SO(2) remains a common air pollutant, almost half of the world's population uses coal and biomass fuels for domestic energy. Limited evidence suggests that exposure to SO(2) may be associated with neurotoxicity and increased risk of hospitalization and mortality of many brain disorders. However, our understanding of the mechanisms by which SO(2) causes harmful insults on neurons remains elusive. To explore the molecular mechanism of SO(2)-induced neurotoxic effects in hippocampal neurons, we evaluated the synaptic plasticity in rat hippocampus after exposure to SO(2)at various concentrations (3.5 and 7 mg m(-3), 6 h d(-1), for 90 d) in vivo, and in primary cultured hippocampal neurons (DIV7 and DIV14) after the treatment of SO2 derivatives in vitro. The results showed that SYP, PSD-95, NR-2B, p-ERK1/2 and p-CREB were consistently inhibited by SO(2)/SO(2) derivatives in more mature hippocampal neurons in vivo and in vitro, while the effects were opposite in young hippocampal neurons. Our results indicated that in young neurons, SO(2) exposure produced neuronal insult is similar to ischemic injury; while in more mature neurons, SO(2) exposure induced synaptic dysfunctions might participate in cognitive impairment. The results implied that SO(2) inhalation could cause different neuronal injury during brain development, and suggested that the molecular mechanisms might be involved in the changes of synaptic plasticity.

作者：Yang, Yun；Gaoyi, Yao；Huifeng, Yue；Lin, Guo；Guohua, Qin；Guangke, Li；Nan, Sang

来源：Chemosphere 2013 年 93卷 10期