Investigation of the effects of short-term inhalation of carbon nanoparticles on brains and lungs of c57bl/6j and p47phox−/− mice

Berlo, Damiën van; Hullmann, Maja; Wessels, Anton; Scherbart, Agnes M.; Cassee, Flemming R.; Gerlofs-Nijland, Miriam E.; Albrecht, Catrin; Schins, Roel P. F.

doi:10.1016/j.neuro.2014.04.008

Cited by 18 publications

(11 citation statements)

References 56 publications

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“…8-Oxoguanine DNA glycosylase 1 (OGG1) is a BER enzyme that removes oxidatively-damaged guanine from double stranded DNA [101,102]. A previous study reported the upregulation of the DNA damage genes OGG1 and APE1 in C57BL/6J mice treated with engineered NPs [103]. DNA damage-induced 45α (GADD45α) has been found to promote DNA repair and remove methylation markers involved in genomic stability.…”

Section: Resultsmentioning

confidence: 99%

Tangeretin-Assisted Platinum Nanoparticles Enhance the Apoptotic Properties of Doxorubicin: Combination Therapy for Osteosarcoma Treatment

et al. 2019

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Osteosarcoma (OS) is the most common type of cancer and the most frequent malignant bone tumor in childhood and adolescence. Nanomedicine has become an indispensable field in biomedical and clinical research, with nanoparticles (NPs) promising to increase the therapeutic efficacy of anticancer drugs. Doxorubicin (DOX) is a commonly used chemotherapeutic drug against OS; however, it causes severe side effects that restrict its clinical applications. Here, we investigated whether combining platinum NPs (PtNPs) and DOX could increase their anticancer activity in human bone OS epithelial cells (U2OS). PtNPs with nontoxic, effective, thermally stable, and thermoplasmonic properties were synthesized and characterized using tangeretin. We examined the combined effects of PtNPs and DOX on cell viability, proliferation, and morphology, reactive oxygen species (ROS) generation, lipid peroxidation, nitric oxide, protein carbonyl content, antioxidants, mitochondrial membrane potential (MMP), adenosine tri phosphate (ATP) level, apoptotic and antiapoptotic gene expression, oxidative stress-induced DNA damage, and DNA repair genes. PtNPs and DOX significantly inhibited U2OS viability and proliferation in a dose-dependent manner, increasing lactate dehydrogenase leakage, ROS generation, and malondialdehyde, nitric oxide, and carbonylated protein levels. Mitochondrial dysfunction was confirmed by reduced MMP, decreased ATP levels, and upregulated apoptotic/downregulated antiapoptotic gene expression. Oxidative stress was a major cause of cytotoxicity and genotoxicity, confirmed by decreased levels of various antioxidants. Furthermore, PtNPs and DOX increased 8-oxo-dG and 8-oxo-G levels and induced DNA damage and repair gene expression. Combination of cisplatin and DOX potentially induce apoptosis comparable to PtNPs and DOX. To the best of our knowledge, this is the first report to describe the combined effects of PtNPs and DOX in OS.

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Section: Resultsmentioning

confidence: 99%

Tangeretin-Assisted Platinum Nanoparticles Enhance the Apoptotic Properties of Doxorubicin: Combination Therapy for Osteosarcoma Treatment

et al. 2019

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“…In addition, metal ions may cause mitochondrial dysfunction by inhibition of electron transfer chain or through reactions with redox active enzymes such as NADPH oxidases [ 184 , 185 ]. Indeed, a range of in vitro and in vivo studies using pharmacological inhibitors, RNA interference, and genetic knock-out models, suggests that increases in intracellular ROS levels in exposed cells as well as tissue levels of ROS in the lung and vasculature of particle-exposed animals, predominately arise from endogenous redox-processes, such as activation of oxidases or mitochondrial respiration [ 231 , 232 , 233 , 234 , 235 , 236 , 237 , 238 , 239 , 240 , 241 , 242 ]. Although the majority of these studies did not address mechanisms of particle-induced inflammation, it seems likely that this endogenous ROS generation may also affect regulation of proinflammatory genes.…”

Section: Central Signaling Pathways and Processes Involved In Partmentioning

confidence: 99%

Activation of Proinflammatory Responses in Cells of the Airway Mucosa by Particulate Matter: Oxidant- and Non-Oxidant-Mediated Triggering Mechanisms

et al. 2015

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Inflammation is considered to play a central role in a diverse range of disease outcomes associated with exposure to various types of inhalable particulates. The initial mechanisms through which particles trigger cellular responses leading to activation of inflammatory responses are crucial to clarify in order to understand what physico-chemical characteristics govern the inflammogenic activity of particulate matter and why some particles are more harmful than others. Recent research suggests that molecular triggering mechanisms involved in activation of proinflammatory genes and onset of inflammatory reactions by particles or soluble particle components can be categorized into direct formation of reactive oxygen species (ROS) with subsequent oxidative stress, interaction with the lipid layer of cellular membranes, activation of cell surface receptors, and direct interactions with intracellular molecular targets. The present review focuses on the immediate effects and responses in cells exposed to particles and central down-stream signaling mechanisms involved in regulation of proinflammatory genes, with special emphasis on the role of oxidant and non-oxidant triggering mechanisms. Importantly, ROS act as a central second-messenger in a variety of signaling pathways. Even non-oxidant mediated triggering mechanisms are therefore also likely to activate downstream redox-regulated events.

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“…Thousands of nanoproducts are already available on the market (JRC, 2014) (Tulve et al, 2015;Vance et al, 2015), raising concerns of massive consumer exposure by inhalation, ingestion, dermal contact, or a combination of these routes. While several studies have already pointed to possible respiratory and cardiovascular system damage following nanoparticle exposure (Cassee et al, 2011;Dockery et al, 1993;Ghio et al, 2012;Liao et al, 2014;McCreanor et al, 2007;Miller et al, 2013;Patel et al, 2013;Pieters et al, 2012;Pope et al, 2008;Pope et al, 2006;Robertson et al, 2012;Robertson et al, 2014;Seaton et al, 1995;Thurston et al, 2016;Xu et al, 2013b;Yamamoto et al, 2013), only few studies have looked at their impact on the highly vulnerable nervous system as underlined in several reviews (Cupaioli et al, 2014;Lung et al, 2014;Suh et al, 2009;van Berlo et al, 2014;Yokel, 2016a;Yokel and Macphail, 2011).…”

Section: Introductionmentioning

confidence: 99%

Nano- and neurotoxicology: An emerging discipline

Bencsik

Lestaevel

Canu

2018

Progress in Neurobiology

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The present critical review analyzes the question of how nanoparticles from continuously growing industrial production and use of nanomaterials may impact human brain health. Available evidence suggests incomplete effectiveness of protective barriers of the brain against nanoparticles translocation to the brain. This raises concerns of potential effects of manufactured nanoparticles on brain functions, given that nanoparticle's potential to induce oxidative stress, inflammation, death by apoptosis, or changes in the level of expression of certain neurotransmitters. Most concerns have not been studied sufficiently and many questions are still open: Are the findings in animals transposable to humans? What happens when exposure is chronic or protracted? What happens to the developing brain when exposure occurs in utero? Are some nanoparticles more deleterious, given their ability to alter protein conformations and aggregation? Aside from developments in nanomedicine, the evidence already available fully justifies the need to specifically evaluate the interactions between nanoparticles and the nervous system. The available data clearly indicates the need for original dedicated experimental models and tools for neurotoxicological research on the one hand, and the need for epidemiological studies of neurodegenerative diseases in manufactured nanoparticle-exposed populations, on the other. A combination of nanotoxicology with neurology in a novel discipline, with its specific tools and methods of investigation, should enable answering still unresolved questions.

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Investigation of the effects of short-term inhalation of carbon nanoparticles on brains and lungs of c57bl/6j and p47phox−/− mice

Cited by 18 publications

References 56 publications

Tangeretin-Assisted Platinum Nanoparticles Enhance the Apoptotic Properties of Doxorubicin: Combination Therapy for Osteosarcoma Treatment

Tangeretin-Assisted Platinum Nanoparticles Enhance the Apoptotic Properties of Doxorubicin: Combination Therapy for Osteosarcoma Treatment

Activation of Proinflammatory Responses in Cells of the Airway Mucosa by Particulate Matter: Oxidant- and Non-Oxidant-Mediated Triggering Mechanisms

Nano- and neurotoxicology: An emerging discipline

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