Gas-Phase Reaction Kinetic Study of a Series of Methyl-Butenols with Ozone under Atmospherically Relevant Conditions.

Methyl-butenols are a category of oxygenated biogenic volatile organic compounds emitted by plants as part of their natural metabolic processes. This study examines the gas-phase reactions of ozone (O3) with five methyl-butenols (2-methyl-3-buten-2-ol, 3-methyl-2-buten-1-ol, 3-methyl-3-buten-1-ol, 2-methyl-3-buten-1-ol, and 3-methyl-3-buten-2-ol) under atmospheric conditions at a temperature of (298 ± 2) K and pressure of (1000 ± 10) mbar. The experimental values for the gas-phase reaction rate coefficients obtained in this study, by using the relative rate method, are as follows (in cm3 molecule-1 s-1): k(3-methyl-2-buten-1-ol + O3) = (311 ± 20) × 10-18, k(2-methyl-3-buten-2-ol + O3) = (9.55 ± 1.04) × 10-18, k(3-methyl-3-buten-1-ol + O3) = (7.29 ± 0.46) × 10-18, k(2-methyl-3-buten-1-ol + O3) = (4.25 ± 0.29) × 10-18, and k(3-methyl-3-buten-2-ol + O3) = (62.9 ± 6.8) × 10-18. The results are discussed in detail, with particular emphasis on the degree and type of substitutions of the double bond. The determined rate coefficient values are also compared to the available literature data and with estimates of the structure-activity relationship. Additionally, the atmospheric implications toward the tropospheric lifetime and photochemical ozone generation potential for the investigated compounds are provided, which highlight the atmospheric impact of methyl-butenol decomposition into the lower atmosphere.

Gas-Phase Kinetic Investigation of the OH-Initiated Oxidation of a Series of Methyl-Butenols under Simulated Atmospheric Conditions.

Five biogenic unsaturated alcohols have been investigated under simulated atmospheric conditions regarding their gas-phase OH reactivity. The gas-phase rate coefficients of OH radicals with 2-methyl-3-buten-2-ol (k1), 3-methyl-2-buten-1-ol (k2), 3-methyl-3-buten-1-ol (k3), 2-methyl-3-buten-1-ol (k4), and 3-methyl-3-buten-2-ol (k5) at 298 ± 2 K and 1000 ± 10 mbar total pressure of synthetic air were determined under low- and high-NOx conditions using the relative kinetic technique. The present work provides for the first time the rate coefficients of gas-phase reactions of hydroxyl radicals with 2-methyl-3-buten-1-ol and 3-methyl-3-buten-2-ol. The following rate constants were measured (in 10-11 cm3 molecule-1 s-1): k1 = 6.32 ± 0.49, k2 = 14.55 ± 0.93, k3 = 10.04 ± 0.78, k4 = 5.31 ± 0.37, and k5 = 11.71 ± 1.29. No significant differences in the measured rate coefficients were obtained when either 365 nm photolysis of CH3ONO in the presence of NO or 254 nm photolysis of H2O2 was used as a source of OH radicals. Reactivity toward other classes of related compounds such as alkenes and saturated alcohols is discussed. A comparison of the structure-activity relationship (SAR) estimates derived from the available accepted methodologies with experimental data available for unsaturated alcohols is provided. Atmospheric lifetimes for the investigated series of alkenols with respect to the main atmospheric oxidants are given and discussed.

Lipopolysaccharide-induced fever depends on prostaglandin E2 production specifically in brain endothelial cells.

Immune-induced prostaglandin E2 (PGE2) synthesis is critical for fever and other centrally elicited disease symptoms. The production of PGE2 depends on cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (mPGES-1), but the identity of the cells involved has been a matter of controversy. We generated mice expressing mPGES-1 either in cells of hematopoietic or nonhematopoietic origin. Mice lacking mPGES-1 in hematopoietic cells displayed an intact febrile response to lipopolysaccharide, associated with elevated levels of PGE2 in the cerebrospinal fluid. In contrast, mice that expressed mPGES-1 only in hematopoietic cells, although displaying elevated PGE2 levels in plasma but not in the cerebrospinal fluid, showed no febrile response to lipopolysaccharide, thus pointing to the critical role of brain-derived PGE2 for fever. Immunohistochemical stainings showed that induced cyclooxygenase-2 expression in the brain exclusively occurred in endothelial cells, and quantitative PCR analysis on brain cells isolated by flow cytometry demonstrated that mPGES-1 is induced in endothelial cells and not in vascular wall macrophages. Similar analysis on liver cells showed induced expression in macrophages and not in endothelial cells, pointing at the distinct role for brain endothelial cells in PGE2 synthesis. These results identify the brain endothelial cells as the PGE2-producing cells critical for immune-induced fever.