scholarly journals Redox Regulation in Aging Lungs and Therapeutic Implications of Antioxidants in COPD

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1429
Author(s):  
Hirofumi Kiyokawa ◽  
Yuma Hoshino ◽  
Kazuhiro Sakaguchi ◽  
Shigeo Muro ◽  
Junji Yodoi
Keyword(s):  
Oxidative Stress ◽  
Respiratory System ◽  
Redox Regulation ◽  
Wide Spectrum ◽  
Redox System ◽  
Cellular Aging ◽  
Future Directions ◽  
Therapeutic Implications ◽  
Chronic Lung Diseases ◽  
Cellular Apoptosis

Mammals, including humans, are aerobic organisms with a mature respiratory system to intake oxygen as a vital source of cellular energy. Despite the essentiality of reactive oxygen species (ROS) as byproducts of aerobic metabolism for cellular homeostasis, excessive ROS contribute to the development of a wide spectrum of pathological conditions, including chronic lung diseases such as COPD. In particular, epithelial cells in the respiratory system are directly exposed to and challenged by exogenous ROS, including ozone and cigarette smoke, which results in detrimental oxidative stress in the lungs. In addition, the dysfunction of redox regulation due to cellular aging accelerates COPD pathogenesis, such as inflammation, protease anti-protease imbalance and cellular apoptosis. Therefore, various drugs targeting oxidative stress-associated pathways, such as thioredoxin and N-acetylcysteine, have been developed for COPD treatment to precisely regulate the redox system. In this review, we present the current understanding of the roles of redox regulation in the respiratory system and COPD pathogenesis. We address the insufficiency of current COPD treatment as antioxidants and discuss future directions in COPD therapeutics targeting oxidative stress while avoiding side effects such as tumorigenesis.

scholarly journals Oxidative Stress as a Common Key Event in Developmental Neurotoxicity

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yuhei Nishimura ◽  
Yasunari Kanda ◽  
Hideko Sone ◽  
Hiroaki Aoyama
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Adverse Outcome ◽  
Redox System ◽  
Autism Spectrum ◽  
Developmental Neurotoxicity ◽  
Free Oxygen Radicals ◽  
Future Directions ◽  
Cellular Events ◽  
Adverse Outcome Pathways

The developing brain is extremely sensitive to many chemicals. Perinatal exposure to neurotoxicants has been implicated in several neurodevelopmental disorders, including autism spectrum disorder, attention-deficit hyperactive disorder, and schizophrenia. Studies of the molecular and cellular events related to developmental neurotoxicity have identified a number of “adverse outcome pathways,” many of which share oxidative stress as a key event. Oxidative stress occurs when the balance between the production of free oxygen radicals and the activity of the cellular antioxidant system is dysregulated. In this review, we describe some of the developmental neurotoxins that target the antioxidant system and the mechanisms by which they elicit stress, including oxidative phosphorylation in mitochondria and plasma membrane redox system in rodent models. We also discuss future directions for identifying adverse outcome pathways related to oxidative stress and developmental neurotoxicity, with the goal of improving our ability to quickly and accurately screen chemicals for their potential developmental neurotoxicity.

scholarly journals Redox Regulation in Cancer: A Double-edged Sword with Therapeutic Potential

2010 ◽  
Vol 3 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Asha Acharya ◽  
Ila Das ◽  
Des Chandhok ◽  
Tapas Saha
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Significant Role ◽  
Redox Regulation ◽  
Therapeutic Potential ◽  
Redox Homeostasis ◽  
Redox System ◽  
Tumor Formation ◽  
Antioxidant Defenses ◽  
Environmental Carcinogens

Oxidative stress, implicated in the etiology of cancer, results from an imbalance in the production of reactive oxygen species (ROS) and cell’s own antioxidant defenses. ROS deregulate the redox homeostasis and promote tumor formation by initiating an aberrant induction of signaling networks that cause tumorigenesis. Ultraviolet (UV) exposures, γ-radiation and other environmental carcinogens generate ROS in the cells, which can exert apoptosis in the tumors, thereby killing the malignant cells or induce the progression of the cancer growth by blocking cellular defense system. Cancer stem cells take the advantage of the aberrant redox system and spontaneously proliferate. Oxidative stress and gene-environment interactions play a significant role in the development of breast, prostate, pancreatic and colon cancer. Prolonged lifetime exposure to estrogen is associated with several kinds of DNA damage. Oxidative stress and estrogen receptor-associated proliferative changes are suggested to play important roles in estrogen-induced breast carcinogenesis. BRCA1, a tumor suppressor against hormone responsive cancers such as breast and prostate cancer, plays a significant role in inhibiting ROS and estrogen mediated DNA damage; thereby regulate the redox homeostasis of the cells. Several transcription factors and tumor suppressors are involved during stress response such as Nrf2, NFκB and BRCA1. A promising strategy for targeting redox status of the cells is to use readily available natural substances from vegetables, fruits, herbs and spices. Many of the phytochemicals have already been identified to have chemopreventive potential, capable of intervening in carcinogenesis.

Oxidative Stress in the Pathogenesis of Alzheimer’s Disease and Cerebrovascular Disease with Therapeutic Implications

2020 ◽  
Vol 19 (2) ◽  
pp. 94-108 ◽  
Author(s):  
Anamaria Jurcau ◽  
Aurel Simion
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Preventive Measures ◽  
Current Knowledge ◽  
Antioxidant Treatment ◽  
Future Directions ◽  
Therapeutic Implications

The significant gain in life expectancy led to an increase in the incidence and prevalence of dementia. Although vascular risk factors have long and repeatedly been shown to increase the risk of Alzheimer’s Disease (AD), translating these findings into effective preventive measures has failed. In addition, the finding that incident ischemic stroke approximately doubles the risk of a patient to develop AD has been recently reinforced. Current knowledge and pathogenetic hypotheses of AD are discussed. The implication of oxidative stress in the development of AD is reviewed, with special emphasis on its sudden burst in the setting of acute ischemic stroke and the possible link between this increase in oxidative stress and consequent cognitive impairment. Current knowledge and future directions in the prevention and treatment of AD are discussed outlining the hypothesis of a possible beneficial effect of antioxidant treatment in acute ischemic stroke in delaying the onset/progression of dementia.

Immune checkpoints and cancer development: therapeutic implications and future directions

2021 ◽  
pp. 153485
Author(s):  
Saber Mehdizadeh ◽  
Hashem Bayatipoor ◽  
Salar Pashangzadeh ◽  
Roghayeh Jafarpour ◽  
Zeinab Shojaei ◽  
...  
Keyword(s):  
Cancer Development ◽  
Immune Checkpoints ◽  
Future Directions ◽  
Therapeutic Implications

scholarly journals How N-Acetylcysteine Supplementation Affects Redox Regulation, Especially at Mitohormesis and Sarcohormesis Level: Current Perspective

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 153
Author(s):  
Aslı Devrim-Lanpir ◽  
Lee Hill ◽  
Beat Knechtle
Keyword(s):  
Oxidative Stress ◽  
Oxidative Metabolism ◽  
Adaptive Response ◽  
Redox Regulation ◽  
Therapeutic Agent ◽  
Metabolic Effects ◽  
Metabolic Adaptations ◽  
Current Perspective ◽  
Exercise Induced ◽  
Response To Exercise

Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) has been applied as a therapeutic agent in treating many diseases in humans due to its precursory role in the production of hepatic glutathione, a natural antioxidant. Several studies have investigated NAC’s possible therapeutic role in oxidative metabolism and adaptive response to exercise in the athletic population. However, still conflicting questions regarding NAC supplementation need to be clarified. This narrative review aims to re-evaluate the metabolic effects of NAC on exercise-induced oxidative stress and adaptive response developed by athletes against the exercise, especially mitohormetic and sarcohormetic response.

scholarly journals An unusual thioredoxin system in the facultative parasite Acanthamoeba castellanii

2021 ◽  
Vol 78 (7) ◽  
pp. 3673-3689
Author(s):  
David Leitsch ◽  
Alvie Loufouma Mbouaka ◽  
Martina Köhsler ◽  
Norbert Müller ◽  
Julia Walochnik
Keyword(s):  
Oxidative Stress ◽  
Stop Codon ◽  
Acanthamoeba Castellanii ◽  
Methionine Sulfoxide ◽  
Redox System ◽  
Methionine Sulfoxide Reductase ◽  
Methionine Sulfoxide Reductase A ◽  
Protein Levels ◽  
Thioredoxin System ◽  
Facultative Parasite

AbstractThe free-living amoeba Acanthamoeba castellanii occurs worldwide in soil and water and feeds on bacteria and other microorganisms. It is, however, also a facultative parasite and can cause serious infections in humans. The annotated genome of A. castellanii (strain Neff) suggests the presence of two different thioredoxin reductases (TrxR), of which one is of the small bacterial type and the other of the large vertebrate type. This combination is highly unusual. Similar to vertebrate TrxRases, the gene coding for the large TrxR in A. castellanii contains a UGA stop codon at the C-terminal active site, suggesting the presence of selenocysteine. We characterized the thioredoxin system in A. castellanii in conjunction with glutathione reductase (GR), to obtain a more complete understanding of the redox system in A. castellanii and the roles of its components in the response to oxidative stress. Both TrxRases localize to the cytoplasm, whereas GR localizes to the cytoplasm and the large organelle fraction. We could only identify one thioredoxin (Trx-1) to be indeed reduced by one of the TrxRases, i.e., by the small TrxR. This thioredoxin, in turn, could reduce one of the two peroxiredoxins tested and also methionine sulfoxide reductase A (MsrA). Upon exposure to hydrogen peroxide and diamide, only the small TrxR was upregulated in expression at the mRNA and protein levels, but not the large TrxR. Our results show that the small TrxR is involved in the A. castellanii’s response to oxidative stress. The role of the large TrxR, however, remains elusive.

N6-methyladenosine(m6A) demethylase FTO regulates cellular apoptosis following cobalt-induced oxidative stress

2021 ◽  
pp. 118749
Author(s):  
Jianping Tang ◽  
Qianqian Su ◽  
Zhenkun Guo ◽  
Jinfu Zhou ◽  
Fuli Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cellular Apoptosis

scholarly journals Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kyota Fujita ◽  
Yusaku Nakabeppu ◽  
Mami Noda
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Models ◽  
Animal Studies ◽  
Clinical Symptoms ◽  
Therapeutic Effects ◽  
Therapeutic Approaches ◽  
Cellular Apoptosis ◽  
6 Hydroxydopamine

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

Cellular aging and oxidative stress

1995 ◽  
pp. 35-43 ◽  
Author(s):  
M. Matsuo ◽  
H. Yuan ◽  
S. Honda
Keyword(s):  
Oxidative Stress ◽  
Cellular Aging ◽  
And Oxidative Stress

scholarly journals The Role of HO-1 and Its Crosstalk with Oxidative Stress in Cancer Cell Survival

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2401
Author(s):  
Shih-Kai Chiang ◽  
Shuen-Ei Chen ◽  
Ling-Chu Chang
Keyword(s):  
Oxidative Stress ◽  
Redox Regulation ◽  
Oxidative Status ◽  
Multiple Roles ◽  
Mitochondrial Enzymes ◽  
Heme Oxygenases ◽  
Downstream Effects ◽  
Cancer Cell Survival ◽  
And Oxidative Stress

Heme oxygenases (HOs) act on heme degradation to produce carbon monoxide (CO), free iron, ferritin, and biliverdin. Upregulation of cellular HO-1 levels is signature of oxidative stress for its downstream effects particularly under pro-oxidative status. Subcellular traffics of HO-1 to different organelles constitute a network of interactions compromising a variety of effectors such as pro-oxidants, ROS, mitochondrial enzymes, and nucleic transcription factors. Some of the compartmentalized HO-1 have been demonstrated as functioning in the progression of cancer. Emerging data show the multiple roles of HO-1 in tumorigenesis from pathogenesis to the progression to malignancy, metastasis, and even resistance to therapy. However, the role of HO-1 in tumorigenesis has not been systematically addressed. This review describes the crosstalk between HO-1 and oxidative stress, and following redox regulation in the tumorigenesis. HO-1-regulated signaling pathways are also summarized. This review aims to integrate basic information and current progress of HO-1 in cancer research in order to enhance the understandings and facilitate following studies.

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