PubMed · 3766296
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D W Wilson, H J Segall, M W Lamé. 1986. Hepatic pathological changes due to hydroxyalkenals.. https://doi.org/10.1007/978-1-4684-5134-4_81
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Recently alpha-chloro fatty aldehydes have been shown to be products of reactive chlorinating species targeting the vinyl ether bond of plasmalogens utilizing a cell-free system. Accordingly, the present experiments were designed to show that alpha-chloro fatty aldehydes are produced by activated neutrophils and to determine their physiologic effects. A sensitive gas chromatography-mass spectrometry technique was developed to detect pentafluorobenzyl oximes of alpha-chloro fatty aldehydes utilizing negative ion chemical ionization. Phorbol 12-myristate 13-acetate activation of neutrophils resulted in the production of both 2-chlorohexadecanal and 2- chlorooctadecanal through a myeloperoxidase-dependent mechanism that likely involved the targeting of both 16 and 18 carbon vinyl ether-linked aliphatic groups present in the sn-1 position of neutrophil plasmalogens. 2-Chlorohexadecanal was also produced by fMLP-treated neutrophils. Additionally, reactive chlorinating species released from activated neutrophils targeted endothelial cell plasmalogens resulting in 2-chlorohexadecanal production. Physiologically relevant concentrations of 2-chlorohexadecanal induced neutrophil chemotaxis in vitro suggesting that alpha-chloro fatty aldehydes may have a role in neutrophil recruitment. Taken together, these studies demonstrate for the first time a novel biochemical mechanism that targets the vinyl ether bond of plasmalogens during neutrophil activation resulting in the production of alpha-chloro fatty aldehydes that may enhance the recruitment of neutrophils to areas of active inflammation.
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The function of the blood-brain barrier (BBB) can be impaired by free radicals. Since free radicals have only a limited diffusion capacity, we tested the possibility whether one of the major secondary lipid peroxidation product - 4-hydroxynonenal, is able to influence the permeability of the BBB. Therefore, we established an in vitro BBB model and tested its capacity to degrade 4-hydroxynonenal. Although, endothelial cells and astrocytes, possess the ability to degrade 4-hydroxynonenal the aldehyde is able to increase the permeability of the BBB. Since aldehydic lipid peroxidation products are metabolized via conjugation with glutathione we proofed that a decrease in glutathione is also able to increase the permeability of the BBB. We concluded that 4-hydroxynonenal is able to impair the BBB function via the decrease of reduced glutathione.