title: Role of oxidative stress in carbon nanotube-generated health effects.
abstract: The development of products containing carbon nanotubes (CNTs) is a major achievement of nanotechnology, although concerns regarding risk of toxic effects linger if the hazards associated with these materials are not thoroughly investigated. Exposure to CNTs has been associated with depletion of antioxidants, increased intracellular production of reactive oxygen species and pro-inflammatory signaling in cultured cells with primary function in the immune system as well as epithelial, endothelial and stromal cells. Pre-treatment with antioxidants has been shown to attenuate these effects, indicating a dependency of oxidative stress on cellular responses to CNT exposure. CNT-mediated oxidative stress in cell cultures has been associated with elevated levels of lipid peroxidation products and oxidatively damaged DNA. Investigations of oxidative stress endpoints in animal studies have utilized pulmonary, gastrointestinal, intravenous and intraperitoneal exposure routes, documenting elevated levels of lipid peroxidation products and oxidatively damaged DNA nucleobases especially in the lungs and liver, which to some extent occur concomitantly with altered levels of components in the antioxidant defense system (glutathione, superoxide dismutase or catalase). CNTs are biopersistent high aspect ratio materials, and some are rigid with lengths that lead to frustrated phagocytosis and pleural accumulation. There is accumulating evidence showing that pulmonary exposure to CNTs is associated with fibrosis and neoplastic changes in the lungs, and cardiovascular disease. As oxidative stress and inflammation responses are implicated in the development of these diseases, converging lines of evidence indicate that exposure to CNTs is associated with increased risk of cardiopulmonary diseases through generation of a pro-inflammatory and pro-oxidant milieu in the lungs.
authors.affiliation: Section of Environmental Health, Department of Public Health, University of Copenhagen, Øster Farimagsgade 5A, Building 5B, 2nd Floor, 1014, Copenhagen K, Denmark, pemo@sund.ku.dk.
authors.forename: Peter
authors.initials: P
authors.lastname: Møller
authors.forename: Daniel Vest
authors.initials: DV
authors.lastname: Christophersen
authors.forename: Ditte Marie
authors.initials: DM
authors.lastname: Jensen
authors.forename: Ali
authors.initials: A
authors.lastname: Kermanizadeh
authors.forename: Martin
authors.initials: M
authors.lastname: Roursgaard
authors.forename: Nicklas Raun
authors.initials: NR
authors.lastname: Jacobsen
authors.forename: Jette Gjerke
authors.initials: JG
authors.lastname: Hemmingsen
authors.forename: Pernille Høgh
authors.initials: PH
authors.lastname: Danielsen
authors.forename: Yi
authors.initials: Y
authors.lastname: Cao
authors.forename: Kim
authors.initials: K
authors.lastname: Jantzen
authors.forename: Henrik
authors.initials: H
authors.lastname: Klingberg
authors.forename: Lars-Georg
authors.initials: LG
authors.lastname: Hersoug
authors.forename: Steffen
authors.initials: S
authors.lastname: Loft
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism* / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000139:chemically induced / Q000503:physiopathology; D004249:DNA Damage / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008171:Lung Diseases / Q000139:chemically induced / Q000503:physiopathology; D036103:Nanotechnology; D037742:Nanotubes, Carbon / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D037742:Nanotubes, Carbon; D017382:Reactive Oxygen Species