Use of Coated Silver Nanoparticles to Understand the Relationship of Particle Dissolution and Bioavailability to Cell and Lung Toxicological Potential
Since more than 30% of consumer products that include engineered nanomaterials contain nano‐Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)‐coated Ag NPs induce...
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| Published in | Small (Weinheim an der Bergstrasse, Germany) Vol. 10; no. 2; pp. 385 - 398 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Germany
Blackwell Publishing Ltd
29.01.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1613-6810 1613-6829 1613-6829 |
| DOI | 10.1002/smll.201301597 |
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| Abstract | Since more than 30% of consumer products that include engineered nanomaterials contain nano‐Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)‐coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag+. In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag+ release leading to a sub‐chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub‐chronic lung injury potential.
Twenty and 110 nm Ag nanoparticles coated with PVP or citrate are used to determine their toxicity in vitro and in vivo. Small particles (20 nm) generate higher acute lung toxicity than big particles because of their high dissolution rate. However, large particles (110 nm) induce chronic lung fibrosis due to their slow dissolution rate and persistence in lungs. |
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| AbstractList | Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag(+) . In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag(+) release leading to a sub-chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential. Since more than 30% of consumer products that include engineered nanomaterials contain nano‐Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)‐coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag+. In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag+ release leading to a sub‐chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub‐chronic lung injury potential. Twenty and 110 nm Ag nanoparticles coated with PVP or citrate are used to determine their toxicity in vitro and in vivo. Small particles (20 nm) generate higher acute lung toxicity than big particles because of their high dissolution rate. However, large particles (110 nm) induce chronic lung fibrosis due to their slow dissolution rate and persistence in lungs. Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag super(+). In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag super(+) release leading to a sub-chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential. Twenty and 110 nm Ag nanoparticles coated with PVP or citrate are used to determine their toxicity in vitro and in vivo. Small particles (20 nm) generate higher acute lung toxicity than big particles because of their high dissolution rate. However, large particles (110 nm) induce chronic lung fibrosis due to their slow dissolution rate and persistence in lungs. Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag+. In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag+ release leading to a sub-chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential. [PUBLICATION ABSTRACT] Since more than 30 % of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, we used Ag nanoparticles (NPs) to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there was also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 had less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag + . In contrast to the more intense acute pulmonary effects of C20, C110 induced mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag + release leading to a sub-chronic injury response. Interestingly, the released metallic Ag gets incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential. Since more than 30% of consumer products that include engineered nanomaterials contain nano‐Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)‐coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag + . In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag + release leading to a sub‐chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub‐chronic lung injury potential. Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag(+) . In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag(+) release leading to a sub-chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential.Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern. In this study, Ag nanoparticles (NPs) are used to demonstrate that 20 nm polyvinylpyrrolidone (PVP or P) and citrate (C)-coated Ag NPs induce more cellular toxicity and oxidative stress than larger (110 nm) particles due to a higher rate of dissolution and Ag bioavailability. Moreover, there is also a higher propensity for citrate 20 nm (C20) nanoparticles to generate acute neutrophilic inflammation in the lung and to produce chemokines compared to C110. P110 has less cytotoxic effects than C110, likely due to the ability of PVP to complex released Ag(+) . In contrast to the more intense acute pulmonary effects of C20, C110 induces mild pulmonary fibrosis at day 21, likely as a result of slow but persistent Ag(+) release leading to a sub-chronic injury response. Interestingly, the released metallic Ag is incorporated into the collagen fibers depositing around airways and the lung interstitium. Taken together, these results demonstrate that size and surface coating affect the cellular toxicity of Ag NPs as well as their acute versus sub-chronic lung injury potential. |
| Author | Sun, Bingbing Zink, Jeffrey I. Wang, Meiying Liao, Yu-Pei Chang, Chong Hyun Meng, Huan Pinkerton, Kent E. Wang, Xiang Ji, Zhaoxia Winkle, Laura Van Lin, Sijie Li, Ruibin Xia, Tian Zhang, Haiyuan Nel, André E. |
| Author_xml | – sequence: 1 givenname: Xiang surname: Wang fullname: Wang, Xiang organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, CA, 90095, Los Angeles, USA – sequence: 2 givenname: Zhaoxia surname: Ji fullname: Ji, Zhaoxia organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, CA, 90095, Los Angeles, USA – sequence: 3 givenname: Chong Hyun surname: Chang fullname: Chang, Chong Hyun organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, CA, 90095, Los Angeles, USA – sequence: 4 givenname: Haiyuan surname: Zhang fullname: Zhang, Haiyuan organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, CA, 90095, Los Angeles, USA – sequence: 5 givenname: Meiying surname: Wang fullname: Wang, Meiying organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 6 givenname: Yu-Pei surname: Liao fullname: Liao, Yu-Pei organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 7 givenname: Sijie surname: Lin fullname: Lin, Sijie organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, CA, 90095, Los Angeles, USA – sequence: 8 givenname: Huan surname: Meng fullname: Meng, Huan organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 9 givenname: Ruibin surname: Li fullname: Li, Ruibin organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 10 givenname: Bingbing surname: Sun fullname: Sun, Bingbing organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 11 givenname: Laura Van surname: Winkle fullname: Winkle, Laura Van organization: Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California at Davis, CA, 95616, Davis, USA – sequence: 12 givenname: Kent E. surname: Pinkerton fullname: Pinkerton, Kent E. organization: Center for Health and the Environmen, University of California at Davis, CA, 95616, Davis, USA – sequence: 13 givenname: Jeffrey I. surname: Zink fullname: Zink, Jeffrey I. organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 14 givenname: Tian surname: Xia fullname: Xia, Tian organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA – sequence: 15 givenname: André E. surname: Nel fullname: Nel, André E. email: anel@mednet.ucla.edu organization: Center for Environmental Implications of Nanotechnology, California NanoSystems Institute, University of California at Los Angeles, 90095, Los Angeles, CA, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24039004$$D View this record in MEDLINE/PubMed |
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| Snippet | Since more than 30% of consumer products that include engineered nanomaterials contain nano‐Ag, the safety of this material is of considerable public concern.... Since more than 30% of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern.... Since more than 30 % of consumer products that include engineered nanomaterials contain nano-Ag, the safety of this material is of considerable public concern.... |
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| SubjectTerms | Animals Biocompatibility Biological Availability Cell Line Citrates cytotoxicity Dissolution Female Humans Lung - drug effects lung inflammation Lungs Male Metal Nanoparticles - chemistry Metal Nanoparticles - toxicity Mice Microscopy, Electron, Transmission nanoparticle Nanoparticles Nanostructure Nanotechnology Rats Silver Silver - chemistry Silver - pharmacokinetics Silver - toxicity Solubility Toxicity Toxicity Tests, Subchronic |
| Title | Use of Coated Silver Nanoparticles to Understand the Relationship of Particle Dissolution and Bioavailability to Cell and Lung Toxicological Potential |
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