Detailed Information on Publication Record

DUMKOVÁ, Jana, T. SMUTNÁ, Lucie VRLÍKOVÁ, Philippe LE COUSTUMER, Z. VEČEŘA, B. DOČEKAL, P. MIKUŠKA, L. ČAPKA, P. FICTUM, Aleš HAMPL and marcela BUCHTOVÁ. Sub-chronic inhalation of lead oxide nanoparticles revealed their broad distribution and tissue-specific subcellular localization in target organs. Particle and Fibre Toxicology. London: Biomed Central, 2017, vol. 14, December, p. nestránkováno, 19 pp. ISSN 1743-8977. Available from: https://dx.doi.org/10.1186/s12989-017-0236-y.

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Basic information
Original name	Sub-chronic inhalation of lead oxide nanoparticles revealed their broad distribution and tissue-specific subcellular localization in target organs
Authors	DUMKOVÁ, Jana (203 Czech Republic, belonging to the institution), T. SMUTNÁ (203 Czech Republic), Lucie VRLÍKOVÁ (203 Czech Republic), Philippe LE COUSTUMER (250 France), Z. VEČEŘA (203 Czech Republic), B. DOČEKAL (203 Czech Republic), P. MIKUŠKA (203 Czech Republic), L. ČAPKA (203 Czech Republic), P. FICTUM (203 Czech Republic), Aleš HAMPL (203 Czech Republic, belonging to the institution) and marcela BUCHTOVÁ (203 Czech Republic, belonging to the institution).
Edition	Particle and Fibre Toxicology, London, Biomed Central, 2017, 1743-8977.

Other information
Original language	English
Type of outcome	Article in a journal
Field of Study	30108 Toxicology
Country of publisher	United Kingdom of Great Britain and Northern Ireland
Confidentiality degree	is not subject to a state or trade secret
WWW	URL
Impact factor	Impact factor: 6.105
RIV identification code	RIV/00216224:14310/17:00099051
Organization unit	Faculty of Science
Doi	http://dx.doi.org/10.1186/s12989-017-0236-y
UT WoS	000418716600001
Keywords in English	nanoparticles; lead oxide; electron microscopy; toxicity; inhalation; lung; liver; kidney; spleen; brain
Tags	NZ, rivok
Tags	International impact, Reviewed
Changed by	Changed by: Ing. Nicole Zrilić, učo 240776. Changed: 12/4/2018 09:59.

Abstract
Background: Lead is well known environmental pollutant, which can cause toxic effects in multiple organ systems. However, the influence of lead oxide nanoparticles, frequently emitted to the environment by high temperature technological processes, is still concealed. Therefore, we investigate lead oxide nanoparticle distribution through the body upon their entry into lungs and determine the microscopic and ultramicroscopic changes caused by the nanoparticles in primary and secondary target organs. Methods: Adult female mice (ICR strain) were continuously exposed to lead oxide nanoparticles (PbO-NPs) with an average concentration approximately 106 particles/cm3 for 6 weeks (24 h/day, 7 days/week). At the end of the exposure period, lung, brain, liver, kidney, spleen, and blood were collected for chemical, histological, immunohistochemical and electron microscopic analyses. Results: Lead content was found to be the highest in the kidney and lungs, followed by the liver and spleen; the smallest content of lead was found in brain. Nanoparticles were located in all analysed tissues and their highest number was found in the lung and liver. Kidney, spleen and brain contained lower number of nanoparticles, being about the same in all three organs. Lungs of animals exposed to lead oxide nanoparticles exhibited hyperaemia, small areas of atelectasis, alveolar emphysema, focal acute catarrhal bronchiolitis and also haemostasis with presence of siderophages in some animals. Nanoparticles were located in phagosomes or formed clusters within cytoplasmic vesicles. In the liver, lead oxide nanoparticle exposure caused hepatic remodeling with enlargement and hydropic degeneration of hepatocytes, centrilobular hypertrophy of hepatocytes with karyomegaly, areas of hepatic necrosis, occasional periportal inflammation, and extensive accumulation of lipid droplets. Nanoparticles were accumulated within mitochondria and peroxisomes forming aggregates enveloped by an electron-dense mitochondrial matrix. Only in some kidney samples, we observed areas of inflammatory infiltrates around renal corpuscles, tubules or vessels in the cortex. Lead oxide nanoparticles were dispersed in the cytoplasm, but not within cell organelles. There were no significant morphological changes in the spleen as a secondary target organ. Thus, pathological changes correlated with the amount of nanoparticles found in cells rather than with the concentration of lead in a given organ. Conclusions: Sub-chronic exposure to lead oxide nanoparticles has profound negative effects at both cellular and tissue levels. Notably, the fate and arrangement of lead oxide nanoparticles were dependent on the type of organs.

Abstract

Background: Lead is well known environmental pollutant, which can cause toxic effects in multiple organ systems. However, the influence of lead oxide nanoparticles, frequently emitted to the environment by high temperature technological processes, is still concealed. Therefore, we investigate lead oxide nanoparticle distribution through the body upon their entry into lungs and determine the microscopic and ultramicroscopic changes caused by the nanoparticles in primary and secondary target organs. Methods: Adult female mice (ICR strain) were continuously exposed to lead oxide nanoparticles (PbO-NPs) with an average concentration approximately 106 particles/cm3 for 6 weeks (24 h/day, 7 days/week). At the end of the exposure period, lung, brain, liver, kidney, spleen, and blood were collected for chemical, histological, immunohistochemical and electron microscopic analyses. Results: Lead content was found to be the highest in the kidney and lungs, followed by the liver and spleen; the smallest content of lead was found in brain. Nanoparticles were located in all analysed tissues and their highest number was found in the lung and liver. Kidney, spleen and brain contained lower number of nanoparticles, being about the same in all three organs. Lungs of animals exposed to lead oxide nanoparticles exhibited hyperaemia, small areas of atelectasis, alveolar emphysema, focal acute catarrhal bronchiolitis and also haemostasis with presence of siderophages in some animals. Nanoparticles were located in phagosomes or formed clusters within cytoplasmic vesicles. In the liver, lead oxide nanoparticle exposure caused hepatic remodeling with enlargement and hydropic degeneration of hepatocytes, centrilobular hypertrophy of hepatocytes with karyomegaly, areas of hepatic necrosis, occasional periportal inflammation, and extensive accumulation of lipid droplets. Nanoparticles were accumulated within mitochondria and peroxisomes forming aggregates enveloped by an electron-dense mitochondrial matrix. Only in some kidney samples, we observed areas of inflammatory infiltrates around renal corpuscles, tubules or vessels in the cortex. Lead oxide nanoparticles were dispersed in the cytoplasm, but not within cell organelles. There were no significant morphological changes in the spleen as a secondary target organ. Thus, pathological changes correlated with the amount of nanoparticles found in cells rather than with the concentration of lead in a given organ. Conclusions: Sub-chronic exposure to lead oxide nanoparticles has profound negative effects at both cellular and tissue levels. Notably, the fate and arrangement of lead oxide nanoparticles were dependent on the type of organs.