1):19444.
doi: 10.1038/s41598-022-24018-7.

Electron microscopy study on the transport of lead oxide nanoparticles into brain structures following their subchronic intranasal administration in rats

Marina P Sutunkova  1 , Ilzira A Minigalieva  1   2 , Ivan G Shelomencev  1 , Larisa I Privalova  1   2 , Yuliya V Ryabova  1   2 , Anastasiya V Tazhigulova  1 , Lev A Amromin  1 , Regina F Minigalieva  1   2 , Yuliya M Sutunkova  1   2 , Vladimir B Gurvich  1 , Eugenya V Makoveeva  2 , Liubov V Toropova  3   4
Affiliations

Electron microscopy study on the transport of lead oxide nanoparticles into brain structures following their subchronic intranasal administration in rats

Marina P Sutunkova et al. Sci Rep. .

Abstract

White outbred female rats were exposed intranasally to 50-µL of suspension of lead oxide nanoparticles (PbO NPs) at a concentration of 0.5 mg/mL thrice a week during six weeks. A control group of rats was administered deionized water in similar volumes and conditions. The developed intoxication was manifested by altered biochemical and cytochemical parameters, as well as behavioral reactions of animals. Using electron microscopy and energy-dispersive X-ray spectroscopy techniques, we revealed deposition of PbO NPs in the olfactory bulb, but not in basal ganglia, and an increase in the number of axons with damage to the myelin sheath in the tissues of olfactory bulb and basal ganglia, changes in the ultrastructure of mitochondria of neurons in the tissues of olfactory bulb and basal ganglia of the brain, and differences in the mitochondrial profile of neurons in different regions of the rat brain. Our results collectively suggest that the central nervous system may be a target of low-level toxicity of lead oxide nanoparticles.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
(a) STEM image of the olfactory bulb tissues with deposits of lead oxide nanoparticles; (b), (c) EDS spectra of the regions marked on image (a).
Figure 2
Figure 2
Representative STEM images of normal (a) and damaged (b) myelin morphotypes.
Figure 3
Figure 3
Damages to the ultrastructure of myelin sheaths of axons in the control and PbO NPs exposure groups of rats. Note: Values are given as a fraction of axons with damaged sheaths in the total number of axons detected. Significant differences in damage to the ultrastructure of the myelin sheaths of axons between brain regions in both groups were not found.
Figure 4
Figure 4
STEM images of damaged axons with loose myelin sheaths in the olfactory bulb of the rats exposed to PbO NPs.
Figure 5
Figure 5
Representative STEM images of normal (A), normal vesicular (B), vesicular (C), swollen vesicular (D), and swollen (E) mitochondrial morphotypes found in the tissues of both studied groups.
Figure 6
Figure 6
Neuronal mitochondrial ultrastructure damages in the control group and PbO NP exposure groups by brain regions. Notes: Values are given as the arithmetic mean of the fraction of mitochondria in the total number of neuronal mitochondria found; whiskers show the standard error of the mean.
Figure 7
Figure 7
Results of the open field test of the experimental animals: (A) the number of head dips into holes; (B) locomotor activity; (C) the number of defecations. The abscissa shows the exposure time in weeks, the ordinate shows the magnitude of effect.
Figure 8
Figure 8
Changes in the activity of succinate dehydrogenase in rat blood lymphocytes (A), the concentration of reduced glutathione in blood hemolysate (B) and ceruloplasmin in blood serum (C) under effect of PbO NPs. The magnitude of the effect is marked on the y axis. Note *Statistically different from the control group (p < 0.05).
Figure 9
Figure 9
Description of PbO nanoparticles used in the experiment: (a) a scanning transmission electron microscopy image of PbO nanoparticles in the suspension at 29,640 × magnification, and (b) the function of PbO nanoparticle size distribution.
Figure 10
Figure 10
Sampling and sample preparation for electron microscopy.
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