In the late ‘70s Zilversmit hypothesized that the dramatic postprandial modification of the plasma lipid pattern could have a significant effect on atherogenesis. Since then, several evidence has been collected, and it has been demonstrated that many events happening during the postprandial phase, such as oxidative stress and inflammation, are strongly linked to atherosclerosis.
At the moment, there is clear scientific evidence that during the postprandial phase there is an impairment of the redox status (postprandial oxidative stress) that could be determined by (1) the aspecific intake of macronutrients, whose catabolism can lead to the production of oxygen-radical species, or (2) the intake of oxidized/ prooxidant species, which, when absorbed, can directly modify the redox balance.
Thus eating regular meals throughout the day can result in a constant oxidative condition that depends on the relative intake of oxidizable or oxidized nutrients and that of antioxidants. This chapter will focus on the role of dietary lipid hydroper oxides and antioxidants in determining the extent of postprandial oxidative stress.
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Natella, F., Ramberti, A., Scaccini, C. (2008). Postprandial Events as a Trigger for Redox Unbalance: Role of Dietary Lipid Hydroperoxides and Antioxidants. In: Valacchi, G., Davis, P.A. (eds) Oxidants in Biology. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-8399-0_16
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