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

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.

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Local anesthetic Ropivacaine protects rats from myocardial ischemia/reperfusion injury by inhibition of COX-2

Archives of Medical Science ◽

10.5114/aoms/132472 ◽

2021 ◽

Author(s):

Zhou Yu ◽

Sufang Sun ◽

Fang Hu

Keyword(s):

Oxidative Stress ◽

Creatine Kinase ◽

Ischemia Reperfusion ◽

Inos Expression ◽

Ischaemic Injury ◽

Cardiac Tissues ◽

Tnf Α ◽

Creatine Kinase Mb ◽

Cellular Apoptosis ◽

Cox 2

IntroductionMyocardial ischaemia/reperfusion (I/R) injury is the leading cause of morbidity and mortality worldwide. Despite novel advances in therapeutics, the management of myocardial I/R is still an unmet medical need. Therefore, in the present study, we have demonstrated the protective effect of ropivacaine (RPC) on the myocardial infarction in rats and its underlying mechanism.Material and methodsInitially, the effect of RPC was determined on the infarct size and histopathology of cardiac tissues. The effect of RPC was also determined on the levels of various cardiac biomarkers such as creatine kinase (CK), creatine kinase MB (CK-MB), alanine aminotransferase (ALT), asparganine aminotransferase (AST), and lactate dehydrogenase (LDH), and biomarkers of oxidative stress (MDA, SOD, and GSH) and inflammation (tumour necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6). RPC effect was also quantified on cellular apoptosis and COX-2 and iNOS expression via western blot analysis. The RPC was further docked into the active site of COX-2.ResultsIt has been found that RPC reduces the improves haemodynamics of (LVSP and ± dp/dtmax, and LVEDP), infarct percentage and architecture of cardiac tissues of rats. It also reduces the level of studies cardiac injury biomarkers together with a reduction of oxidative stress (MDA, SOD, and GSH) and inflammation (TNF-α, IL-1β, and IL-6). Upon administration of RPC, the rate of cellular apoptosis was found to be greatly reduced, with a reduction in COX-2 and iNOS expression. In docking analysis, RPC creates van der Waals forces and pi-interactions with Tyr381, Arg106, Val102, Leu345, Val509, Ser339, Leu338, Val335, Ala513, His75, and Leu517 at the catalytic site of COX-2.ConclusionsCollectively, our results demonstrated that ropivacaine showed significant benefit against myocardial ischaemic injury.

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Oxidative Stress/FOXO Pathway is Enhanced in Hepatocellular Carcinoma by Interferon α-2b Treatment Favoring Cellular Apoptosis and Slowing Down Oncogenesis

Frontiers in Anti-Cancer Drug Discovery ◽

10.2174/9781681081496115060004 ◽

2015 ◽

pp. 66-90

Keyword(s):

Oxidative Stress ◽

Hepatocellular Carcinoma ◽

Interferon Α ◽

Slowing Down ◽

Cellular Apoptosis

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Mitochondrial Dysfunction in Aging and Neurodegeneration

Advances in Medical Diagnosis, Treatment, and Care - Handbook of Research on Critical Examinations of Neurodegenerative Disorders ◽

10.4018/978-1-5225-5282-6.ch004 ◽

2019 ◽

pp. 76-101

Author(s):

Vaibhav Walia ◽

Munish Garg

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Mitochondrial Dysfunction ◽

Neurodegenerative Disorders ◽

Electron Transport Chain ◽

Tricarboxylic Acid ◽

Atp Production ◽

Important Target ◽

Transport Chain ◽

Cellular Apoptosis

Mitochondria are a dynamic organelle of the cell involved in the various biological processes. Mitochondria are the site of the adenosine triphosphate (ATP) production, electron transport chain (ETC), oxidation of fatty acids, tricarboxylic acid (TCA), and cellular apoptosis. Besides these, mitochondria are the site of production of reactive oxygen species (ROS), which further disrupts the normal functioning of this organelle also making mitochondria itself as an important target of oxidative stress. Thus, mitochondria serve as an important target in the process of neurodegeneration. In the present chapter, the authors describe mitochondria and its functioning, dynamics, and the mitochondrial dysfunction in aging and neurodegenerative disorders (NDs).

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Effects of elevated temperature on gonadal functions, cellular apoptosis, and oxidative stress in Atlantic sea urchin Arbacia punculata

Marine Environmental Research ◽

10.1016/j.marenvres.2019.05.017 ◽

2019 ◽

Vol 149 ◽

pp. 40-49 ◽

Cited By ~ 2

Author(s):

Jackson Johnstone ◽

Sarah Nash ◽

Eleazar Hernandez ◽

Md Saydur Rahman

Keyword(s):

Oxidative Stress ◽

Elevated Temperature ◽

Sea Urchin ◽

Cellular Apoptosis ◽

And Oxidative Stress

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Solid Lipid Nanoparticles of Myricitrin Have Antioxidant and Antidiabetic Effects on Streptozotocin-Nicotinamide-Induced Diabetic Model and Myotube Cell of Male Mouse

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/7496936 ◽

2018 ◽

Vol 2018 ◽

pp. 1-18 ◽

Cited By ~ 13

Author(s):

Akram Ahangarpour ◽

Ali Akbar Oroojan ◽

Layasadat Khorsandi ◽

Maryam Kouchak ◽

Mohammad Badavi

Keyword(s):

Oxidative Stress ◽

C2c12 Cell ◽

In Vitro Study ◽

Homogenization Method ◽

Solid Lipid ◽

Muscle Tissues ◽

Diabetic Model ◽

Cellular Apoptosis

Type 2 diabetes mellitus (T2DM) may occur via oxidative stress. Myricitrin is a plant-derived antioxidant, and its solid lipid nanoparticle (SLN) may be more potent. Hence, the present study was conducted to evaluate the effects of myricitrin SLN on streptozotocin-nicotinamide- (STZ-NA-) induced T2DM of the mouse and hyperglycemic myotube. In this experimental study, cold homogenization method was used to prepare SLN. Then, 120 adult male NMRI mice were divided into 7 groups: control, vehicle, diabetes (received STZ 65 mg/kg 15 min after injected NA 120 mg/kg), diabetes + SLN containing myricitrin 1, 3, and 10 mg/kg, and diabetes + metformin. For in vitro study, myoblast (C2C12) cell line was cultured and divided into 6 groups (n=3): control, hyperglycemia, hyperglycemia + SLN containing myricitrin 1, 3, and, 10 μM, and hyperglycemia + metformin. After the last nanoparticle treatment, plasma samples, pancreas and muscle tissues, and myotubes were taken for experimental assessments. Diabetes increased lipid peroxidation and reduced antioxidant defense along with the hyperglycemia, insulin resistance, and pancreas apoptosis. Hyperglycemia induced oxidative stress, antioxidant impairment, and cellular apoptosis. Myricitrin SLN improved diabetes and hyperglycemia complications in the in vivo and in vitro studies. Therefore, SLN of myricitrin showed antioxidant, antidiabetic, and antiapoptotic effects in the mouse and myotube cells.

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DeubiquitinaseUsp18prevents cellular apoptosis from oxidative stress in liver cells

Cell Biology International ◽

10.1002/cbin.10799 ◽

2017 ◽

Vol 41 (8) ◽

pp. 914-921 ◽

Cited By ~ 6

Author(s):

Keng Po Lai ◽

Angela Hoi Yan Cheung ◽

William Ka Fai Tse

Keyword(s):

Oxidative Stress ◽

Liver Cells ◽

Cellular Apoptosis

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CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/9947772 ◽

2021 ◽

Vol 2021 ◽

pp. 1-17

Author(s):

Md Jamal Uddin ◽

Jeewon Jeong ◽

Eun Seon Pak ◽

Hunjoo Ha

Keyword(s):

Oxidative Stress ◽

Acute Kidney Injury ◽

Er Stress ◽

Stress Responses ◽

Kidney Diseases ◽

Kidney Injury ◽

Oxygen Species ◽

Chronic Kidney Diseases ◽

Tubular Cells ◽

Cellular Apoptosis

Acute kidney injury (AKI) most commonly appears in critically ill patients in hospitals. AKI is characterized as a quick deterioration of kidney function and has recently been identified to be tightly interlinked with chronic kidney diseases. The emerging major mediators of AKI include oxidative stress and endoplasmic reticulum (ER) stress. Carbon monoxide (CO) attenuates oxidative stress and ER stress in various cells, while Fyn, a member of the Src kinase family, is activated by oxidative stress and contributes to ER stress in skeletal muscle. Considering these, the objective of the current research was to determine (i) the involvement of Fyn in ER stress-mediated AKI and (ii) the effect of CO-releasing molecule-2 (CORM2) on reactive oxygen species- (ROS-) Fyn-ER stress-mediated AKI. Pretreatment with CORM2 (30 mg/kg) efficiently inhibited LPS (30 mg/kg)-induced oxidative stress, inflammation, and cellular apoptosis during AKI in C57BL/6J mice. Also, CORM2 efficiently suppressed the activation of Fyn and ER stress in AKI mice. Consistently, pretreatment with CORM2 inhibited oxidative stress, Fyn activation, ER stress, inflammation, and apoptosis in LPS- or H2O2-stimulated proximal epithelial tubular cells. Fyn inhibition using siRNA or an inhibitor (PP2) significantly attenuated ER stress responses in the cells. These data suggest that CORM2 may become a potential treatment option against ROS-Fyn-ER stress-mediated AKI.

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

Antioxidants ◽

10.3390/antiox10091429 ◽

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.

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