Role of Lipid Peroxidation Process in Neurodegenerative Disorders

Abstract

Lipid peroxidation is one of the primary events of the cell injury process. In pathophysiological condition, it is undergoing the initiation of organ damage. Various free radicals are playing a key role in this lipid peroxidation process. Free radical associated organ damage involves the three major phases, that is, initiation, propagation and termination. The primary source of various free radical formations is mediated through the pathophysiological function of mitochondria. Lipid peroxidation is contributed to the multiple neurodegenerative disorders. Thus, the various endogenous cellular anti-oxidant systems are regulated lipid peroxidation process and control the neurodegenerative action. Some of the molecules are targeted to attenuate the lipid peroxidation and their mediators for the prevention of neurodegeneration.

The Neuromelanin Paradox and Its Dual Role in Oxidative Stress and Neurodegeneration

“…Cellular membranes and organelle membranes are especially susceptible to ROS damage, due to their high polyunsaturated fatty acids. ROS-induced lipid peroxidation exerts its deleterious effects through two general mechanisms: (i) loss of the integrity of cellular membranes (it is important to note that this process affects not only the cell membrane, but also the mitochondria, endoplasmic reticulum, and nuclear membranes), and (ii) generation of intermediate and end products, such as lipid hydroperoxides, MDA, 4-HNE, and acrolein that leads to genotoxicity, cytotoxicity, and ultimately, cellular death [ 16 , 17 , 18 , 19 , 20 ]. This type of regulated non-apoptotic peroxidation-driven and iron-dependent cell death mechanism is called “ferroptosis” [ 21 ].…”

Characterization of Sesuvium sesuvioides Using High-Performance Liquid Chromatography and Validation of Its In Vivo Anti-hyperthyroidism Effect via Suppressing Oxidative Stress and Inflammatory Markers

“…Moreover, it was investigated that thyroxine-induced thyroid dysfunction enhanced lipid peroxidation (LPO) reactions and reactive oxygen species (ROS) that may lead to cellular damage and enhance cell death. 32 LPO is responsible for the decreased level of SOD and GSH in hyperthyroid animals and indicative of the decreased oxidative defense system in the body. MDA is a terminal product of LPO, 33 and a marked increased level of MDA was observed in hyperthyroid animals.…”

Detrimental Effects of Lipid Peroxidation in Type 2 Diabetes: Exploring the Neutralizing Influence of Antioxidants

“…However, elevated levels of MDA-mediated adducts have been associated with inflammation and cellular injury, contributing to the development of cardiovascular and chronic liver diseases [ 44 , 45 ]. Additionally, increased levels of MDA have been associated with the pathogenesis of diabetes mellitus, aging, and other neurodegenerative diseases [ 46 , 47 ]. Malondialdehyde has been reported to inhibit cardiac contractile function through phosphorylation of p38 MAP kinase [ 48 ].…”