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Ageing, Neurodegeneration and Alzheimer's Disease
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Richard J. Elsworthy, Sarah Aldred
Lipid peroxidation has also been measured in AD by monitoring relatively stable products of fatty acid oxidation. The enzymatic and radical-mediated oxidation of arachidonic and docosahexaenoic acid produces prostaglandin-like F2-Isoprostanes and neuroprostanes respectively, which are commonly used for quantifying oxidative distress ‘in vivo’ (Yoshida et al., 2013). Although oxidative distress is widely regarded as a consistent feature of AD, there have been studies showing little to no change in total lipid and protein oxidation (Zabel et al., 2018). This apparent contradiction from research studies may be explained by differences in the time of sampling in relation to disease progression, or by the tissue or fluid compartment being analysed (Peña-Bautista et al., 2019). As previously mentioned, evidence of increased oxidative distress has been reported early in the pathogenies of AD but does not persist with disease progression (Nunomura et al., 2001). Therefore, rather than assess non-specific, global markers of oxidative distress, it is more informative to analyse oxidative modification to specific biomolecules at chosen stages of disease progression to better establish the role of oxidative distress in AD (Aldred et al., 2010; Sultana et al., 2010).
Micronutrients in Improvement of the Standard Therapy in Traumatic Brain Injury
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
High levels of active Peroxiredoxin 6 (prdx6), a major antioxidant enzyme normally found in astrocytes, were detected in the CSF of healthy control subject; however, it was oxidized (inactive form) in patients with TBI.82 Enhanced oxidative damage in the brain and higher levels of markers of oxidative damage F2-isoprostane and F4-neuroprostane in the CSF were present in patients with TBI.83 Increased serum concentration of thioredoxin, a marker of oxidative damage, was associated with severe TBI symptoms including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, and posttraumatic cerebral infarction.84
Beneficial Effects of Omega-3 Fatty Acids on Cardiovascular Disease
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Estela Guerrero De León, Mahabir Prashad Gupta, Juan Antonio Morán-Pinzón
A recent publication by Roy et al. (2015), indicates that the antiarrhythmic effect of DHA is related to the non-enzymatic oxidation carried out by ROS, where neuroprostanes are generated. These mediators are recognized biomarkers of oxidative stress and therefore would be expected to have a harmful effect. However, these researchers demonstrated experimentally that neuroprostanes, primarily 4RS-4F4t-neuroprostane and 10(S)-10-F4t-neuroprostane, can regulate the function of the ryanodine receptor (RyR2), decreasing calcium efflux from the sarcoplasmic reticulum leading to a reduction in calcium sparks and the risk of arrhythmias (Roy et al., 2015). Under this premise, it would be expected that in chronic conditions of oxidative stress, which are common in cardiovascular diseases (ischemia, atherosclerosis, AMI, cardiac post-surgery, etc.) (Luscher, 2015; Islam et al., 2016; Yalta and Yalta, 2018), ω-3 PUFAs generate the production of neuroprostanes which participate in the antiarrhythmic effects induced by these fatty acids.
Liquid biopsy markers for stroke diagnosis
Published in Expert Review of Molecular Diagnostics, 2020
Harshani Wijerathne, Malgorzata A. Witek, Alison E. Baird, Steven A. Soper
Oxidative stress and lipid peroxidation take place because of neuro-inflammation during neuronal injury. Some of the biomarkers related to these events are redox sensitive molecular chaperones, lipid oxidation products like malondialdehyde and oxidized low-density lipoproteins [67]. Unfortunately, many of these oxidative stress markers are not specific to brain injury. Attention is paid to lipids, however, they are highly enriched in the brain. As an example, the F4-neuroprostane, which is a byproduct of free radical-induced oxidation of docosahexaenoic acid, is a fatty acid that is highly enriched in the CNS [68].
A review on neuropharmacological role of erucic acid: an omega-9 fatty acid from edible oils
Published in Nutritional Neuroscience, 2022
J. B. Senthil Kumar, Bhawna Sharma
Among the various factors, mitochondria have been increasingly studied as the critical participants in the aging process and NDs [66]. The free radical theory of aging is well accepted as mitochondria are the principle source of intracellular reactive oxygen species (ROS). This hypothesis suggested a central role for the mitochondrion in normal mammalian aging [67]. The major source of ROS is due to the some premature electron leak inevitably occuring at the respiratory chain during oxidative phosphorylation in particular, complexes I and III [68]. Production of ROS can cause oxidative damage to cell structures, including alterations in membrane lipids, proteins, and DNA [69]. In turn, it may trigger cellular organelle dysfunction that finally leads to neuronal death. Oxidative stress could be overcome by the cellular antioxidant defence system such as catalase (CAT) & superoxide dismutase (SOD) [70]; and non-enzymatic molecules like vitamins E [71]. However, it has been postulated that, the antioxidant defence in brain decrease with age [72]. Another important cascade of reaction in which the ROS readily attack the double bond of PUFAs to form electrophilic aldehyde is lipid peroxidation [73]. The lipid aldehydes are potent lipid electrophiles that can covalently modify lipid, protein and nucleic acids [74]. In addition to that, lipid hydroperoxyl radicals undergoes endo cyclisation to produce fatty acid esters such as ispoprostanes and neuroprostanes [75]. Presence of these fatty acid esters are potential key biomarkers for oxidative stress status in neurological disorders [74]. One of the major targets of lipid peroxidation process is the central nervous system [76]. Certainly, the brain is highly sensitive to oxidative stress because it consumes about 20%–30% of inhaled oxygen [77], contains high levels of PUFAs, ideal target of free radical attack, and high levels of redox transition metals [78]. Most of the mitochondrial lipids are produced in the endoplasmic reticulum (ER) and carried to the mitochondria [79], whereas, lipids such as cardiolipin and phosphatidylethanolamine are known to be biosynthesised within the inner membrane of the mitochondria and are critical for maintaining the unique mitochondrial membrane architecture [80]. An increase in ROS production may further aggravate mitochondrial dysfunction, partly via lipid peroxidation leading to neuronal damage. As ageing process continues, mitochondria become one of the source for the ROS that directly attack various cellular constituents such as fatty acids. Similarly, mutations in the mitochondrial enoyl-CoA/ACP (acyl carrier protein) reductase carrying out the last step of mitochondrial fatty acid synthesis leads to neurodegeneration in mice [81].