Abstract

Non-enzymatic modification of aminophospholipids by lipid peroxidation-derived aldehydes and reducing sugars through carbonyl-amine reactions are thought to contribute to the age-related deterioration of cellular membranes and to the pathogenesis of diabetic complications. Much evidence demonstrates the modification of aminophospholipids by glycation, glycoxidation and lipoxidation reactions. Therefore, a number of early and advanced Maillard reaction-lipid products have been detected and quantified in different biological membranes. These modifications may be accumulated during aging and diabetes, introducing changes in cell membrane physico-chemical and biological properties.

Highlights

  • Maillard reaction-derived molecular damage is a natural consequence of aerobic life

  • Despite the fact that non-enzymatic modification of aminophospholipids by glycation, carboxymethylation and lipid peroxidation has been described, they represent only a limited range of the possible products that can likely be formed by the Maillard reaction

  • In a liquid chromatography (LC)-mass spectrometry (MS)-based study, it was reported that 1.2% and 2.3% of total PE were glycated in human red blood cells (RBC) and in plasma lipids, respectively

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Summary

Introduction

The wide range of processes in which phospholipids are involved explains the need for diversity in phospholipid structures and fatty acid composition [6,10]. Aminophospholipids have been implicated in a diverse array of processes ranging from cell proliferation to cell death, from catabolism to inflammation [12] In this scenario, asymmetry is maintained by active ATP-dependent processes, suggesting that is critical to normal cell function. In eukaryotic cells from vertebrate species, the average chain length of a biological membrane is strictly maintained by around 18 carbon atoms, and the relative distribution between saturated and unsaturated fatty acids follows the ratio. The mechanisms of the homeostatic regulation of the membrane composition, the mechanisms that create lipid asymmetry and their functional implications, and the full definition of the utility of the eukaryotic lipid repertoire are beginning to be understood, being an exciting and rapidly expanding field

Membrane Unsaturation and Lipid Peroxidation
Non-Enzymatic Modification of Cellular Components
Chemical Modification of Aminophospholipids by Carbonyl-Amine Reactions
Biological Significance of MRPs in Aminophospholipids
Physiological Significance of MRPs in Lipids
Findings
Summary
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