“…2). Unidentified peaks were not included in the calculation of the percentage in total fatty acid [5, 6]. Values are expressed as % total fatty acids, and total fatty acid concentration (nmol/g viscera) was calculated by comparison of gas chromatography peak areas relative to that of the C17:0 internal standard.Fig.…”
BackgroundTo investigate the changes of polyunsaturated fatty acids (PUFAs) and their downstream eicosanoids in patients with asthma, the levels of erythrocyte membrane lipids and plasma lipid metabolites were examined.MethodsErythrocyte membrane lipids were extracted and esterificated, and then fatty acid compositions were determined by gas chromatography. The concentrations of six eicosanoids of PGE2, TXA2, LTB4, PGE1, 6-k-PGF1α and PGF2α in plasma were measured by ELISA.ResultsThe results showed that the contents of erythrocyte membrane fatty acids in patients with asthma were mainly composed of C16:0, C18:0, C18:1, C18:2(n-6), and C20:4(n-6). The ratio n-6/n-3 PUFAs in patients and health persons were (4.42 ± 1.33):1 and (3.21 ± 0.79):1 (p < 0.01), showing statistically significant differences. ELISA results showed that the levels of plasma PGE2, TXB2, and PGE1 in patients were higher than health persons; and the levels of eicosanoids of PGF2α and 6-k-PGF1α were significantly lower in patient group than healthy group (p < 0.05), but LTB4 was no obvious difference (p = 0.09). Increased ratio of n-6/n-3 PUFAs is consistent to the increased levels of pro-inflammatory PGE2 and TXB2 and anti-inflammatory PGE1 originated from C20:4(n-6) and C18:2(n-6), indicating that increased ratio of n-6/n-3 PUFAs and eicosanoids from n-6 PUFAs might promote the progress of airway inflammation of asthma.ConclusionChanges of erythrocyte fatty acids, n-6/n-3 PUFAs ratio and the levels of plasma PGE2, TXB2, and PGE1 in patients with asthma were relevant to airway inflammation in some extent. Therefore, it could be proposed that increase of n-3/n-6 PUFAs ratio by diet supplementation of n-3 PUFAs might effectively improve airway inflammation in asthma.
“…2). Unidentified peaks were not included in the calculation of the percentage in total fatty acid [5, 6]. Values are expressed as % total fatty acids, and total fatty acid concentration (nmol/g viscera) was calculated by comparison of gas chromatography peak areas relative to that of the C17:0 internal standard.Fig.…”
BackgroundTo investigate the changes of polyunsaturated fatty acids (PUFAs) and their downstream eicosanoids in patients with asthma, the levels of erythrocyte membrane lipids and plasma lipid metabolites were examined.MethodsErythrocyte membrane lipids were extracted and esterificated, and then fatty acid compositions were determined by gas chromatography. The concentrations of six eicosanoids of PGE2, TXA2, LTB4, PGE1, 6-k-PGF1α and PGF2α in plasma were measured by ELISA.ResultsThe results showed that the contents of erythrocyte membrane fatty acids in patients with asthma were mainly composed of C16:0, C18:0, C18:1, C18:2(n-6), and C20:4(n-6). The ratio n-6/n-3 PUFAs in patients and health persons were (4.42 ± 1.33):1 and (3.21 ± 0.79):1 (p < 0.01), showing statistically significant differences. ELISA results showed that the levels of plasma PGE2, TXB2, and PGE1 in patients were higher than health persons; and the levels of eicosanoids of PGF2α and 6-k-PGF1α were significantly lower in patient group than healthy group (p < 0.05), but LTB4 was no obvious difference (p = 0.09). Increased ratio of n-6/n-3 PUFAs is consistent to the increased levels of pro-inflammatory PGE2 and TXB2 and anti-inflammatory PGE1 originated from C20:4(n-6) and C18:2(n-6), indicating that increased ratio of n-6/n-3 PUFAs and eicosanoids from n-6 PUFAs might promote the progress of airway inflammation of asthma.ConclusionChanges of erythrocyte fatty acids, n-6/n-3 PUFAs ratio and the levels of plasma PGE2, TXB2, and PGE1 in patients with asthma were relevant to airway inflammation in some extent. Therefore, it could be proposed that increase of n-3/n-6 PUFAs ratio by diet supplementation of n-3 PUFAs might effectively improve airway inflammation in asthma.
“…Moreover, we did not find conservation of the iron liganding residues suggesting that the sequences of interest may not encode for functional LOXs. The occurrence of LOX in single cell organisms, in plants and lower metazoa [15–17] has been reviewed before but distribution of LOX isoforms in multicellular vertebrates has not been summarized systematically.…”
Section: Lipoxygenase Distribution Classification and Propertiesmentioning
Lipoxygenases (LOXs) form a heterogeneous class of lipid peroxidizing enzymes, which have been implicated in cell proliferation and differentiation but also in the pathogenesis of various diseases with major public health relevance. As other fatty acid dioxygenases LOX oxidize polyunsaturated fatty acids to their corresponding hydroperoxy derivatives, which are further transformed to bioactive lipid mediators (eicosanoids and related substances). On the other hand, lipoxygenases are key players in regulation of the cellular redox homeostasis, which is an important element in gene expression regulation. Although the first mammalian lipoxygenases were discovered 40 years ago and although the enzymes have been well characterized with respect to their structural and functional properties the biological roles of the different lipoxygenase isoforms are not completely understood. This review is aimed at summarizing the current knowledge on the physiological roles of different mammalian LOX-isoforms and their patho-physiological function in inflammatory, metabolic, hyperproliferative, neurodegenerative and infectious disorders.
“…Lipoxygenases (LOXs) form a heterogeneous family of fatty acid dioxygenases (Haeggstrom & Funk, ), which frequently occur in higher plants (Andreou & Feussner, ) and mammals (Kuhn, Banthiya, & Leyen, ) but have also been detected in lower organisms (Anterola et al, ; Hansen et al, ; Horn et al, ; Mortimer, Järving, Brash, Samel, & Järving, ; Yuan et al, ). In mammals, LOXs have been implicated in cell differentiation and maturation (Brash, Yu, Boeglin, & Schneider, ; Krieg & Furstenberger, ; Rapoport & Schewe, ; van Leyen, Duvoisin, Engelhardt, & Wiedmann, ) but also play important roles in human pathologies (Ackermann, Hofheinz, Zaiss, & Kronke, ; Chen, Sheller, Johnson, & Funk, ; Colakoglu, Tuncer, & Banerjee, ; Eckl et al, ; Haeggstrom & Funk, ; Harats et al, ; Kronke et al, ; Kuhn et al, ).…”
Lipoxygenases are lipid peroxidizing enzymes, which frequently occur in higher plants and mammals. These enzymes are also expressed in lower multicellular organisms but here they are not widely distributed. In bacteria, lipoxygenases rarely occur and evaluation of the currently available bacterial genomes suggested that <0.5% of all sequenced bacterial species carry putative lipoxygenase genes. We recently rescreened the public bacterial genome databases for lipoxygenase‐like sequences and identified two novel lipoxygenase isoforms (
MF‐LOX1 and MF‐LOX2
) in the halotolerant
Myxococcus fulvus
. Both enzymes share a low degree of amino acid conservation with well‐characterized eukaryotic lipoxygenase isoforms but they involve the catalytically essential iron cluster. Here, we cloned the
MF‐LOX1
cDNA, expressed the corresponding enzyme as N‐terminal hexa‐his‐tag fusion protein, purified the recombinant enzyme to electrophoretic homogeneity, and characterized it with respect to its protein‐chemical and enzymatic properties. We found that
M. fulvus
expresses a catalytically active intracellular lipoxygenase that converts arachidonic acid and other polyunsaturated fatty acids enantioselectively to the corresponding n‐9 hydroperoxy derivatives. The enzyme prefers C
20
‐ and C
22
‐polyenoic fatty acids but does not exhibit significant membrane oxygenase activity. The possible biological relevance of
MF‐LOX1
will be discussed in the context of the suggested concepts of other bacterial lipoxygenases.
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