Acrolein [HRP]

Accidents related to spilling of chemicals and chemical wastes are never ceasing, especially as our reliance on chemical products increases continuously. For the sake of workers' safety and maintenance of our environment, it is important to not only reduce the frequency of such accidents but also minimize the damage from each accident through proper spill control methods. Our focus here is to address the issues regarding rapid evaporation of the hazardous volatile organic liquids spills and propose a potential sorbent material, cellulose acetate, which can significantly reduce the rate of evaporation of highly volatile chemicals such as acetone, acrolein, and propylene oxide. Compared to conventional chemical sorbents such as activated carbon, expanded vermiculite, and cellulose, cellulose acetate not only exhibits higher vapor retention abilities, but also demonstrates comparable sorption efficiencies for sorption of acetone, acrolein, and propylene oxide. Cellulose acetate is also an environmentally friendly and economical material that is safe to use even for sorption of highly flammable chemicals, thus, its potential as a new class of commercial chemical sorbent is very promising. [GRAPHICS] .

Clinically, high levels of acrolein (a highly reactive alpha, beta-unsaturated aldehyde) and acrolein adducts are detected in the brain of patients with CNS neurodegenerative diseases, including Alzheimer's disease and spinal cord injury. Our previous study supports this notion by showing acrolein as a neurotoxin in a Parkinsonian animal model. In the present study, the effect of AZD6244 (an ATP non-competitive MEK1/2 inhibitor) on acrolein-induced neuroinflammation was investigated using BV-2 cells and primary cultured microglia. Our immunostaining study showed that lipopolysaccharide (LPS, an inflammation inducer as a positive control) increased co-localized immunoreactivities of phosphorylated ERK and ED-1 (a biomarker of activated microglia) in the treated BV-2 cells. Similar elevation in co-localized immunoreactivities of phosphorylated ERK and ED-1 was detected in the acrolein-treated BV-2 cells. Furthermore, Western blot assay showed increases in phosphorylated ERK in BV-2 cells subjected to LPS (1 mu g/mL) or acrolein (30 mu M); these increases were blocked by AZD6244 (10 mu M). At the same time, AZD6244 attenuated LPS-induced TNF-alpha (a pro-inflammatory cytokine) and cyclooxygenase-II (COX II, a pro-inflammatory enzyme). Consistently, AZD6244 reduced acrolein-induced elevations in COX-II mRNA and COX-II protein expression. In addition, AZD6244 inhibited acrolein-induced increases in activated caspase 1 (a biomarker of inflammasome activation) and heme oxygenase-1 (a redox-regulated chaperone protein) in BV-2 cells. Using a transwell migration assay, AZD6244 attenuated acrolein (5 mu M)-induced migration of BV-2 cells and primary cultured microglia. In conclusion, our study shows that acrolein is capable of inducing neuroinflammation which involved ERK activation in microglia. Furthermore, AZD6244 is capable of inhibiting acrolein-induced neuroinflammation. Our study suggests that ERK inhibition may be a neuroprotective target against acrolein-induced neuroinflammation in the CNS neurodegenerative diseases.