Abstract
Epidemiological data suggest that plant-derived phenolics beneficial effects include an inhibition of LDL oxidation. After applying a screening method based on 2,4-dinitrophenyl hydrazine- protein carbonyl reaction to 21 different plant-derived phenolic acids, we selected the most antioxidant ones. Their effect was assessed in 5 different oxidation systems, as well as in other model proteins. Mass-spectrometry was then used, evidencing a heterogeneous effect on the accumulation of the structurally characterized protein carbonyl glutamic and aminoadipic semialdehydes as well as for malondialdehyde-lysine in LDL apoprotein. After TOF based lipidomics, we identified the most abundant differential lipids in Cu++-incubated LDL as 1-palmitoyllysophosphatidylcholine and 1-stearoyl-sn-glycero-3-phosphocholine. Most of selected phenolic compounds prevented the accumulation of those phospholipids and the cellular impairment induced by oxidized LDL. Finally, to validate these effects in vivo, we evaluated the effect of the intake of a phenolic-enriched extract in plasma protein and lipid modifications in a well-established model of atherosclerosis (diet-induced hypercholesterolemia in hamsters). This showed that a dietary supplement with a phenolic-enriched extract diminished plasma protein oxidative and lipid damage. Globally, these data show structural basis of antioxidant properties of plant-derived phenolic acids in protein oxidation that may be relevant for the health-promoting effects of its dietary intake.
Highlights
The oxidative stress hypothesis of atherosclerosis is based on the fact that free radical-derived damage participates in atherogenesis pathophysiology by means of LDL modification, among other mechanisms [1,2,3]
These primary lipid oxidation products are fragmented into secondary lipid oxidation products, such as malonyldialdehyde or 4-hydroxynonenal, which can react with the Ng-amino group of lysine residues from LDL apoprotein (Apo B-100)
The antioxidant capacity was quantified after Western Blot of DNP reactive carbonyls in LDL apoproteins (Figure 1A) being the value corresponding to oxLDL considered 0% of antioxidant capacity
Summary
The oxidative stress hypothesis of atherosclerosis is based on the fact that free radical-derived damage participates in atherogenesis pathophysiology by means of LDL modification, among other mechanisms [1,2,3]. The conversion of native LDL into highly modified LDL via oxidative processes can occur by two major mechanisms: In the first case, the events start with the complete loss of LDL’s endogenous antioxidants (i.e., a-tocopherol, ubiquinol-10), followed by the conversion of a majority of the polyunsaturated fatty acids (PUFA) into their corresponding hydroperoxides. These primary lipid oxidation products are fragmented into secondary lipid oxidation products, such as malonyldialdehyde or 4-hydroxynonenal, which can react with the Ng-amino group of lysine residues from LDL apoprotein (Apo B-100). Apoprotein oxidative modifications have been not studied as extensively as lipid-phase ones
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