Collapse of redox homeostasis during aging and stress

Feleciano, Diogo R.; Kirstein, Janine

doi:10.1080/23723556.2015.1091060

Cited by 7 publications

(18 citation statements)

References 9 publications

(8 reference statements)

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“…Protein homeostasis (proteostasis) is central to maintaining the functional cellular proteome, a dynamic complex process involving response to different physiological and pathological conditions [ 6 , 7 ]. Proteostasis comprises synchronization from protein synthesis in the ribosome through to posttranslational modification, trafficking to each subcellular compartment, assembly into protein macro-complexes, signaling, and degradation [ 7 , 8 ], depending on proper protein folding and transport by chaperones [ 9 , 10 ].…”

Section: The Sensitive-cysteine Redox Proteome (Cysteinet)mentioning

confidence: 99%

“…This technique identifies reactive cysteine residues in catalytic critical sites in complex proteomes [ 42 ]. Protein homeostasis is one of the essential mechanisms of cells maintaining the adequate functional proteome in each organelle and its integration in different stress-inducing conditions, including cellular aging, which is associated with a decline in proteostasis [ 6 , 7 ]. Proteostasis is a high-energy-dependent part of the proteome that involves different functions, such as editing, transfer, folding, and degradation of proteins across cellular organelles, including the cytosol, nucleus, mitochondria, and endoplasmic reticulum (ER) [ 6 , 7 , 26 ].…”

Section: The Sensitive-cysteine Redox Proteome (Cysteinet) In Agingmentioning

confidence: 99%

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N-Acetyl-Cysteine: Modulating the Cysteine Redox Proteome in Neurodegenerative Diseases

Martínez-Banaclocha

2022

Antioxidants

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In the last twenty years, significant progress in understanding the pathophysiology of age-associated neurodegenerative diseases has been made. However, the prevention and treatment of these diseases remain without clinically significant therapeutic advancement. While we still hope for some potential genetic therapeutic approaches, the current reality is far from substantial progress. With this state of the issue, emphasis should be placed on early diagnosis and prompt intervention in patients with increased risk of neurodegenerative diseases to slow down their progression, poor prognosis, and decreasing quality of life. Accordingly, it is urgent to implement interventions addressing the psychosocial and biochemical disturbances we know are central in managing the evolution of these disorders. Genomic and proteomic studies have shown the high molecular intricacy in neurodegenerative diseases, involving a broad spectrum of cellular pathways underlying disease progression. Recent investigations indicate that the dysregulation of the sensitive-cysteine proteome may be a concurrent pathogenic mechanism contributing to the pathophysiology of major neurodegenerative diseases, opening new therapeutic opportunities. Considering the incidence and prevalence of these disorders and their already significant burden in Western societies, they will become a real pandemic in the following decades. Therefore, we propose large-scale investigations, in selected groups of people over 40 years of age with decreased blood glutathione levels, comorbidities, and/or mild cognitive impairment, to evaluate supplementation of the diet with low doses of N-acetyl-cysteine, a promising and well-tolerated therapeutic agent suitable for long-term use.

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Section: The Sensitive-cysteine Redox Proteome (Cysteinet)mentioning

confidence: 99%

Section: The Sensitive-cysteine Redox Proteome (Cysteinet) In Agingmentioning

confidence: 99%

N-Acetyl-Cysteine: Modulating the Cysteine Redox Proteome in Neurodegenerative Diseases

Martínez-Banaclocha

2022

Antioxidants

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“…Paradoxically, it is possible to have too much and too little oxidation at the same time within the same cell. For example, aging is associated with excessive oxidation in the cytosol, but a loss of oxidizing potential in the endoplasmic reticulum, which is essential for the proper folding of proteins (Feleciano and Kirstein 2016). In contrast to focusing exclusively on free radicals as being responsible for aging and disease, redox dysregulation appears to be a more accurate proposition.…”

Section: Redox Dysregulationmentioning

confidence: 99%

Hydrogen gas: from clinical medicine to an emerging ergogenic molecule for sports athletes

LeBaron

Laher

Kura

et al. 2019

Can. J. Physiol. Pharmacol.

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H2 has been clinically demonstrated to provide antioxidant and anti-inflammatory effects, which makes it an attractive agent in exercise medicine. Although exercise provides a multiplicity of benefits including decreased risk of disease, it can also have detrimental effects. For example, chronic high-intensity exercise in elite athletes, or sporadic bouts of exercise (i.e., noxious exercise) in untrained individuals, result in similar pathological factors such as inflammation, oxidation, and cellular damage that arise from and result in disease. Paradoxically, exercise-induced pro-inflammatory cytokines and reactive oxygen species largely mediate the benefits of exercise. Ingestion of conventional antioxidants and anti-inflammatories often impairs exercise-induced training adaptations. Disease and noxious forms of exercise promote redox dysregulation and chronic inflammation, changes that are mitigated by H2 administration. Beneficial exercise and H2 administration promote cytoprotective hormesis, mitochondrial biogenesis, ATP production, increased NAD+/NADH ratio, cytoprotective phase II enzymes, heat-shock proteins, sirtuins, etc. We review the biomedical effects of exercise and those of H2, and we propose that hydrogen may act as an exercise mimetic and redox adaptogen, potentiate the benefits from beneficial exercise, and reduce the harm from noxious exercise. However, more research is warranted to elucidate the potential ergogenic and therapeutic effects of H2 in exercise medicine.

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“…During the process of aging, the equilibrium between redox state and antioxidant agents changes [92]. These alterations interfere with cellular and tissue regeneration [93].…”

Section: Paraoxonases and Agingmentioning

confidence: 99%

Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview

2019

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Aging is defined as the accumulation of progressive organ dysfunction. There is much evidence linking the involvement of oxidative stress in the pathogenesis of aging. With increasing age, susceptibility to the development of diseases related to lipid peroxidation and tissue injury increases, due to chronic inflammatory processes, and production of reactive oxygen species (ROS) and free radicals. The paraoxonase (PON) gene family is composed of three members (PON1, PON2, PON3) that share considerable structural homology and are located adjacently on chromosome 7 in humans. The most studied member product is PON1, a protein associated with high-density lipoprotein with paraoxonase/esterase activity. Nevertheless, all the three proteins prevent oxidative stress. The major aim of this review is to highlight the importance of the role of PON enzymes in the aging process, and in the development of the main diseases present in the elderly: cardiovascular disease, diabetes mellitus, neurodegenerative diseases, and cancer.

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Collapse of redox homeostasis during aging and stress

Cited by 7 publications

References 9 publications

N-Acetyl-Cysteine: Modulating the Cysteine Redox Proteome in Neurodegenerative Diseases

N-Acetyl-Cysteine: Modulating the Cysteine Redox Proteome in Neurodegenerative Diseases

Hydrogen gas: from clinical medicine to an emerging ergogenic molecule for sports athletes

Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview

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