Local Stress-Limiting Systems and their Cardioprotective Effects
Felix Z. Meerson, Alexander V. Galkin in Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
In assessing the mechanism of enhancement of free-radical oxidation in ischemia and reperfusion, it should be borne in mind that in mitochondria, as electrons are transferred to cytochrome oxidase, under normal conditions there can occur a single-electron “side-drop” to dioxygen, giving rise to the active oxygen forms which react with the endogenous substrates in the cell structures, first and foremost with phospholipids. This free-radical lipid oxidation yields peroxide compounds and accordingly the whole process has been termed lipid peroxidation. Our data in Table 1 show that the LPO products are always present and hence the process is always operative in the normal ventricular myocardium. It can also be seen that the intensity of LPO is inversely correlated with the activity of the natural antioxidant agents.
Micronutrients in Healthy Aging and Age-Related Decline in Organ Functions
Kedar N. Prasad in Micronutrients in Health and Disease, 2019
In addition to reactive oxygen and nitrogen species, there are other damaging molecules produced by lipid peroxidation. For example, peroxidation of membrane phospholipids acyl chains generates reactive carbonyl species (alpha-, beta-unsaturated aldehydes, di-aldehydes, and keto-aldehydes), which are relatively stable. These carbonyl species can diffuse from one subcellular compartment to another within the same cell or they can escape from the cells and damage targets far away from the site of formation. These carbonyl species react with cellular constituents and form advanced lipoxidation end products (ALEs), and they play an important role in accelerating aging process.24This is supported by the fact that the level of ALEs in several tissues and species increases with age, and dietary restriction that increases the lifespan and decreases the levels of AELs.
Ageing
Henry J. Woodford in Essential Geriatrics, 2022
Proteins can be affected by oxidation and also glycation, which is the binding of carbohydrates to form advanced glycation end-products (AGE). This can lead to reduced enzyme activity or the accumulation of protein aggregates, including amyloid plaques. Lipid peroxidation can harm bodily membranes. Nucleic acids can also be damaged. This is particularly likely to occur with mitochondrial DNA due to its proximity to free radical production and its more limited repair capacity. Damage to mitochondria can reduce energy availability within the cell. Natural repair mechanisms exist and greatly limit the damage done, but they are imperfect and are highly energy-dependent. Thus, mitochondrial damage may reduce energy availability for cellular repair, further promoting the ageing process.
ALSUntangled No. 47: RT001
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2019
Richard Bedlack
Excess free radicals are the molecular cause of cellular oxidative stress. Free radicals are toxic to cells because they damage DNA and key cellular proteins; however, they also have important physiologic roles in cell signaling and pathogen defense. Most antioxidants work by neutralizing a single free radical. Retrotope postulates that RT001 might be more effective than other antioxidants because it works at the level of lipid (i.e. fatty acid) peroxidation (1). Lipid peroxidation is a chemical reaction in which a free radical converts a fatty acid into a fatty acid peroxide. This chemical reaction also results in another free radical that can peroxidize more fatty acids. This process continues as a self-propagating chain reaction that results in extensive lipid peroxidation. The many resulting fatty acid peroxides are unstable and can form additional free radicals, thus multiplying the initial oxidative stress and causing more cellular injury (8). Deuterium atoms are heavier than hydrogen atoms, therefore peroxidation of D-PUFAs is slower than peroxidation of PUFAs. The slower lipid peroxidation of D-PUFA may lessen or interrupt some of the downstream cellular damage associated with oxidative stress (1). Cell culture studies and animal models of Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease support the idea that RT001 and other D-PUFAs decrease oxidative stress (1, 9–17), but we could not find experimental evidence that D-PUFAs were more potent in a biological context compared to most other antioxidants.
Neuroprotective properties of solanum leaves in transgenic Drosophila melanogaster model of Alzheimer's disease
Published in Biomarkers, 2022
Opeyemi B. Ogunsuyi, Tosin A. Olasehinde, Ganiyu Oboh
In AD, oxidative stress has been reported to mediate a number of pathological events culminating in cognitive dysfunction (Tönnies and Trushina 2017). This therefore, agrees with the result from this study in which the ROS content of AD flies is significantly elevated (p < 0.05), compared to the wcontrol flies. The observed elevation in ROS in the AD fly heads also correlated with elevated production of H2O2 and lipid peroxidation levels. H2O2 is a major source of endogenous ROS capable of being oxidised to the highly reactive OH radical which is capable of eliciting macromolecular damages including lipid peroxidation (Chen et al. 2012). Lipid peroxidation is caused by free radicals through a series of reactions which leads to the oxidation of polyunsaturated lipids, and has been shown to increase in AD; Bourdel-Marchasson et al. (2001) found plasma level of lipid peroxidation higher in AD patients than in healthy controls. This study revealed that the level of lipid peroxidation in the AD flies was significantly higher (p < 0.05) than the wcontrol flies. However, the levels of lipid peroxidation in the AD flies treated with the dietary inclusions of AE and BN leaves are significantly lower (p < 0.05) than the AD flies. This also correlated with significant reduction in ROS and H2O2 levels in these groups of flies suggesting the antioxidant properties of the leaves at reducing free radical production and lipid peroxidation.
Assessment of titanium dioxide nanoparticles toxicity via oral exposure in mice: effect of dose and particle size
Published in Biomarkers, 2019
Sanaa A. Ali, Maha Z. Rizk, Manal A. Hamed, Ezzat I. Aboul-Ela, Nagy S. El-Rigal, Hanan F. Aly, Abdel-Hamid Z. Abdel-Hamid
Marked toxicity of TiO2NPs is reflected on the increase in reactive oxygen species (ROS) resulting in oxidative stress and consequently disorders in different biological functions (Colvin 2003, Long et al. 2006, Jia et al. 2017). There is definitive balance between ROS generation and their elimination by antioxidant defence system. Lipid peroxidation is a chain reaction where oxidants create the breakdown of membrane phospholipids that have polyunsaturated fatty acids (Serdar et al. 2018). Lipid peroxidation causes the damage to bio-membranes which can have important consequences for living organisms (Jemec et al. 2012). During oxidative stress, cells mostly increase their levels of antioxidant enzymes such as glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and CAT (Valavanidis et al. 2006, Yildirim et al. 2018).
Related Knowledge Centers
- Fatty Acid
- Hydroxyl Radical
- Reactive Oxygen Species
- Cell Membrane
- Lipid
- Redox
- Radical
- Polyunsaturated Fat
- Methylene Bridge
- Hydrogen