Pulmonary exposure to metallic nanomaterials during pregnancy irreversibly impairs lung development of the offspring

Paul, Emmanuel N.; Franco-Montoya, Marie-Laure; Paineau, Erwan; Angeletti, Bernard; Vibhushan, Shamila; Ridoux, Audrey; Tiendrébéogo, Arnaud Jean Florent; Salomé, Murielle; Hesse, Bernhard; Vantelon, Delphine; Rose, Jérôme; Canouï‐Poitrine, Florence; Boczkowski, Jorge; Lanone, Sophie; Delacourt, Christophe; Pairon, Jean‐Claude

doi:10.1080/17435390.2017.1311381

Cited by 51 publications

(63 citation statements)

References 53 publications

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“…In addition, the hematological results showed a significant increase in WBC and PLT counts in those exposed to higher doses of ZnO. These observations were in accordance with previous researches which indicted that exposure to NPs could induce inflammation in mice [20,21]. The organ coefficient data showed a significant decrease in thymus weight/body weight which implied that the exposure to ZnO NPs may have disturbed the inflammation system during pregnancy that was consistent with the hematological results.…”

Section: Discussionsupporting

confidence: 90%

Nano Zinc Oxide Induced Fetal Mice Growth Restriction, Based on Oxide Stress and Endoplasmic Reticulum Stress

et al. 2020

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ZnO NPs have been assessed to show adverse effects on reproductive organs, but the molecular mechanisms of reproductive toxicity have not been sufficiently studied. In this research, the dosage effects from the oral exposure of ZnO NPs (30 nm) to pregnant mice in gestation day 10.5 to 17.5 was analyzed. Pregnant mice exposed to ZnO NPs induced dam injury, mice fetal growth restriction, and the fetus number decreased. The pathological evaluation showed that ZnO NPs exposure caused placental spongiotrophoblast area decease and structural damage. The RT-qPCR and immunocytochemistry data indicated that ZnO NPs could induce placenta oxide stress, endoplasmic reticulum stress responses, apoptosis, and altered placental function. These findings indicated that ZnO NPs could induce dam injury and fetal growth restriction. Reproductive toxicity of ZnO NPs may be due to placental injury and function alteration caused by apoptosis, oxide stress, and endoplasmic reticulum stress after ZnO NPs exposure.

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Section: Discussionsupporting

confidence: 90%

Nano Zinc Oxide Induced Fetal Mice Growth Restriction, Based on Oxide Stress and Endoplasmic Reticulum Stress

et al. 2020

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“…In conclusion, many in vivo animal studies reported in the literature have shown the fetotoxicity of nanoparticles after maternal pulmonary exposure, especially in rodents [11,23,33,34]. Table 1 -Population characteristics in terms of demographic data, medical history and data about the amniocentesis.…”

Section: Discussionmentioning

confidence: 99%

Elemental fingerprint of human amniotic fluids and relationship with potential sources of maternal exposure

Raia-Barjat

Prieux

Leclerc

et al. 2020

Journal of Trace Elements in Medicine and Biology

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Background-The impact of nanoparticles we are increasingly exposed to remains largely unknown. Of particular concern is the exposure of pregnant women and potential impact on fetal development. Indeed, many in vitro and in vivo animal studies have shown that nanoparticles are able to cross the placental barrier and induce toxic effects to the fetus. However, little is known in humans. Objective-The aim and originality of this study were to investigate the nanoparticle burden of amniotic fluids in pregnant women. Methods-To that purpose, 100 amniotic fluids collected for clinical purposes were used to determine the nanoparticle quantity and nature by inductively coupled plasma atomic emission spectroscopy (NAMIOTIC, ClinicalTrials.gov Identifier: NCT02720887). Results-The prevalence of patients with a substantial concentration for the essential trace elements Cu, Fe and Zn was high, while that of patients with a substantial concentration of Al, Ag, Be, Co, Cr, Ni, Si, Ti and W was relatively low (under 20%). It was generally higher in the fraction containing nanoparticles and ions than in the fraction containing micro-and submicroparticles. No correlation was found between the nanoparticle burden and the different potential sources of exposure to nanoparticles (smoking status of the patient, living area, heating source, mode of transport, leisure, use of hygiene products and cosmetics and occupational activities). Conclusion-Our results showing low concentrations and low prevalence of most of the assessed elements in amniotic fluids are reassuring. Further research is needed to draw firm conclusions on the developmental toxicity of engineered nanoparticles in humans but the present paper can provide a useful basis for further evaluation of the fetal toxicity of nanoparticles.

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“…Mice were sacri ced 24 h, 1 or 4 weeks later. A broncho-alveolar lavage (BAL) was performed, and the lungs were harvested and collected for further analysis as previously described (34). A subset of mice were treated with Clodronate or liposome as negative control as previously described (35).…”

Section: Experimental Model Of Lung Brosismentioning

confidence: 99%

Deficient macrophage autophagy protects mice from Cerium Oxide nanoparticle-induced lung fibrosis

Annangi¹,

Lu²,

Bruniaux³

et al. 2020

Preprint

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BackgroundCerium (Ce) is a rare earth element, rapidly oxidizing to form CeO2, and currently used in numerous commercial applications, especially as nanoparticles (NP). The potential health effects of Ce remain uncertain, but literature indicates the development of rare earth pneumoconiosis accompanied with granuloma formation, interstitial fibrosis and inflammation. The exact underlying mechanisms are yet not completely understood, and we propose that autophagy could be an interesting target to study, particularly in macrophages. Therefore, the objective of our study was to investigate the role of macrophagic autophagy after pulmonary exposure to CeO2 NP in mice. Mice lacking the early autophagy gene Atg5 in their myeloid lineage and their wildtype counterparts were exposed to CeO2 NP by single oropharyngeal administration and sacrificed up to one month after. At that time, lung remodeling was thoroughly characterized (inflammatory cells infiltration, expression of fibrotic markers such as αSMA, TGFβ1, total and type I and III collagen deposition), as well as macrophage infiltration (quantification and M1/M2 phenotype). Results: Such pulmonary exposure to CeO2 NP induces a progressive and dose-dependent lung fibrosis in the bronchiolar and alveolar walls, together with the activation of autophagy. Blockade of macrophagic autophagy protects from alveolar but not bronchiolar fibrosis, via the modulation of macrophage polarization towards M2 phenotype. Conclusion: In conclusion, our findings bring novel insight on the role of macrophagic autophagy in lung fibrogenesis, and add to the current awareness of pulmonary macrophages as potential new therapeutic targets for future anti-fibrotic therapies.

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Pulmonary exposure to metallic nanomaterials during pregnancy irreversibly impairs lung development of the offspring

Cited by 51 publications

References 53 publications

Nano Zinc Oxide Induced Fetal Mice Growth Restriction, Based on Oxide Stress and Endoplasmic Reticulum Stress

Nano Zinc Oxide Induced Fetal Mice Growth Restriction, Based on Oxide Stress and Endoplasmic Reticulum Stress

Elemental fingerprint of human amniotic fluids and relationship with potential sources of maternal exposure

Deficient macrophage autophagy protects mice from Cerium Oxide nanoparticle-induced lung fibrosis

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