SO(2) inhalation induces protein oxidation, DNA-protein crosslinks and apoptosis in rat hippocampus.

Previous studies provide evidence for the possible neurotoxicity of SO(2), but little information is available about its mechanisms. In the present study, SO(2) inhalation-induced effects on the protein oxidation, DNA-protein crosslinks and apoptosis in rat hippocampus were studied, by exposing Wistar rats to SO(2) at 14, 28 and 56mg/m(3). The results indicate that the protein carbonyl content, an indicator of protein oxidation, and DNA-protein crosslink coefficient were significantly augmented with concentration-dependent properties. In addition, SO(2) inhalation at all concentrations tested caused the increases of caspase-3 activity and number of TUNEL positive staining neuron and the statistical difference was observed after 28 and 56mg/m(3) exposure, suggesting the occurrence of apoptosis. The results imply that attacking protein, nucleic acids and lipids by free radicals, generated via SO(2) derivatives in vivo, is one of the main mechanisms for SO(2)-induced injuries in central neuronal system.