Reactive Oxygen Species, Oxidative Damage and Cell Death

Ghosh, Nandini; Das, Amitava; Chaffee, Scott; Roy, Sashwati; Sen, Chandan K.

doi:10.1016/b978-0-12-805417-8.00004-4

Cited by 83 publications

(62 citation statements)

References 91 publications

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“…Oxidative stress, an imbalance in reactive ROS and antioxidant levels, plays an important role in the development and progression of diabetes and its complications [ 61 ]. ROS exerts damage onto proteins and lipid components of cells via oxidation, oxidizing lipids into reactive lipid peroxides [ 62 ]. Mitochondrial ROS have also been related to the increased activity of uncoupling proteins (UCP), which uncouple ATP synthesis from electron transport.…”

Section: Involvement Of Mitochondria Dysfunction In Diabetic Cardimentioning

confidence: 99%

Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids

Jubaidi

Zainalabidin

Mariappan

et al. 2020

IJMS

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As the powerhouse of the cells, mitochondria play a very important role in ensuring that cells continue to function. Mitochondrial dysfunction is one of the main factors contributing to the development of cardiomyopathy in diabetes mellitus. In early development of diabetic cardiomyopathy (DCM), patients present with myocardial fibrosis, dysfunctional remodeling and diastolic dysfunction, which later develop into systolic dysfunction and eventually heart failure. Cardiac mitochondrial dysfunction has been implicated in the development and progression of DCM. Thus, it is important to develop novel therapeutics in order to prevent the progression of DCM, especially by targeting mitochondrial dysfunction. To date, a number of studies have reported the potential of phenolic acids in exerting the cardioprotective effect by combating mitochondrial dysfunction, implicating its potential to be adopted in DCM therapies. Therefore, the aim of this review is to provide a concise overview of mitochondrial dysfunction in the development of DCM and the potential role of phenolic acids in combating cardiac mitochondrial dysfunction. Such information can be used for future development of phenolic acids as means of treating DCM by alleviating the cardiac mitochondrial dysfunction.

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Section: Involvement Of Mitochondria Dysfunction In Diabetic Cardimentioning

confidence: 99%

Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids

Jubaidi

Zainalabidin

Mariappan

et al. 2020

IJMS

View full text Add to dashboard Cite

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“…[3] However, uncontrolled ROS levels, not adequately balanced by endogenous and exogenous antioxidant defenses, can lead to an oxidative stress status giving rise to cell damage and various diseases. [4] Oxidative stress is known to hasten the aging process, significantly contribute to pathophysiology of a broad variety of disorders or diseases such as cardiovascular diseases, inflammatory bowel disease, rheumatoid arthritis, and others. [5] Moreover, a considerable body of evidence has shown that ROS trigger NF-кB which activates and/or further amplifies the pro-inflammatory response regulating pro-inflammatory mediators, such as nitric oxide (NO).…”

Section: Introductionmentioning

confidence: 99%

Effect of Non‐Volatile Constituents of Elsholtzia ciliata (Thunb.) Hyl. from Southern Vietnam on Reactive Oxygen Species and Nitric Oxide Release in Macrophages

Nguyen

Hung

Schwaiger

et al. 2020

Chemistry & Biodiversity

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The extract of Elsholtzia ciliata aerial parts was subjected to bio-guided isolation using the intercellular ROS reduction in J774A.1 macrophages to monitor the anti-oxidative activity. Fifteen compounds were isolated from the active fractions including eleven flavonoids (vitexin, pedalin, luteolin-7-O-β-D-glucopyranoside, apigenin-5-Oβ-D-glucopyranoside, apigenin-7-O-β-D-glucopyranoside, chrysoeriol-7-O-β-D-glucopyranoside, 7,3'-dimethoxyluteolin-6-O-β-D-glucopyranoside, luteolin, 5,6,4'-trihydroxy-7,3'-dimethoxyflavone, 5-hydroxy-6,7-dimethoxyflavone (compound 13), 5-hydroxy-7,8-dimethoxyflavone); three hydroxycinnamic acid derivatives (caffeic acid, 4-(E)-caffeoyl-L-threonic acid, 4-O-(E)-p-coumaroyl-L-threonic acid) and one fatty acid (α-linolenic acid). The biological evaluation of these compounds (10-2.5 μM) indicated that all of them exerted good antioxidant and anti-inflammatory activities, in particular compound 13.

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“…Reactive oxygen species can be derived from many sources including endogenous (mitochondria, peroxisomes, lipoxygenases, NADPH oxidase, cytochrome p450) or exogenous inputs (UV, ionizing radiation, chemotherapeutics, inflammatory cytokines, environmental toxins). They can lead to impaired physiological function, a shift in the homeostasis of normal growth and development, as well as cause damage to signaling pathways [6][7][8]. It was suggested in the 1950s by Denham Harman, that endogenous free radicals were responsible for the "free-radical theory" of ageing and that toxic radicals generated in cells resulted in a pattern of cumulative damage [9].…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

“…ROS are also capable of causing damage to the lipids of cell membranes whereby the bonds between fatty acids become prone to damage or abstraction. Lipid peroxidation may result in a self-perpetuating process as certain radicals are both reaction initiators as well as the products of lipid peroxidation and will attack lipid membranes thus altering membrane fluidity, permeability and could affect cellular metabolic functions as well [8]. Fortunately, numerous protective mechanisms exist to mitigate this damage and one such model of oxidative-stress tolerance is mammalian hibernation.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

“…As oxygen consumption at body temperatures approaching 0˚C is typically around 1-5% of euthermic values [17], hibernation generally provides an energy savings of 90-95% of energy expenditures compared with the euthermic state [13,18,19,21]. This is accompanied by several physiological changes (for ground squirrels) including a significant decrease in breathing rates (from 40 breaths per minute to less than 1), heart rate (from 350-400 beats per minute to [5][6][7][8][9][10], and tissue perfusion rates (down to 10% of euthermic). These and other physiological parameters are rapidly reversed upon exit from torpor during intermittent arousals, where a 10-20-fold surge in oxygen consumption occurs as the squirrel rewarms to 37˚C [17,22].…”

Section: Hibernationmentioning

confidence: 99%

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Regulation of Antioxidant Defenses, DNA Damage Repair, the Immune Response, and Neuroprotection During Hibernation in the Thirteen-Lined Ground Squirrel

Szereszewski¹

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Hibernation is a fascinating survival adaptation that allows animals to transition into a torpid state to survive the winter by coordinating a strong suppression of metabolic rate, conservation of fuel/energy, and reduction of body temperature. This strategy permits thirteen-lined ground squirrels (Ictidomys tridecemlineatus) and other hibernating mammals to endure the harsh winter season when there is little access to food. Many energy-expensive cellular processes are suppressed, including gene transcription and protein synthesis/turnover, but are reactivated rapidly when animals arouse back to euthermia. Both torpor and arousal can have damaging consequences; for example, during arousal, reactive oxygen species flood the cell causing oxidative damage to numerous cellular components. Therefore, hibernation requires many pro-survival mechanisms to mitigate multiple types of damage: e.g. from oxidative damage, DNA damage, and pathogen attack, among others. The research reported in this thesis on damage control processes in hibernators shows that antioxidant enzymes such as PRDXs are upregulated in key tissues but in an isoform-specific and time-specific manner over the torpor-arousal cycle. PRDX2, 3, 4 and 6 were found to be significantly upregulated in specific tissues.Similarly, DNA damage repair is initiated during torpor and is characterized by the binding of repair proteins such as Ku80 and the MRN complex to the site of breaks, but ligation (with XLF) reactions to fully repair DNA do not appear to occur until the arousal period.Pro-inflammatory mechanisms are also used to deal with pathogens; these remain active at basal levels in a tissue-specific manner during torpor, but are up-regulated in the final stages just before arousal or only during arousal depending on the tissue, such as the induction of CCL5, a recruiter of monocytes. A cyto/neuro-protective mitochondrial peptide, shumanin, was also identified that is induced in a tissue-specific manner, helping to protect key organs such as the brain cortex and adipose tissues. The results show that hibernation is a complex, multi-faceted process that employs specific adaptations of damage prevention/repair pathways to protect squirrel tissues from damage not only during prolonged torpor but over the transitional states to/from torpor and does so expertly while conserving energy until such a time that repair mechanisms may be fully initiated.iv

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Reactive Oxygen Species, Oxidative Damage and Cell Death

Cited by 83 publications

References 91 publications

Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids

Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids

Effect of Non‐Volatile Constituents of Elsholtzia ciliata (Thunb.) Hyl. from Southern Vietnam on Reactive Oxygen Species and Nitric Oxide Release in Macrophages

Regulation of Antioxidant Defenses, DNA Damage Repair, the Immune Response, and Neuroprotection During Hibernation in the Thirteen-Lined Ground Squirrel

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