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Oxidant stress and essential fatty acids in patients with risk and established ARDS

Oxygen free radicals are important mediators of both physiological and pathological events. In acute lung injury, the activated lymphocytes stimulate tumor necrosis factor (TNF) and other cytokines. These lymphokines augment free radical generation by polymorphonuclear leukocytes (PMNLs), macrophage...

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Bibliographic Details
Published in:Clinica chimica acta 2000-08, Vol.298 (1), p.111-120
Main Authors: Kumar, K.Vijay, Rao, S.Manimala, Gayani, R, Mohan, I.Krishna, Naidu, M.U.R
Format: Article
Language:English
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Summary:Oxygen free radicals are important mediators of both physiological and pathological events. In acute lung injury, the activated lymphocytes stimulate tumor necrosis factor (TNF) and other cytokines. These lymphokines augment free radical generation by polymorphonuclear leukocytes (PMNLs), macrophages and other cells which may ultimately produce acute respiratory distress syndrome (ARDS). This is supported by our results presented here in that there is a significant increase in lipid peroxidation products in patients with established ARDS. The amount of lipid peroxidation was significantly higher in the established ARDS group compared to patients who are at risk for ARDS. Nitric oxide concentrations were significantly decreased in established ARDS compared to the control and those who are at risk for ARDS. Fatty acid analysis of the plasma phospholipid fraction revealed a significant decreased in linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid levels of n-6 series and alpha-linolenic acid, eicosapentaenoic acid, docosa-hexanenoic acid of n-3 series. Patients who are at risk for ARDS have decreased levels of gamma-linolenic acid of the n-6 series, alpha-linolenic acid and eicosapentaenoic acid of the n-3 series. These results suggest that lipid peroxides and alteration in essential fatty acid metabolism may have a role in the pathogenesis of ARDS.
ISSN:0009-8981
1873-3492
DOI:10.1016/S0009-8981(00)00264-3