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Lipidomic Insight into Membrane Remodeling in Aging and Neurodegenerative Diseases
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Lipid peroxidation generates hydroperoxides as well as endoperoxides, which undergo fragmentation to produce a broad range of reactive intermediates called reactive carbonyl species with three to nine carbons, the most reactive being α, β-unsaturated aldehydes [4-hydroxy-2-nonenal (HNE) and acrolein], dialdehydes [malondialdehyde (MDA) and glyoxal], and keto-aldehydes [4-oxo-2-nonenal (ONE) and isoketals].
Chronic obstructive pulmonary disease
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
Julie Milot, Mathieu Morissette
COPD is characterized by an increase in oxidative pulmonary stress and it has been shown that the lungs of patients afflicted with COPD have high levels of 4-hydroxy-2-nonenal (4-HNE) [47] and 8-isoprostane [48], two oxidized lipids. The two most important sources of ROS in COPD are tobacco smoke inhalation and the “oxidative burst” of inflammatory phagocytes.
Oxidative Stress and the Aging Brain: From Theory to Prevention
Published in David R. Riddle, Brain Aging, 2007
Carmelina Gemma, Jennifer Vila, Adam Bachstetter, Paula C. Bickford
Aging also is accompanied by changes in membrane fatty acid composition, including a decrease in the levels of polyunsaturated fatty acids (PUFAs) and an increase in monosaturated fatty acids. PUFAs, such as arachidonic acid (AA), are abundant in the aging brain and are highly susceptible to free radical attack. A correlation between the concentration of AA and long-term potentiation has been shown [33, 34], suggesting that oxidative depletion of AA levels may relate to a cognitive deficit in rats. For example, levels of AA are decreased in the hippocampus of aged rats with impaired ability to sustain long-term potentiation. Oxidative damage to lipids can also occur indirectly through the production of highly reactive aldehydes. Peroxidation of AA forms malondialdehyde (MDA), which induces DNA damage by reacting with amino acids in protein to form adducts that disrupt DNA base-pairing. Increased levels of MDA have been found in the aged canine brain [35]. In the aged human brain, increased levels of MDA have been found in inferior temporal cortex and in the cytoplasm of neurons and astrocytes [36], as well as in the hippocampus and cerebellum of aged rodents [37, 38]. Peroxidation of linoleic acid forms 4-hydroxy-2-nonenal (HNE). HNE is more stable than free radicals and it is able to migrate to sites that are distant from its formation, resulting in greater damage. The most damaging effect of HNE is its ability to form covalent adducts with histidine, lysine, and cysteine residues in proteins, enabling a modification in their activity [39]. It has been shown that the HNE-modified proteins, along with neurofibrillary tangles, are present in the senile plaques in aged dogs [40]. Increased levels of HNE have also been found in Alzheimer’s and Parkinson’s disease [41, 42]. These findings support the hypothesis that lipid peroxidation contributes to the deterioration of central nervous system (CNS) function.
Hydrogen sulfide: a target to modulate oxidative stress and neuroplasticity for the treatment of pathological anxiety
Published in Expert Review of Neurotherapeutics, 2020
Mary Chen, Caroline Pritchard, Diandra Fortune, Priyadurga Kodi, Marco Grados
In cell culture model systems, H2S significantly inhibits the potent oxidant ONOO− (peroxynitrite), which may play a role in the tyrosine nitration of α-synuclein and other key neural components. Tyrosine nitration has been implicated in Parkinson’s disease (α-synuclein aggregation), Alzheimer disease (tyrosine-nitrated tau protein), Pick’s disease and corticobasal degeneration [91]. Similarly, 4-hydroxy-2-nonenal (4-HNE), generated by oxidation of polyunsaturated fatty acids, is another cytotoxic oxidative stress biomarker. In SH-SY5Y cells, which are sensitive to ONOO−, H2S is able to avert 4-HNE neurotoxicity by acting as a simple low molecular weight thiol [92]. Administration of NaHS can rescue hypoxic-induced neuronal damage in the same SH-SY5Y cell line by acting through the K(ATP)/PKC/ERK1/Hsp90 pathway. Interestingly, this pathway is also a transduction signaling step in neuroplasticity [93].
Intake of New Zealand Blackcurrant Powder Affects Skin-Borne Volatile Organic Compounds in Middle-Aged and Older Adults
Published in Journal of Dietary Supplements, 2022
M. E. T. Willems, M. Todaka, M. Banic, M. D. Cook, Y. Sekine
Emission of VOCs that are associated with body odor in older adults were lowered, that is, 2-nonenal (Haze et al. 2001) and 6-methyl-5-hepten-2-one (Ozeki and Moro 2016). 2-nonenal has a greasy and grassy odor that is perceived as unpleasant (Haze et al. 2001). Haze et al. (2001) provided evidence that 2-nonenal is produced by the oxidative degradation of unsaturated fatty acids, that is, by lipid peroxidation of fatty acids produced in the sebaceous glands (Ishino et al. 2010). Observations of 2-nonenal skin emissions have been observed in Japanese persons older than 39 years (Haze et al. 2001) and non-Japanese populations between 41 and 70 years of age (Gallagher et al. 2008), so likely a difference in dietary intake (i.e., higher intake of marine-based foods in Japanese persons) between those groups was not a likely explanation for the production of 2-nonenal in older adults. Age-induced lipid peroxidation is upregulated in older adults independent of dietary intake and therefore expected to be present in the participants of the present study. Intake of NZBC in humans has been shown to reduce lipid peroxidation by lowering the amounts of exercise-induced plasma carbonyls (Lyall et al. 2009). The present study therefore provides indirect observations of the ability of blackcurrant intake to reduce biochemical consequences of age-related oxidative stress in the sebaceous glands. The ketone 6-methyl-5-hepten-2-one results from oxidative degradation of the sebaceous gland product squalene (Ozeki and Moro 2016). Lower values for the emission rate of the skin VOC 6-methyl-5-hepten-2-one maybe due to reduced synthesis of squalene and subsequently a smaller amount of squalene being available for oxidative degradation. 6-methyl-5-hepten-2-one is suppressed in older adults (mean age 84.5 years) by inhibition of squalene peroxidation by 6 weeks use of soap containing the antifungal miconazole nitrate (Ozeki and Moro 2016). Overall, the reduction of the body odor components 2-nonenal and 6-methyl-5-hepten-2-one by intake of NZBC powder may have application for the well-being of older adults with concern for their body odor.
Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice
Published in Inhalation Toxicology, 2018
Keiki Ogino, Kenjiro Nagaoka, Tatsuo Ito, Kei Takemoto, Tomoaki Okuda, Shoji F. Nakayama, Noriyoshi Ogino, Yuka Seki, Hiroki Hamada, Shogo Takashiba, Yoshihisa Fujikura
The effects of PM2.5 and treated PM2.5 on oxidative stress were assessed according to the level of 4-OH-2-nonenal measured in lung tissue (Figure 7). 4-OH-2-nonenal was not augmented in the PM2.5 group but was significantly increased in the treated PM2.5 group.