PubMed · 11289698
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R Brommage, H Vafai. 2000. Rapid embedding protocol for visualizing bone mineral and matrix.. https://doi.org/10.1007/s002230001187
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Previous studies have shown that reactive oxygen species (ROS) enhance arachidonic acid (AA) release and the subsequent AA metabolism in macrophages. The purpose of this study was determined the implication of phospholipases A2 (PLA2s) in these events. Our results show that oxidative stress induced by exogenous adding of hydrogen peroxide or superoxide anion in macrophage RAW 264.7 and mouse peritoneal macrophage cultures caused a marked enhancement of calcium-independent PLA2 (iPLA2) activity,whereas the increment of secreted PLA2 (sPLA2) and calcium-dependent cytosolic PLA2 (cPLA2) activities were slight. This increase of iPLA2 activity by ROS was rapid and dose-dependent. ROS also induced a significant [3H] arachidonic acid (AA) release. The iPLA2 selective inhibitor, bromoenol lactone, almost completely suppressed the mobilization of [3H]AA induced by ROS whereas antisense oligonucleotide against cPLA2 did not have any appreciable effect. Thus, our data show that iPLA2 activity is involved in the mechanism by which ROS increases the availability of free AA in macrophages RAW 264.7. Moreover, the protein kinase C (PKC) inhibitor, calphostin C, and calcium chelators had no effect on the [3H]AA release induced by ROS, suggesting this is a regulatory role of iPLA2.
[reaction: see text] The enantioselective aldol reaction using a novel binuclear zinc catalyst of acetone with several aldehydes gave products in good yields (62-89%) with a high level of enantioselectivity (ee = 76-92%).
The modulation of frontal cortical EEG activation to noxious somatosensory (tail pressure) and olfactory (acetone) stimulation by the basal amygdala was examined in urethane-anesthetized rats. Mild tail pressure produced no EEG activation, while acetone (sniffed by freely breathing rats or drawn across the olfactory epithelium in tracheotomized rats) produced a moderate suppression of large-amplitude synchronized EEG patterns. Concurrent, low-intensity 100 Hz stimulation of the basal amygdala permitted EEG activation to tail pressure to occur, and strongly enhanced olfactory-induced cortical activation. These results indicate that excitation of the basal amygdala potentiates frontal cortical responsiveness to aversive sensory events. This may provide a mechanism to facilitate cortical excitability and processing by amygdaloid neuronal activity.