Are Polyunsaturated Fatty Acid Metabolites, the Protective Effect of 4‑hydroxytyrosol on Human Red Blood Cell Membranes and Oxidative Damage (4‑hydroxyalkenals) Compatible in Hypertriglyceridemic Patients?

Background: Increased levels of malondialdehyde (MDA) and 4‑hydroxynonenal (HNE) are demonstrated in plasma of uremic patients. A study showed that the comparison of erythrocytes of healthy and diseased patients (obese, hypertensive, and Type 2 diabetics) with age is associated to a disturbed oxidant/antioxidant balance when obesity is associated with hypertension. 4‑hydroxytyrosol is shown to significantly protect red blood cells (RBCs) from oxidative damage (4‑HNE). In literature, there are partial discussions on the role of lipids and their oxidation products. The products of degradation of membrane proteins are observed as self‑consisting products without interrelations with membrane lipids. Objective: The aim of this study is to evaluate the role of polyunsaturated fatty acid (PUFA) metabolites on oxidative damage (4‑hydroxy‑alkenals) in RBCs of hypertriglyceridemic patients after membrane treatment with 4‑hydroxytyrosol. Materials and Methods: The authors optimize the isolation of RBC ghosts and spectrophotometric method to measure free 4‑hydroxyalkenals in human RBC membranes and investigated the effect on oxidative damage in human erythrocyte membranes and in vitro 4‑hydroxytyrosol treatment to evaluate the membrane lipids reducible by this phenol. Results: Plasma triglyceride levels in patients are clearly higher than in controls. Moreover, total membrane proteins data are similar to previous described. The normalized alkenals levels are significantly enhanced in hyperlipemic patients in comparison to normoglyceridemic controls. After the 4‑hydroxytyrosol action, lipid metabolites substantially decrease. The ratio of oxidized lipids (MDA + HNE) and membrane proteins data are similar to previously described ones. Conclusion: According to experimental data, the accumulation of the alkenals in RBC membrane could be produced either by partial PUFA oxidation contained in glycerides and plasma glycerides and by glycerides into plasma membrane recycled RBC.