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  • 1
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The role of cytokines and arachidonic acid metabolites in the regulation of IgE production in healthy persons and in atopic dermatitis patients with elevated IgE levels was studied. Interleukin-4 (IL-4) induced IgE production in peripheral blood mononuclear cells (PBMCs) of all donors, and no significant difference was found between the amounts of IgE produced by healthy persons and atopic dermatitis patients. Similarly, recombinant interferon (IFN)-α and IFN-γ, as well as IL-2, inhibited IL-4-induced IgE production to a similar extent in both study groups. To evaluate the role of arachidonic acid (AA) metabolites in the regulation of IgE production, we added indomethacin, an inhibitor of the cyclooxygenase pathway, or nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway, to IL-4-treated cultures. Both indomethacin and NDGA strongly inhibited IL-4-induced IgE production. They also inhibited IL-4-induced IgG4 synthesis. No significant difference in the amount of inhibition was found between the two study groups. We were unable to restore the NDGA-induced inhibition of IgE-production by adding leukotrienes B4, C4, D4, or 5-HETE to the NDGA-treated cultures. PGE2 also failed to restore the indomethacin-mediated inhibitory effect. Consequently, NDGA- and indomethacin-mediated inhibitory effects do not appear to be mediated by any single factor studied. Collectively, our results show IFNs and IL-2 to be similar in effect in the modulation of IL-4-induced IgE synthesis in healthy and atopic persons. In addition, our results show the importance of AA metabolites in the regulation of IgE and IgG4 synthesis in normal persons as well as in atopic dermatitis patients.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Progress in Lipid Research 25 (1986), S. 405-406 
    ISSN: 0163-7827
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0090-6980
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 125 (1991), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of solar-simulated UV-irradiation on the activity of antioxidant enzymes and the amount of diene conjugation were studied in human epidermis in vivo. A single dose of UV-irradiation was found to result in a transient reduction in superoxide dismutase activity and this was followed by increased amounts of conjugated diene double bonds, an index for oxidative stress. This suggests that in-vivo exposure of human epidermis to solar-simulated UV-irradiation causes changes in the enzymic antioxidant defence system which, in turn, are accompanied by increased level of oxidative stress.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 280 (1988), S. 103-107 
    ISSN: 1432-069X
    Keywords: Arachidonic acid ; Retinoids ; Fatty acids ; Keratinocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the effect of etretin (Ro 10-1670), the active metabolite of the widely used antipsoriatic drug etretinate (Ro 10-9359), on the incorporation and release of arachidonic acid in human skin keratinocytes. During 24-h culture, radioactive 14C-arachidonic acid was avidly incorporated into the cellular lipids of the keratinocytes. When the cells were cultured for another 48 h in fresh medium, 8.8%±0.3% of the incorporated radioactivity was released from the cells. The presence of etretin (10-8 M to 10-5 M) in the medium stimulated the release of radiolabel. With 10-5 M etretin in the culture medium, 13.0%±0.4% of the incorporated radioactivity was released, and this was accompanied by decreased labelling of phosphatidylethanolamine. This suggests that phosphatidylethanolamine may be an important source of the released arachidonic acid. Etretin pretreatment reduced the incorporation of 14C-arachidonic acid into diacylglycerols, triacylglycerols, and cholesteryl esters. Pretreatment for 48 h with 10-5 M etretin reduced subsequent 14C-arachidonic acid incorporation into nonphosphorus lipids from a mean total of 8.2%±0.2% to 3.2%±0.1% (p〈0.001). These findings suggest that etretin interferes with the esterification of arachidonic acid into nonphosphorus lipids. Etretin was also found to cause changes in the fatty acid composition of keratinocytes. Following 48 h culture with etretin, the percentage amount of the fatty acids belonging to the n3 series was increased whereas that of palmitic acid (16:0) and palmitoleic acid (16:1n7) was decreased. In conclusion, our study suggests that etretin in therapeutical concentrations affects fatty acid metabolism in human keratinocytes in culture.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 115 (1989), S. 575-578 
    ISSN: 1432-1335
    Keywords: Fatty acids ; Breast cancer ; Phospholipids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The fatty acid composition of fractionated phospholipids and neutral lipids was analyzed in human breast cancer tissues and the surrounding, apparently healthy tissue. In the cancer tissues the relative amounts of unsaturated fatty acids were increased in all the phospholipid subclasses analyzed. The differences were more marked in phosphatidylethanolamine than in the other phospholipid fractions and, furthermore, the relative amount of phosphatidylethanolamine was increased in cancerous tissue. In blood-erythrocyte phospholipids, no differences in fatty acid composition could be found between breast cancer and control patients. The present study suggests that the lipid composition of cancerous breast tissues differs from that of the surrounding tissue and may be involved in carcinogenesis.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 120 (1994), S. 374-377 
    ISSN: 1432-1335
    Keywords: Breast cancer ; Antioxidants ; Lipids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have analysed products of lipid peroxidation reactions and activities of antioxidant enzymes in cancerous breast tissue and in corresponding reference tissue. In addition, the serum lipid peroxidation and peroxyl-radical-trapping capacity of breast cancer patients were compared to those of healthy subjects. A total of 23 patients with breast cancer participated in this study. In the cancerous tissue, catalase activity was lower than in the reference tissue, while the activities of superoxide dismutase, glutathione peroxidase and the hexose monophosphate shunt were elevated. The content of thiobarbituric-acid-reactive material was slightly lower in the cancerous tissues, but the levels in serum were found to be elevated in patients with breast cancer. The amounts of conjugated diene double bonds were essentially equal both in the cancerous and in the reference tissue. Moreover, in breast cancer patients the serum levels of diene conjugation and the peroxyl-radical-scavenging capacity did not differ from those measured in healthy subjects. This study indicates that the antioxidant defence system is altered in cancerous breast tissues, but does not support the hypothesis suggesting that formation of lipid peroxides in the tumour tissue itself is of primary importance in the carcinogenesis.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 278 (1986), S. 441-444 
    ISSN: 1432-069X
    Keywords: Keratinocyte ; Arachidonic acid ; UV irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Following labeling of human keratinocytes in culture for 48 h with 14C-arachidonic acid (800,000 cpm), 86.8±0.5% (mean±SEM) of the radioactivity was incorporated into the cells. Two hours after exposure to UVB irradiation at doses up to 392 mJ/cm2 of erythemally effective (EE) UVB irradiation, only slight changes in the distribution of arachidonic acid could be detected. However, 24 h after irradiation the release of arachidonic acid into the culture medium was significantly increased. The distribution of arachidonic acid was also changed: there was a considerable loss in the amount of radioactivity associated with phosphatidylethanolamine. With doses up to 174 mJ/cm2 (EE) of UVB, the decrease in the labeling of phospholipids was accompanied by an increased arachidonic acid content in the nonphosphorus lipids, especially in the triacylglycerols. Following a high dose of UVB (392 mJ/cm2, EE), a substantial release of label was detected, but the labeling of triacylglycerols was unaltered. The present study suggests that in human keratinocytes UVB irradiation induces the release of arachidonic acid from the cellular lipids and that the major source of the released arachidonic acid is phosphatidylethanolamine.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 20 (1996), S. 451-459 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Exposure to ultraviolet (UV) light impairs the function of inflammatory cells. Urocanic acid (UCA) in an stratum corneum has been suggested as a mediator in the immunosuppression of lymphoid cells detected after irradiation with UVB (UV wavelengths 280–320 nm). In this study, we examined the effects of the two UCA isomers,trans andcis UCA on human polymorphonuclear leukocytes, neutrophils. It was found that treatment of cells with eithertrans ofcis UCA isomers inhibited the opsonized zymosan-induced respiratory burst activity, measured with luminolenhanced chemiluminescence assay. Both isomers were also able to partially block the up-regulation of complement receptors 1 (CR1; CD35) and 3 (CR3; CD11b/CD18) in N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated neutrophils. These results indicate that the isomerization oftrans UCA toeis UCA is not essential for the action of UCA on neutrophils. Neither of the UCA isomers were found to induce cyclic AMP (cAMP) formation in 3-isobutyl-1-methylxanthine treated cells, suggesting that the activation of adenylate cyclase-cAMP system is not involved in UCA provoked suppression of neutrophils. It is concluded that the function of UCA may be protective, to suppress the activation of human neutrophils in inflamed, sunburned epidermis.
    Type of Medium: Electronic Resource
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