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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
LIPID PEROXIDATION IN OXIDATIVE HOMEOSTASIS
Abstract number: S56
Zarkovic1 N
1Rudjer Boskovic, Institute, Zagreb, Croatia
Although oxidative stress is commonly considered as excess in production of "toxic oxygen free radicals" due to the fact that reactive oxygen species (ROS) have not only toxic but also important physiological effects oxidative stress does not necessarily imply pathology but often important physiological process, too. Furthermore, in case of progressive chain reactions of lipid peroxidation triggered by oxidative stress usually we also consider mostly pathological aspects of various disorders, such as cancer, cardiovascular pathologies and (neuro)degenerative processes. Even the end products of lipid peroxidation, reactive aldehydes, are denoted as a "second toxic messengers of free radicals" although they are not free radicals, not even ROS, but interact with bioactive macromolecules achieving biological effects that resemble activities of free radicals. However, in recent years biological effects of 4-hydroxynonenal (HNE) considered as major bioactive marker of lipid peroxidation, revealed some of physiological effects of this aldehyde suggesting also certain physiological roles of lipid peroxidation. That might be relevant for cell signaling and regulation of various essential cellular processes such as proliferation, differentiation and apoptosis in particular in case of inflammation, healing and adaptation to stress. The findings of regulatory roles of HNE and oxidative stress are further supported by findings of HNE presence even in the form of protein adducts under physiological circumstances in normal tissues. Therefore, "oxidative homeostasis" is suggested as a novel term implying physiology of oxidative stress and lipid peroxidation that might be important for both physiology and pathophysiology.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :S56