scholarly journals Oxidative Stress and Its Association with COVID-19: A Narrative Review

2020 ◽  
pp. 97-105 ◽  
Author(s):  
Hardi Rafat Baqi ◽  
Halgord Ali M. Farag ◽  
Abdel Hamid H. El Bilbeisi ◽  
Rafee Habib Askandar ◽  
Amany M. El Afifi

The naturalness of severe acute respiratory syndrome coronavirus 2 infections (SARS-Cov-2) appears to impact the respiratory system and lungs, however, the etiology of many cases exhibited several various features of the disease. The Coronavirus disease 2019 (COVID-19) symptoms are not limited to the virus’s first definitions. This review gathered the contemporary information throughout PubMed, Scopus, and Science Direct databases regarding possible effects of the virus in generating reactive oxygen species and causing oxidative stress. However, this ensures a hypothesis for now, yet from the literature and incidence of COVID-19 symptoms along with comorbidities we can observe the potentials of the virus in the generation of oxidative stress. Especially the virus’s route to cell entry via angiotensin-converting enzyme 2 (ACE2) receptor is well known that leads to pathogenesis in angiotensin II (AT II) which are critical in NADH/NADPH oxidase inducing ROS generation. Moreover, the virus’s activity to replicate seems to be reduced in high antioxidant glutathione level concentrations. The outcome of the review proposes a hypothesis that COVID-19 is associated with reactive oxygen species and its comorbidities mostly joined with oxidative stress including hypertension, cardiovascular, thrombosis, obesity, and diabetes besides of chronic obstructive pulmonary disease and asthma.

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1537
Author(s):  
Akihiko Taniguchi ◽  
Mitsuru Tsuge ◽  
Nobuaki Miyahara ◽  
Hirokazu Tsukahara

The respiratory system is continuously exposed to endogenous and exogenous oxidants. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the airways, leading to the destruction of lung parenchyma (emphysema) and declining pulmonary function. It is increasingly obvious that reactive oxygen species (ROS) and reactive nitrogen species (RNS) contribute to the progression and amplification of the inflammatory responses related to this disease. First, we described the association between cigarette smoking, the most representative exogenous oxidant, and COPD and then presented the multiple pathophysiological aspects of ROS and antioxidative defense systems in the development and progression of COPD. Second, the relationship between nitric oxide system (endothelial) dysfunction and oxidative stress has been discussed. Third, we have provided data on the use of these biomarkers in the pathogenetic mechanisms involved in COPD and its progression and presented an overview of oxidative stress biomarkers having clinical applications in respiratory medicine, including those in exhaled breath, as per recent observations. Finally, we explained the findings of recent clinical and experimental studies evaluating the efficacy of antioxidative interventions for COPD. Future breakthroughs in antioxidative therapy may provide a promising therapeutic strategy for the prevention and treatment of COPD.


2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Amrit Kaur Bansal ◽  
G. S. Bilaspuri

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Mads Emil Bjørn ◽  
Hans Carl Hasselbalch

Reactive oxygen species (ROS) have been implicated in a wide variety of disorders ranging between traumatic, infectious, inflammatory, and malignant diseases. ROS are involved in inflammation-induced oxidative damage to cellular components including regulatory proteins and DNA. Furthermore, ROS have a major role in carcinogenesis and disease progression in the myeloproliferative neoplasms (MPNs), where the malignant clone itself produces excess of ROS thereby creating a vicious self-perpetuating circle in which ROS activate proinflammatory pathways (NF-κB) which in turn create more ROS. Targeting ROS may be a therapeutic option, which could possibly prevent genomic instability and ultimately myelofibrotic and leukemic transformation. In regard to the potent efficacy of the ROS-scavenger N-acetyl-cysteine (NAC) in decreasing ROS levels, it is intriguing to consider if NAC treatment might benefit patients with MPN. The encouraging results from studies in cystic fibrosis, systemic lupus erythematosus, and chronic obstructive pulmonary disease warrant such studies. In addition, the antioxidative potential of the widely used agents, interferon-alpha2, statins, and JAK inhibitors, should be investigated as well. A combinatorial approach using old agents with anticancer properties together with novel JAK1/2 inhibitors may open a new era for patients with MPNs, the outlook not only being “minimal residual disease” and potential cure but also a marked improvement in inflammation-mediated comorbidities.


2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Yang Sun ◽  
Sachiko Ito ◽  
Naomi Nishio ◽  
Yuriko Tanaka ◽  
Nana Chen ◽  
...  

Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2αin GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Roland Akhigbe ◽  
Ayodeji Ajayi

AbstractOxidative stress, an alteration in the balance between reactive oxygen species (ROS) generation and antioxidant buffering capacity, has been implicated in the pathogenesis of cardiometabolic disorders (CMD). At physiological levels, ROS functions as signalling mediators, regulates various physiological functions such as the growth, proliferation, and migration endothelial cells (EC) and smooth muscle cells (SMC); formation and development of new blood vessels; EC and SMC regulated death; vascular tone; host defence; and genomic stability. However, at excessive levels, it causes a deviation in the redox state, mediates the development of CMD. Multiple mechanisms account for the rise in the production of free radicals in the heart. These include mitochondrial dysfunction and uncoupling, increased fatty acid oxidation, exaggerated activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), reduced antioxidant capacity, and cardiac metabolic memory. The purpose of this study is to discuss the link between oxidative stress and the aetiopathogenesis of CMD and highlight associated mechanisms. Oxidative stress plays a vital role in the development of obesity and dyslipidaemia, insulin resistance and diabetes, hypertension via various mechanisms associated with ROS-led inflammatory response and endothelial dysfunction.


2020 ◽  
Vol 23 (1) ◽  
pp. 57-64
Author(s):  
M. A. Shirshakova ◽  
Elena A. Morozova

A smokers lips are more likely to change because of exposure to reactive oxygen species that contain oxygen in large quantities in tobacco smoke. Oxidative stress is a crucial factor in the development of smoking-related diseases, such as oral cancer, lung cancer, and chronic obstructive pulmonary diseases. The damaging effect occurs because of the imbalance between the generation of reactive oxygen species and their detoxification. Markers of oxidative stress include parameters of lipid peroxidation, the activity of glutathione and antioxidant enzymes, and oxidative DNA damage. The destruction of hyaluronic acid (HA), the only drug used to correct lip changes, in smokers is accelerated by its participation in reactions with active oxygen forms, and not just by pathemization because of enzymatic cleavage by hyaluronidase. Mannitol has strong antioxidant properties, which makes it an ideal auxiliary substance in the composition of fillers based on HA. The role of reactive oxygen species in the aging process and their effects on both endogenous HA and HA-based drugs developed for esthetic use are discussed. A review of drugs, based on mannitol with hyaluronic fillers, is provided. The inclusion of mannitol in hyaluronic fillers is an effective and safe way to improve both short-term and long-term esthetic effects of the HA injection.


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