scholarly journals Role of reactive oxygen species in cell physiology and pathology and their pharmacological regulation

2014 ◽  
Vol 12 (4) ◽  
pp. 13-21 ◽  
Author(s):  
Vasiliy Egorovich Novikov ◽  
Olga Sergeevna Levchenkova ◽  
Yelena Vasilyevna Pozhilova

This review is devoted to analysis of modern scientific investigations about role of reactive oxygen species (ROS) in physiology and pathophysiology of cell. Key issues of ROS generation, their function in signaling pathways, role in the cellular pathology, functioning of antioxidant system are discussed in the paper. The review also summarizes literature data about possibility of pharmacological regulation of the activity of free radical oxidation reactions, which have practical value for effective pharmacotherapy of diseases in pathogenesis of which destructive action of ROS is present.

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
Meera Ramanujam ◽  
Rengarajulu Puvanakrishnan

Neutrophil infiltration plays a major role in the pathogenesis of myocardial injury. Oxidative injury is suggested to be a central mechanism of the cellular damage after acute myocardial infarction. This study is pertained to the prognostic role of a tetrapeptide derivative PEP1261 (BOC-Lys(BOC)-Arg-Asp-Ser(tBu)-OtBU), a peptide sequence (39–42) of lactoferrin, studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation, lysosomal enzymes release, and enhanced expression of C proteins. The groundwork experimentation was concerned with the isolation of neutrophils from the normal and acute myocardial infarct rats to find out the efficacy of PEP1261 in the presence of a powerful neutrophil stimulant, phorbol 12-myristate 13 acetate (PMA). Stimulation of neutrophils with PMA resulted in an oxidative burst of superoxide anion and enhanced release of lysosomal enzymes and expression of complement proteins. The present study further demonstrated that the free radicals increase the complement factors in the neutrophils confirming the role of ROS. PEP1261 treatment significantly reduced the levels of superoxide anion and inhibited the release of lysosomal enzymes in the stimulated control and infarct rat neutrophils. This study demonstrated that PEP1261 significantly inhibited the effect on the ROS generation as well as the mRNA synthesis and expression of the complement factors in neutrophils isolated from infarct heart.


2015 ◽  
Vol 51 (89) ◽  
pp. 16139-16142 ◽  
Author(s):  
Yuyuan Yao ◽  
Bin Jiang ◽  
Yajun Mao ◽  
Juan Chen ◽  
Zhenfu Huang ◽  
...  

A positive role of PFRs in enhancing reactive oxygen species (ROS) generation for an extreme rate enhancement in environmental pollutant decomposition is reported.


Nanoscale ◽  
2018 ◽  
Vol 10 (34) ◽  
pp. 15911-15917 ◽  
Author(s):  
Erik Jacques ◽  
Manuel Ahumada ◽  
Brianna Rector ◽  
Goonay Yousefalizadeh ◽  
Constanza Galaz-Araya ◽  
...  

Free radical oxidation of CLP-Trp peptides@AgNPs was studied using steady state & ultrafast spectroscopy and molecular dynamics.


2019 ◽  
Vol 100 (4) ◽  
pp. 636-641 ◽  
Author(s):  
E F Galimova ◽  
Z G Khaibullina ◽  
D A Enikeev ◽  
Yu L Bortsova ◽  
K S Mochalov ◽  
...  

Aim. The study of free radical oxidation processes in an experiment on model systems using the anti-inflammatory drug bromfenac (nakwan) widely used in ophthalmology for the treatment of infectious and inflammatory diseases of the anterior chamber of the eye. Methods. The antioxidant capacity of the drug was evaluated by chemiluminescence registration and analysis of model systems that generate reactive oxygen species and reproduce lipid peroxidation processes using the chemiluminomer CL-003. The following parameters of spontaneous and induced chemiluminescence were determined: light sum and maximum luminescence amplitude, duration of latent period, amplitude of fast and slow flash. Results. When tested in vitro in two different model systems, a high antioxidant activity of the studied drug was established, up to complete suppression of chemiluminescence when 90 μg of bromfenac was added to the incubation medium, which characterizes the inhibition of the generation of reactive oxygen species. A significant increase in total antioxidant activity with bromfenac was also demonstrated, which is reflected by the integral parameter of chemiluminescence — light sum which decreased with the introduction of 10 μg of the drug by 1.2 times, and with 90 μg by 1.5 times. A comparative analysis of the antioxidant properties of various nonsteroidal anti-inflammatory drugs used in ophthalmic practice demonstrated a more pronounced efficacy of bromfenac compared to ketorolac, the use of which was not accompanied by statistically significant changes in chemiluminescence. A very important mechanism of the positive effect of bromfenac is the direct dependence of the action on its quantity in the reaction medium, which opens up prospects for the controlled correction of free radical phenomena and the excessive activation of lipid peroxidation in the imbalance of the pro- and antioxidant processes in biological systems. Conclusion. It is suggested that the protective effects of the drug in various infectious-inflammatory lesions of the eye can be determined, along with previously known properties, its antioxidant activity, restriction of increased production of reactive oxygen species and oxidative stress phenomena.


2019 ◽  
Vol 20 (14) ◽  
pp. 3576 ◽  
Author(s):  
Taiwo Samuel Agidigbi ◽  
Chaekyun Kim

Reactive oxygen species (ROS) and free radicals are essential for transmission of cell signals and other physiological functions. However, excessive amounts of ROS can cause cellular imbalance in reduction–oxidation reactions and disrupt normal biological functions, leading to oxidative stress, a condition known to be responsible for the development of several diseases. The biphasic role of ROS in cellular functions has been a target of pharmacological research. Osteoclasts are derived from hematopoietic progenitors in the bone and are essential for skeletal growth and remodeling, for the maintenance of bone architecture throughout lifespan, and for calcium metabolism during bone homeostasis. ROS, including superoxide ion (O2−) and hydrogen peroxide (H2O2), are important components that regulate the differentiation of osteoclasts. Under normal physiological conditions, ROS produced by osteoclasts stimulate and facilitate resorption of bone tissue. Thus, elucidating the effects of ROS during osteoclast differentiation is important when studying diseases associated with bone resorption such as osteoporosis. This review examines the effect of ROS on osteoclast differentiation and the efficacy of novel chemical compounds with therapeutic potential for osteoclast related diseases.


Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 454 ◽  
Author(s):  
Kuznetsov ◽  
Javadov ◽  
Margreiter ◽  
Grimm ◽  
Hagenbuchner ◽  
...  

Mitochondria play a critical role in maintaining cellular function by ATP production. They are also a source of reactive oxygen species (ROS) and proapoptotic factors. The role of mitochondria has been established in many aspects of cell physiology/pathophysiology, including cell signaling. Mitochondria may deteriorate under various pathological conditions, including ischemia-reperfusion (IR) injury. Mitochondrial injury can be one of the main causes for cardiac and other tissue injuries by energy stress and overproduction of toxic reactive oxygen species, leading to oxidative stress, elevated calcium and apoptotic and necrotic cell death. However, the interplay among these processes in normal and pathological conditions is still poorly understood. Mitochondria play a critical role in cardiac IR injury, where they are directly involved in several pathophysiological mechanisms. We also discuss the role of mitochondria in the context of mitochondrial dynamics, specializations and heterogeneity. Also, we wanted to stress the existence of morphologically and functionally different mitochondrial subpopulations in the heart that may have different sensitivities to diseases and IR injury. Therefore, various cardioprotective interventions that modulate mitochondrial stability, dynamics and turnover, including various pharmacologic agents, specific mitochondrial antioxidants and uncouplers, and ischemic preconditioning can be considered as the main strategies to protect mitochondrial and cardiovascular function and thus enhance longevity.


Nanomedicine ◽  
2021 ◽  
Author(s):  
Shichong Jia ◽  
Shengfang Ge ◽  
Xianqun Fan ◽  
Kam W Leong ◽  
Jing Ruan

The radiotherapy enhancement effect of numerous nanosensitizers is based on the excessive production of reactive oxygen species (ROS), and only a few systematic reviews have focused on the key strategy in nanosensitizer-mediated radiotherapy. To clarify the mechanism underlying this effect, it is necessary to understand the role of ROS in radiosensitization before clinical application. Thus, the source of ROS and their principle of tumor inhibition are first introduced. Then, nanomaterial-mediated ROS generation in radiotherapy is reviewed. The double-edged sword effect of ROS and the potential dangers they may pose to cancer patients are subsequently addressed. Finally, future perspectives regarding ROS-regulated nanosensitizer applications and development are discussed.


2014 ◽  
Vol 3 (1) ◽  
pp. 2-13
Author(s):  
Akram Ranjbar ◽  
Hassan Ghasemi ◽  
Farshad Rostampour‎

Metals can cause oxidative stress by increasing the formation of reactive oxygen species (ROS), which make antioxidants incapable of defiance against growing amounts of free radicals. Metal toxicity is related to their oxidative state and reactivity with other compounds. However, several reports about metals have been published in the recent years. Mitochondria, as a site of cellular oxygen consumption and energy production, can be a target for metals toxicity. Dysfunction of Mitochondrial oxidative phosphorylation led to the production of some metals toxicities metals through alteration in the activities of I, II, III, IV and V complexes and disruption of mitochondrial membrane. Reductions of adenosine triphosphate (ATP) synthesis or induction of its hydrolysis can impair the cellular energy production. In the present review study, the researchers have criticized reviews and some evidence about the oxidative stress as a mechanism of toxicity of metals. The metals disrupt cellular and antioxidant defense, reactive oxygen species (ROS) generation, and promote oxidative damage. The oxidative injuries induced by metals can be restored by use of antioxidants such as chelators, vitamin E and C, herbal medicine, and through increasing the antioxidants level. However, to elucidate many aspect of mechanism toxicity of metals, further studies are yet to be carried out.


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