SO2 inhalation causes synaptic injury in rat hippocampus via its derivatives in vivo

• Published in: Chemosphere (Oxford) 2013-11, Vol.93 (10), p.2426-2432
• Main Authors: Yun, Yang, Yao, Gaoyi, Yue, Huifeng, Guo, Lin, Qin, Guohua, Li, Guangke, Sang, Nan
• Format: Article
• Language: English
• Subjects: Air; biofuels; Biological and medical sciences; breathing; central nervous system diseases; Chemical and industrial products toxicology. Toxic occupational diseases; coal; Cognitive impairment; Developing hippocampal neurons; energy; Environmental pollutants toxicology; Gas, fumes; hippocampus; Ischemic injury; Medical sciences; mortality; neurons; neurotoxicity; rats; risk; SO2; sulfur dioxide; Synaptic plasticity; Toxicology
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2013.08.063

•Ambient SO2 exposure was a potential inducer of neurological diseases.•SO2 exposure produced a neuronal insult is similar to ischemic injury in young neurons.•SO2 exposure induced synaptic dysfunctions might participate in cognitive impairment in more mature neurons.•SO2 exposure induced alterations of synaptic plasticity in rat hippocampus via its derivatives in vivo. SO2 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 SO2 may be associated with neurotoxicity and increased risk of hospitalization and mortality of many brain disorders. However, our understanding of the mechanisms by which SO2 causes harmful insults on neurons remains elusive. To explore the molecular mechanism of SO2-induced neurotoxic effects in hippocampal neurons, we evaluated the synaptic plasticity in rat hippocampus after exposure to SO2 at various concentrations (3.5 and 7mgm−3, 6hd−1, for 90d) 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 SO2/SO2 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, SO2 exposure produced neuronal insult is similar to ischemic injury; while in more mature neurons, SO2 exposure induced synaptic dysfunctions might participate in cognitive impairment. The results implied that SO2 inhalation could cause different neuronal injury during brain development, and suggested that the molecular mechanisms might be involved in the changes of synaptic plasticity.