Antioxidant defense disruption by polycyclic aromatic hydrocarbons-coated onto Fe(2)O(3) particles in human lung cells (A549).

We addressed the hypothesis that in vitro short-term exposure to hematite (Fe(2)O(3)) and polycyclic aromatic hydrocarbons (PAHs) is more deleterious by virtue of their combinations being able to cause higher oxidative stress conditions in human lung cells (A549), than either chemical alone. Lipid peroxidation (malondialdehyde; MDA), antioxidant enzyme activities (superoxide dismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glutathione status (reduced glutathione; GSH, oxidized glutathione; GSSG) and alpha-tocopherol (alpha-Toc) consumption were studied in cells exposed to Fe(2)O(3), benzo(a)pyrene (B(a)P) or pyrene, alone or in association. We found that increases in GSSG/GSH (P<0.01) and in alpha-Toc consumption (P<0.01) counteracted Fe(2)O(3)-induced lipid peroxidation. Exposure to B(a)P did not induce oxidative injury because of the involvement of non-enzymatic antioxidants in cell homeostasis. Pyrene did not induce free radicals (FR)-induced injury. Exposure to PAHs-coated onto Fe(2)O(3) particles damaged both the enzymatic (i.e. increases in SOD and GR activities; P<0.01) and the non-enzymatic (i.e. increases in GSSG/GSH; P<0.001, alpha-Toc consumption; P<0.01) antioxidant defenses, thereby allowing lipid peroxidation (i.e. MDA production; P<0.05). Exposure to PAHs-coated onto Fe(2)O(3) particles induced not only higher lipid peroxidation (i.e. MDA production; P<0.05) but also higher antioxidant alterations (i.e. SOD and GR activities; P<0.05, GSSH/GSH; P<0.01 or P<0.05) than either chemical alone. Several mechanisms could account for this result, enhanced uptake of Fe(2)O(3) and/or greater availability of PAHs. Hence, our results indicate that exposure to PAHs-coated onto Fe(2)O(3) particles is more deleterious in lungs than either chemical alone.