Targeting Free Radicals in Oxidative Stress-Related Human Diseases

Poprac, Patrik; Jomová, Klaudia; Šimunková, Miriama; Kollár, Vojtech; Rhodes, Christopher J.; Valko, Marián

doi:10.1016/j.tips.2017.04.005

Cited by 900 publications

(592 citation statements)

References 89 publications

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“…The brain is an organ that consumes one‐third of the metabolic oxygen. In addition, it has high contents of unsaturated fatty acids, which are vulnerable to free radical attack, and has relatively high transition metal content, so the brain is a suitable environment for damage by free radical mediated lipid peroxidation (Poprac et al, ; Schieber & Chandel, ). SOD plays a role in preventing the accumulation of superoxide which can damages and inactivates proteins that contain iron‐sulfur clusters.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies on the treatment of dementia are underway, and the dementia market is also expending (Ahmadi‐Abhari et al, ). Alzheimer’s disease (AD) is a representative category of dementia, and is a neurodegenerative disease characterized by cognitive decline due to increased reactive oxygen species (ROS) and neuronal cell injury caused by aging and antioxidant system imbalance (Poprac et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Aruncus dioicus var. kamtschaticus extract suppresses mitochondrial apoptosis induced‐neurodegeneration in trimethyltin‐injected ICR mice

et al. 2018

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In the present study, we attempt to confirm the effect of the ethyl acetate fraction from Aruncus dioicus var. kamtschaticus (EFAD) against neurodegeneration with various experiments using trimethyltin (TMT). First, learning and memory deterioration caused by TMT was examined with several behavioral tests. EFAD had an improvement effect on TMT‐induced cognitive dysfunction. Second, to assess the oxidative stress caused by TMT, a series of biochemical indicators of the cholinergic and antioxidant system were measured. EFAD showed superb effects on the recovery of the cholinergic system and reduction of oxidative stress. Third, to identify the mitochondrial apoptosis caused by TMT, mitochondrial activity and mitochondrial apoptotic signaling molecules were analyzed. EFAD improved mitochondrial activity and suppressed mitochondrial apoptosis. Finally, dicaffeoylglucose isomers were identified as main compounds of EFAD with ultra‐performance liquid‐quadrupole‐time‐of flight mass spectrometry (UPLC‐QTOF/MS2). Consequently, EFAD showed a protective effect against mitochondrial apoptosis‐induced neurodegeneration in TMT‐injected mice based on antioxidant ability. Practical applications Recently, neurodegenerative disease patients are increasing, and in particular, Alzheimer’s disease (AD) is a representative neurodegeneration, which characterized by mitochondrial damage, neurofibrillary tangles, and neuronal cell death. This study confirmed that the ethyl acetate fraction from A. dioicus var. kamtschaticus ameliorates the impaired cognitive ability by TMT toxicity, which shares the symptoms of AD. Therefore, this study can provide the potential of cognitive functional food material of A. dioicus var. kamtschaticus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aruncus dioicus var. kamtschaticus extract suppresses mitochondrial apoptosis induced‐neurodegeneration in trimethyltin‐injected ICR mice

et al. 2018

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“…Mitochondria, in addition to be the major energy source of the cells, are also considered the main origin of ROS since superoxide radical is generated as a consequence of the electron transport chain, which may give rise to oxidative stress and subsequent cell damage. As result of accumulation of oxidative lesions, several physiological functions can be affected, increasing disease's incidence concomitantly with a reduction in life span [90]. Despite the physiologic relevance of low and intermediary ROS levels that preserve cell survival [91] oxidative stress has been faced as a potential unifying mechanism contributing to several human pathologies since high ROS concentrations, above the clearance capacity of the cell cause oxidative stress, mitochondrial dysfunction, cellular damage, and, in numerous cases, cell death [92].…”

Section: Oxidative Stressmentioning

confidence: 99%

The ups and downs of cellular stress: the “MAM hypothesis” for Bipolar disorder pathophysiology

Pereira¹,

Resende²,

Morais³

et al. 2017

IJCNMH

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Mental health problems constitute the largest single source of world economic burden, with an estimated global cost greater than cardiovascular disease, cancer or diabetes individually. In the European Union mental disorders affect millions of people and these numbers are expected to rise as result of Europe's ageing population. Given the biological causes of many of these disorders, most studies focus on their molecular basis. Bipolar disorder (BD) is characterized by mood swings between depression and mania resulting in cognitive and functional impairments that require lifetime treatment. Recurrent mood episodes, residual symptoms, functional impairment, psychosocial disability with high rates of divorce, unemployment, drug abuse and suicide attempting, and significant medical comorbidities such as metabolic and cardiovascular diseases cannot be efficiently controlled even with proper use of current treatments. Moreover, delayed diagnosis/misdiagnosis is frequent because reliable biomarkers are absent. Therefore, a better understanding of BD pathophysiology is a prerequisite for the design of new drugs and their implementation in clinical practice as well as to develop biomarkers for a more accurate and earlier diagnosis and/or evaluation of therapeutic response. This review summarises the association between decreased cellular resilience towards stress and BD. Since the key stress-response mediator Mitochondria-Associated Membranes (MAMs) modulate several BD relevant processes such as mitochondrial dysfunction and oxidative stress, Ca 2+ deregulation and cytoskeleton abnormalities, endoplasmic reticulum stress responses, loss of proteostasis and inflammasome activation, we propose the "MAM hypothesis" for BD pathophysiology. Targeting MAM-associated signaling pathways can be a promising investigation avenue to identify novel therapeutic strategies.Keywords: Bipolar disorder, Endoplasmic reticulum, Mitochondria, Mitochondria-associated membranes, Cellular resilience, Cellular stress, Plasticity. Bipolar DisorderBD is a chronic psychiatric illness with a remitting course, affecting 2.4% of the general population [1], characterized by mood swings between manic and depressive states that result in cognitive and functional impairments, high health care costs and premature mortality [2,3]. BD is the sixth leading cause of disability worldwide responsible for loss of more disability-adjusted life-years than all forms of cancer and major neurological conditions [4]. BD is associated with greatly impaired quality of life and increased physical health burden [5]. Moreover, BD patients tend to have high rates of divorce, unemployment, drug abuse and crime as consequence of impaired social cognition, and its impact on patients can be devastating, with approximately 23% of patients with BD reported having suicide attempts [6]. Moreover, individuals with BD diagnosis have a high risk of medical comorbidities such as metabolic (diabetes, obesity and metabolic syndrome) and cardiovascular disorders [7].Current knowl...

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“…These extra‐ and intracellular stresses disrupt cellular signaling pathways and homeostasis, causing various diseases such as cancer, stomach ulcers, heart disease, obesity, and diabetes. Especially, oxidative stress resulting from excessive free radical production is known as a fundamental cause of age‐related diseases such as atherosclerosis, metabolic disorder, neurodegenerative disorders, and cancer (Kattoor, Pothineni, Palagiri, & Mehta, ; Poprac et al., ; Rani, Deep, Singh, Palle, & Yadav, ; Salim, ; Shaw, Werstuck, & Chen, ). Free radicals and reactive oxygen species generated during the oxidative phosphorylation process for ATP production in the mitochondria induce cellular oxidative stress (Pero, Roush, Markowitz, & Miller, ).…”

Section: Introductionmentioning

confidence: 99%

Alpha‐Casein and Beta‐Lactoglobulin from Cow Milk Exhibit Antioxidant Activity: A Plausible Link to Antiaging Effects

Kim

Cheon

et al. 2019

Journal of Food Science

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Studies on the discovery and function of antioxidants are consistently being performed because oxidative stress can cause various diseases. Many compounds and natural products have antioxidant activity in vitro; however, it is often difficult to reproduce their effects in vivo. Additionally, methods to measure antioxidant activities in cells are also scarce. Here, we investigated the antioxidant activity of milk proteins by observing the formation of arsenite‐induced stress granules as a tool to evaluate antioxidant activity in cells. Milk proteins not only decreased the formation of stress granules in several cell types but also scavenged 2,2'‐azino‐bis(3‐ethylbenzothiazoline‐6‐sulfonic acid) (ABTS) radical cations in vitro. In addition, milk proteins inhibited cellular senescence based on an SA‐β‐galactosidase assay, and increased differentiation to myotubes from myoblasts isolated from the skeletal muscles of mouse pups. Taken together, our results demonstrate that milk proteins have an antiaging effect, especially prevention of skeletal muscle loss, through their antioxidant activities. Practical Application Our results provide that antioxidant effects of milk proteins containing α‐caseins, β‐caseins, and β‐lactoglobulin can mitigate aging‐related damage induced by oxidative stress through showing inhibition of cellular senescence and increase of differentiation and maturation of myoblast. Therefore, we suggest that milk proteins could be potent health supplements to prevent aging‐associated diseases, especially sarcopenia.

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Targeting Free Radicals in Oxidative Stress-Related Human Diseases

Cited by 900 publications

References 89 publications

Aruncus dioicus var. kamtschaticus extract suppresses mitochondrial apoptosis induced‐neurodegeneration in trimethyltin‐injected ICR mice

Aruncus dioicus var. kamtschaticus extract suppresses mitochondrial apoptosis induced‐neurodegeneration in trimethyltin‐injected ICR mice

The ups and downs of cellular stress: the “MAM hypothesis” for Bipolar disorder pathophysiology

Alpha‐Casein and Beta‐Lactoglobulin from Cow Milk Exhibit Antioxidant Activity: A Plausible Link to Antiaging Effects

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