Benzo(a)pyrene-coated onto Fe 2O 3 particles-induced lung tissue injury: role of free radicals

Abstract

Lipid peroxidation (as malondialdehyde; MDA), activities of some antioxidant enzymes (as superoxide dismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glutathione status, and oxidative DNA damage (as 8-hydroxy-2′-deoxyguanosine; 8-OHdG) were investigated in the lungs of rats exposed to hematite (Fe 2O 3; 3 mg), benzo(a)pyrene (B(a)P; 3 mg), or B(a)P (3 mg)-coated onto Fe 2O 3 particles (3 mg). Approximately 2-fold increases in MDA production were seen in animals exposed to Fe 2O 3, B(a)P, or B(a)P-coated onto Fe 2O 3 particles ( P<0.01). Decreases in SOD activities were observed in rats treated with Fe 2O 3 (1.66-fold, P<0.01), B(a)P (1.66-fold, P<0.001) or B(a)P-coated onto Fe 2O 3 particles (1.43-fold, P<0.01). GPx and GR activities could not be detected. No alteration of the glutathione status was observed. Significant increases in the 8-OHdG formation occurred in response to exposure to B(a)P (2.0-fold, P<0.01) or B(a)P-coated onto Fe 2O 3 particles (23.7-fold, P<0.001). Our results demonstrate also that Fe 2O 3 generates free radical (FR)-induced lung injury and is not an inert carrier. We established that exposure to B(a)P or B(a)P-coated onto Fe 2O 3 particles resulted in lipid peroxidation and SOD inactivation, thereby leading to oxidative damages in DNA. The main findings of this work was that B(a)P-coated onto Fe 2O 3 particles caused higher lung concentrations of 8-OHdG than B(a)P by itself. Hence, our data may explain why exposure to B(a)P-coated onto Fe 2O 3 particles resulted in a decreased latency and an increased incidence of lung tumors in rodents compared to exposure to B(a)P.