Hypoxia-related lipid peroxidation: Evidences, implications and approaches

Claus Behn*, Oscar F. Araneda, Aníbal J. Llanos, Gloria Celedón, Gustavo González

*Autor correspondiente de este trabajo

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

83 Citas (Scopus)


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

Idioma originalInglés
Páginas (desde-hasta)143-150
Número de páginas8
PublicaciónRespiratory Physiology and Neurobiology
EstadoPublicada - 30 sep. 2007
Publicado de forma externa


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