Abstract
Recent evidence suggests that in addition to their well studied toxic effects, reactive oxygen species (ROS) are also essential mediators of cell growth, differentiation and apoptosis (Sen and Packer, 1996; Lander, 1997). Nonetheless, the mechanisms by which ROS alter cell function remain obscure. Since free radicals derived from oxygen are generally short-lived and react predominantly at their site of generation, it is likely that their metabolic as well as the toxic effects are mediated, in part, by their metastable products, particularly those derived from the peroxidation of membrane lipids. Peroxidation of unsaturated fatty acids generates a variety of metastable compounds of which aldehydes are the most abundant end-products (Esterbauer et al., 1991; Witz, 1983). In comparison only minor amounts of ketones, epoxides, hydrocarbons, alcohols and acids are formed (Grosch, 1987). Therefore, in cellular systems, aldehyde burden may be an important consequence of lipid peroxidation.
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Bhatnagar, A., Srivastava, S., Wang, LF., Chandra, A., Ansari, N.H., Srivastava, S.K. (1999). Cardiac Metabolism of Enals. In: Weiner, H., Maser, E., Crabb, D.W., Lindahl, R. (eds) Enzymology and Molecular Biology of Carbonyl Metabolism 7. Advances in Experimental Medicine and Biology, vol 463. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4735-8_27
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DOI: https://doi.org/10.1007/978-1-4615-4735-8_27
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