Origin and pathophysiology of protein carbonylation, nitration and chlorination in age-related brain diseases and aging

Gonos, Efstathios S.; Καπετάνου, Μαριάννα; Sereikaitė, Jolanta; Bartosz, Grzegorz; Naparło, Katarzyna; Grzesik, Michalina; Sadowska-Bartosz, Izabela

doi:10.18632/aging.101450

Cited by 74 publications

(61 citation statements)

References 259 publications

(235 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Levels of nitrites and carbonyl groups, as indicators of nitrosative damage and a protein marker of oxidative stress, respectively, were similar when comparing EGCG-treated and non-treated P23H groups. EGCG reduced levels of both biomarkers in control animals, which were reported to increase with age, probably by modulation of nitric oxide synthase enzymes (NOS) and its free radical scavenger activity [82][83][84][85][86]. EGCG was shown to protect the GSH/glutathione peroxidase system [87], increasing or maintaining the ratio GSH/GSSG, and thereby improving the oxidative status of treated rats [26].…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats

et al. 2020

View full text Add to dashboard Cite

Retinitis pigmentosa (RP) includes a group of genetic disorders that involve the loss of visual function due to mutations mainly in photoreceptors but also in other retinal cells. Apoptosis, retinal disorganization, and inflammation are common in the progression of the disease. Epigallocatechin gallate (EGCG) has been proved as beneficial in different eye diseases. Pigmented heterozygous P23H rat was used as an animal model of RP. Visual function was assessed by optomotor and electroretinogram (ERG) and circadian rhythms were evaluated by telemetry. Hepatic oxidative damage and antioxidant defenses were assessed using biochemical tests. The visual function of the EGCG P23H group was preserved, with a deterioration in the activity period and lower values in the interdaily stability parameter. Control rats treated with EGCG were less active than the sham group. EGCG increased antioxidant levels in P23H rats but reduced total hepatic antioxidant capacity by almost 42% in control rats compared to the sham group. We conclude that treatment with EGCG improves visual function and antioxidant status in P23H rats but diminishes antioxidant defenses in wild-type control animals, and slightly worsens activity circadian rhythms. Further studies are necessary to clarify the beneficial effects in disease conditions and in healthy organisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats

et al. 2020

View full text Add to dashboard Cite

show abstract

“…MPO also oxidizes tyrosine to tyrosyl radical [ 154 ]. MPO mediates protein nitrosylation, forming 3-chlorotyrosine (3-Cl-Tyr) and dityrosine crosslinks [ 155 , 156 ] ( Table 2 ).…”

Section: Oxidative Stressmentioning

confidence: 99%

Monitoring the Redox Status in Multiple Sclerosis

Tanaka

Vécsei

2020

Biomedicines

View full text Add to dashboard Cite

Worldwide, over 2.2 million people suffer from multiple sclerosis (MS), a multifactorial demyelinating disease of the central nervous system. MS is characterized by a wide range of motor, autonomic, and psychobehavioral symptoms, including depression, anxiety, and dementia. The blood, cerebrospinal fluid, and postmortem brain samples of MS patients provide evidence on the disturbance of reduction-oxidation (redox) homeostasis, such as the alterations of oxidative and antioxidative enzyme activities and the presence of degradation products. This review article discusses the components of redox homeostasis, including reactive chemical species, oxidative enzymes, antioxidative enzymes, and degradation products. The reactive chemical species cover frequently discussed reactive oxygen/nitrogen species, infrequently featured reactive chemicals such as sulfur, carbonyl, halogen, selenium, and nucleophilic species that potentially act as reductive, as well as pro-oxidative stressors. The antioxidative enzyme systems cover the nuclear factor erythroid-2-related factor 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) signaling pathway. The NRF2 and other transcriptional factors potentially become a biomarker sensitive to the initial phase of oxidative stress. Altered components of the redox homeostasis in MS were discussed in search of a diagnostic, prognostic, predictive, and/or therapeutic biomarker. Finally, monitoring the battery of reactive chemical species, oxidative enzymes, antioxidative enzymes, and degradation products helps to evaluate the redox status of MS patients to expedite the building of personalized treatment plans for the sake of a better quality of life.

show abstract

“…Oxidative stress due to free radicals gener-ate which attack phospholipid polyunsaturated fatty acids in cellular membrane can lead to lipid peroxidation, thereby results in formation of major end products 4-hydroxyl-2-nonenal (HNE), acrolein, and malondialdehyde, causing neurotoxicity to neurons [39]. HNE reacts with proteins forming stable covalent adducts to lysine, cysteine, and histidine residues, thereby producing carbonyl functionalities to the proteins, leading to oxidative damage called protein oxidation, and these protein carbonyls are mostly abundant in frontal, temporal, occipital, hippocampus, and inferior parietal lobe [40,41]. RNS-like peroxynitrite causes tyrosine nitration of protein (3-nitrotyrosine and di tyrosine).…”

Section: Oxidative Stress and Tau Hyperphosphorylationmentioning

confidence: 99%

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Duggal

Mehan

2019

ADR

View full text Add to dashboard Cite

Neuronal microtubule (MT) tau protein provides cytoskeleton to neuronal cells and plays a vital role including maintenance of cell shape, intracellular transport, and cell division. Tau hyperphosphorylation mediates MT destabilization resulting in axonopathy and neurotransmitter deficit, and ultimately causing Alzheimer's disease (AD), a dementing disorder affecting vast geriatric populations worldwide, characterized by the existence of extracellular amyloid plaques and intracellular neurofibrillary tangles in a hyperphosphorylated state. Pre-clinically, streptozotocin stereotaxically mimics the behavioral and biochemical alterations similar to AD associated with tau pathology resulting in MT assembly defects, which proceed neuropathological cascades. Accessible interventions like cholinesterase inhibitors and NMDA antagonist clinically provides only symptomatic relief. Involvement of microtubule stabilizers (MTS) prevents tauopathy particularly by targeting MT oriented cytoskeleton and promotes polymerization of tubulin protein. Multiple in vitro and in vivo research studies have shown that MTS can hold substantial potential for the treatment of AD-related tauopathy dementias through restoration of tau function and axonal transport. Moreover, anti-cancer taxane derivatives and epothiolones may have potential to ameliorate MT destabilization and prevent the neuronal structural and functional alterations associated with tauopathies. Therefore, this current review strictly focuses on exploration of various clinical and pre-clinical features available for AD to understand the neuropathological mechanisms as well as introduce pharmacological interventions associated with MT stabilization. MTS from diverse natural sources continue to be of value in the treatment of cancer, suggesting that these agents have potential to be of interest in the treatment of AD-related tauopathy dementia in the future.

show abstract

Origin and pathophysiology of protein carbonylation, nitration and chlorination in age-related brain diseases and aging

Cited by 74 publications

References 259 publications

Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats

Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats

Monitoring the Redox Status in Multiple Sclerosis

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Contact Info

Product

Resources

About