Toxic Potential of Materials at the Nanolevel
The establishment of principles and test procedures to ensure safe manufacture and use of nanomaterials in the marketplace is urgently required and achievable.
Understanding biophysicochemical interactions at the nano-bio interface.
Probing the various interfaces of nanoparticle/biological interfaces allows the development of predictive relationships between structure and activity that are determined by nanomaterial properties such as size, shape, surface chemistry, roughness and surface coatings.
Comparison of the mechanism of toxicity of zinc oxide and cerium oxide nanoparticles based on dissolution and oxidative stress properties.
The results demonstrate that metal oxide nanoparticles induce a range of biological responses that vary from cytotoxic to cytoprotective and can only be properly understood by using a tiered test strategy such as that developed for oxidative stress and adapted to study other aspects of nanoparticle toxicity.
Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage.
The studies demonstrate that the increased biological potency of UFPs is related to the content of redox cycling organic chemicals and their ability to damage mitochondria.
Comparison of the abilities of ambient and manufactured nanoparticles to induce cellular toxicity according to an oxidative stress paradigm.
It is demonstrated that ROS generation and oxidative stress are a valid test paradigm to compare NP toxicity, and particle interactions with cellular components are capable of generating oxidative stress.
Air Pollution-Related Illness: Effects of Particles
- A. Nel
- Environmental ScienceScience
- 6 May 2005
Nel describes how the adverse effects of ultrafine air particles are linked to their ability to gain access to the lung and systemic circulation, where toxic components lead to tissue damage and inflammation.
Use of metal oxide nanoparticle band gap to develop a predictive paradigm for oxidative stress and acute pulmonary inflammation.
It is demonstrated that it is possible to predict the toxicity of a large series of MOx nanoparticles in the lung premised on semiconductor properties and an integrated in vitro/in vivo hazard ranking model premisedon oxidative stress.
Particulate air pollutants and asthma. A paradigm for the role of oxidative stress in PM-induced adverse health effects.
Comparison of the Pro-Oxidative and Proinflammatory Effects of Organic Diesel Exhaust Particle Chemicals in Bronchial Epithelial Cells and Macrophages1
It is demonstrated that epithelial cells exhibit a hierarchical oxidative stress response that differs from that of macrophages by more rapid transition from cytoprotective to cytotoxic responses, and not being protected by a thiol antioxidant, N-acetylcysteine, which effectively protects macrophage against cytot toxic DEP chemicals.