Antioxidant defense disruption by polycyclic aromatic hydrocarbons-coated onto Fe2O3 particles in human lung cells (A549)

We addressed the hypothesis that in vitro short-term exposure to hematite ( Fe2O3) and polycyclic aromatic hydrocarbons (PAHs) is more deleterious by v irtue of their combinations being able to cause higher oxidative stress con ditions in human lung cells (A549), than either chemical alone. Lipid perox idation (malondialdehyde; MDA), antioxidant enzyme activities (superoxide d ismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glu tathione status (reduced glutathione; GSH, oxidized glutathione; GSSG) and alpha -tocopherol (alpha -Toc) consumption were studied in cells exposed to Fe2O3, 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 Fe2O3-induced lipid peroxidation. Exposure to B(a)P did n ot induce oxidative injury because of the involvement of non-enzymatic anti oxidants in cell homeostasis. Pyrene did not induce free radicals (FR)-indu ced injury. Exposure to PAHs-coated onto Fe2O3 particles damaged both the e nzymatic (i.e. increases in SOD and GR activities; P < 0.01) and the non-en zymatic (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 Fe2O3 particles induced not only higher lipid peroxidation (i.e. MDA production; P < 0.05) but als o higher antioxidant alterations (i.e. SOD and GR activities; P < 0.05, GSS H/GSH; P < 0.01 or P < 0.05) than either chemical alone. Several mechanisms could account for this result, enhanced uptake of Fe2O3 and/or greater ava ilability of PAHs. Hence, our results indicate that exposure to PAHs-coated onto Fe2O3 particles is more deleterious in lungs than either chemical alo ne. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.