Catalytic Oxidation of Benzyl Alcohol to Benzaldehyde with Fe/Cu-Cross-Linked Montmorillonite

2011 ◽  
Vol 396-398 ◽  
pp. 1891-1894
Author(s):  
Xue Ju Zhang ◽  
He Song ◽  
Xiang Feng Guo ◽  
Li Hua Jia
Keyword(s):  
Hydrogen Peroxide ◽  
Liquid Phase ◽  
Benzyl Alcohol ◽  
Active Oxygen Species ◽  
Active Oxygen ◽  
Oxygen Species ◽  
Reaction Conditions ◽  
Oxidation Of Benzyl Alcohol ◽  
Excellent Activity ◽  
Phase Oxidation

The Fe/Cu-cross-linked montmorillonite catalysts were synthesized with Linan Na-Mont and characterized by BET, SEM, XRD. Liquid-phase oxidation of benzyl alcohol to benzaldehyde by hydrogen peroxide over Fe/Cu-PILC catalyst in the absence of solvent has been thoroughly investigated. The influence of reaction conditions has also been studied. The results show that Fe/Cu(100)-PILC has excellent activity and reusability in the process. The active oxygen species in the reaction is from the absorbed oxygen of Fe/Cu-PILC.

Lung edema due to hydrogen peroxide is independent of cyclooxygenase products

1984 ◽  
Vol 56 (4) ◽  
pp. 900-905 ◽  
Author(s):  
O. Burghuber ◽  
M. M. Mathias ◽  
I. F. McMurtry ◽  
J. T. Reeves ◽  
N. F. Voelkel
Keyword(s):  
Hydrogen Peroxide ◽  
Glucose Oxidase ◽  
Direct Action ◽  
Active Oxygen Species ◽  
Active Oxygen ◽  
Lung Edema ◽  
Oxygen Species ◽  
Edema Formation ◽  
Prostaglandin Production ◽  
Prostaglandin F2 Alpha

Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary vasoreactivity and cause edema. We chemically produced hydrogen peroxide by adding glucose oxidase to a plasma- and cell-free, but beta-D-glucose-containing, solution, which perfused isolated rat lungs. Addition of glucose oxidase to the perfusate caused a marked decrease in pulmonary vasoreactivity, accompanied by an increase in the concentrations of prostacyclin, thromboxane A2, and prostaglandin F2 alpha. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulmonary vasoreactivity, inhibited the increase of the concentration of the measured prostaglandins, and prevented edema formation. Indomethacin effectively blocked lung prostaglandin production but neither prevented the decrease in vasoreactivity nor inhibited edema formation. From these data we conclude that hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Despite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema.

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