Hypoxia-related lipid peroxidation: evidences, implications and approaches.

摘要: Abstract Hypoxia may be intensified by concurrent oxidative stress. Lack of oxygen in relation to aerobic ATP requirements, as hypoxia has been defined, goes along with an increased generation reactive species (ROS). Polyunsaturated fatty acids (PUFAs) range among the molecules most susceptible ROS. Oxidative breakdown n-3 PUFAs compromise not only membrane lipid matrix dynamics, and hence structure function membrane-associated proteins like enzymes, receptors, transporters, but also gene expression. Eicosapentaenoic acid depletion, products peroxidation (LP), well as, lack combine exacerbating activity nuclear factor kappa B (NFκB), ubiquitous pro-inflammatory anti-apoptotic transcription factor. Field studies at high altitude show malondialdehyde (MDA) content exhaled breath condensate (EBC) mountaineers correlate Lake Louis score acute mountain sickness. A pathogenic role LP can therefore expected. By control LP, some seem cope more efficiently than others naturally occurring hypoxia. Limitation potential effects hypoxia-related adequate provision antioxidants contribute increase survival under conditions where is lacking requirements. need for antioxidant intervention, however, should weighed against ROS requirement triggering adaptive processes response demand oxygen.