title: Coal and tire burning mixtures containing ultrafine and nanoparticulate materials induce oxidative stress and inflammatory activation in macrophages.
abstract: Ultra-fine and nano-particulate materials resulting from mixtures of coal and non-coal fuels combustion for power generation release to the air components with toxic potential. We evaluated toxicological and inflammatory effects at cellular level that could be induced by ultrafine/nanoparticles-containing ashes from burning mixtures of coal and tires from an American power plant. Coal fly ashes (CFA) samples from the combustion of high-S coal and tire-derived fuel, the latter about 2-3% of the total fuel feed, in a 100-MW cyclone utility boiler, were suspended in the cell culture medium of RAW 264.7 macrophages. Cell viability, assessed by MTT reduction, SRB incorporation and contrast-phase microscopy analysis demonstrated that CFA did not induce acute toxicity. However, CFA at 1mg/mL induced an increase of approximately 338% in intracellular TNF-α, while release of this proinflammatory cytokine was increased by 1.6-fold. The expression of the inflammatory mediator CD40 receptor was enhanced by 2-fold, the receptor for advanced glycation endproducts (RAGE) had a 5.7-fold increase and the stress response protein HSP70 was increased nearly 12-fold by CFA at 1mg/mL. Although CFA did not induce cell death, parameters of oxidative stress and reactive species production were found to be altered at several degrees, such as nitrite accumulation (22% increase), DCFH oxidation (3.5-fold increase), catalase (5-fold increase) and superoxide dismutase (35% inhibition) activities, lipoperoxidation (4.2 fold-increase) and sulfhydryl oxidation (40% decrease in free SH groups). The present results suggest that CFA containing ultra-fine and nano-particulate materials from coal and tire combustion may induce sub-chronic cell damage, as they alter inflammatory and oxidative stress parameters at the molecular and cellular levels, but do not induce acute cell death.
authors.affiliation: Center of Oxidative Stress Research, Tuiskon Dick Department of Biochemistry, Institute of Health Basic Sciences, Federal University of Rio Grande do Sul (UFRGS) Brazil. Electronic address: Juciano.gasparotto@gmail.com.
authors.forename: Juciano
authors.initials: J
authors.lastname: Gasparotto
authors.forename: Nauana
authors.initials: N
authors.lastname: Somensi
authors.forename: Fernanda F
authors.initials: FF
authors.lastname: Caregnato
authors.forename: Thallita K
authors.initials: TK
authors.lastname: Rabelo
authors.forename: Kátia
authors.initials: K
authors.lastname: DaBoit
authors.forename: Marcos L S
authors.initials: ML
authors.lastname: Oliveira
authors.forename: José C F
authors.initials: JC
authors.lastname: Moreira
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Gelain
mesh_terms: D000818:Animals; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D060729:Coal Ash / Q000009:adverse effects*; D007249:Inflammation / Q000139:chemically induced*; D015227:Lipid Peroxidation / Q000187:drug effects; D008264:Macrophages / Q000737:chemistry / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D053758:Nanoparticles / Q000009:adverse effects*; D009569:Nitric Oxide / Q000096:biosynthesis; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000032:analysis; D012408:Rubber / Q000009:adverse effects*; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D060729:Coal Ash; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D012408:Rubber; D002374:Catalase; D013482:Superoxide Dismutase
keywords: Inflammation; Macrophage; Nano-particulate materials; Oxidative stress