Differential effects between one week and four weeks exposure to same mass of SO2 on synaptic plasticity in rat hippocampus.

Sulfur dioxide (SO2 ) is a ubiquitous air pollutant. The previous studies have documented the adverse effects of SO2 on nervous system health, suggesting that acutely SO2 inhalation at high concentration may be associated with neurotoxicity and increase risk of hospitalization and mortality of many brain disorders. However, the remarkable features of air pollution exposure are lifelong duration and at low concentration; and it is rarely reported that whether there are different responses on synapse when rats inhaled same mass of SO2 at low concentration with a longer term. In this study, we evaluated the synaptic plasticity in rat hippocampus after exposure to same mass of SO2 at various concentrations and durations (3.5 and 7 mg/m(3) , 6 h/day, for 4 weeks; and 14 and 28 mg/m(3) , 6 h/day, for 1 week). The results showed that the mRNA level of synaptic plasticity marker Arc, glutamate receptors (GRIA1, GRIA2, GRIN1, GRIN2A, and GRIN2B) and the protein expression of memory related kinase p-CaMKпα were consistently inhibited by SO2 both in 1 week and 4 weeks exposure cases; the protein expression of presynaptic marker synaptophysin, postsynaptic density protein 95 (PSD-95), protein kinase A (PKA), and protein kinase C (PKC) were increased in 1 week exposure case, and decreased in 4 weeks exposure case. Our results indicated that SO2 inhalation caused differential synaptic injury in 1 week and 4 weeks exposure cases, and implied the differential effects might result from different PKA- and/or PKC-mediated signal pathway. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 820-829, 2016.

Chronic SO2 inhalation above environmental standard impairs neuronal behavior and represses glutamate receptor gene expression and memory-related kinase activation via neuroinflammation in rats.

Sulfur dioxide (SO2), as a ubiquitous air pollutant implicated in the genesis of pulmonary disease, is now being considered to be involved in neurotoxicity and increased risk for hospitalization of brain disorders. However, comparatively little is known about the impact of chronically SO2 inhalation on neuronal function. In the present study, by exposing male Wistar rats to SO2 at 3.50 and 7.00 mg/m(3) (approximately 1225 and 2450 ppb, 4.08-8.16 (24h average concentration) times higher than the EPA standard for environmental air concentrations) or filtered air for 90 days, we investigated the impact of chronic SO2 inhalation on performance in Morris water maze, and probed the accompanying neurobiological effects, including activity-regulated cytoskeletal associated gene (Arc) and glutamate receptor gene expression, memory-related kinase level and inflammatory cytokine release in the hippocampus. Here, we found that SO2 exposure reduced the number of target zone crossings and time spent in the target quadrant during the test session in the spatial memory retention of the Morris water maze. Following the neuro-functional abnormality, we detected that SO2 inhalation reduced the expression of Arc and glutamate receptor subunits (GluR1, GluR2, NR1, NR2A, and NR2B) with a concentration-dependent property in comparison to controls. Additionally, the expression of memory kinases was attenuated statistically in the animals receiving the higher concentration, including protein kinase A (PKA), protein kinase C (PKC) and calcium/calmodulin-dependent protein kinaseIIα (CaMKIIα). And the inflammatory cytokine release was increased in rats exposed to SO2. Taken together, our results suggest that long-term exposure to SO2 air pollution at concentrations above the environmental standard in rats impaired spatial learning and memory, and indicate a close link between the neurobiological changes highlighted in the brain and the behavioral disturbances.

SO(2) inhalation causes synaptic injury in rat hippocampus via its derivatives in vivo.

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.

Analyzing nutrient distribution in different particle-size municipal aged refuse.

To investigate the feasibility of using aged municipal solid waste as farmland soil, it is essential to study its nutritive compositions for plant growth. Previous studies have demonstrated that the properties of different particle-size aged refuse are very different, therefore, the present study was conducted to evaluate the adequacy of three elements (N, P, K) and the fractionation of inorganic P in the aged refuse with a particle-size distribution of 900 to 300, 300 to 150, 150 to 105, 105 to 90 and 90 to 0 µm. The results indicate that (1) total quantities of N, P, K were much larger than that in the general soil and the quantities of available N, P and K were also adequate; (2) total content of P was sufficient, but the ratio of available-P to total P was not high enough; (3) with the decrease of particle size, the contents of these elements presented different trends. The results implicate that total contents of N, P and K were enough for the aged refuse being exploited as cultivated soil, and different gradation of aged refuse could be added to improve poor soils. It provides scientific evidence for utilizing different particle-size aged refuse comprehensively.

SO(2)-induced neurotoxicity is mediated by cyclooxygenases-2-derived prostaglandin E(2) and its downstream signaling pathway in rat hippocampal neurons.

Sulfur dioxide (SO(2)) pollution in atmospheric environment is involved in neurotoxicity and increased risk for hospitalization and mortality of many brain disorders; however, our understanding of the mechanisms by which SO(2) caused harmful insults on neurons remains elusive. Here, we show that SO(2) exposure produced a neuronal insult, and the neurotoxic effect was likely via stimulating cyclooxygenase-2 (COX-2) elevation by activation of nuclear factor-κB (NF-κB) activity and its acting on the promoter-distal NF-κB-binding site of COX-2 promoter. The action of SO(2) on elevating COX-2 ultimately appeared to be dependent on the increased production of arachidonic acid-derived prostaglandins, mainly prostaglandin E(2) (PGE(2)), and functioning of its EP2/4 receptors. Also, the molecular modulating process might be triggered by free radical attack from SO(2) metabolism in vivo and followed by activating cyclic adenosine monophosphate/protein kinase A pathway and enhancing probability of the release of glutamate, upregulating N-methyl-D-aspartic acid receptor expression and causing neuronal apoptosis. Our results reveal a mechanistic basis for exploring an association between SO(2) inhalation and increased risk for neurological disorders and opening up therapeutic approaches of treating, ameliorating, or preventing brain injuries resulting from SO(2) exposure in atmospheric polluting environment.