Distribution of aerobic and oxidative stress related

MicroRNAs are considered to be important mediators that play essential roles in the regulation of diverse aspects of carcinogenesis. Growing studies have demonstrated that the ROS can regulate microRNA biogenesis and expression mainly through modulating biogenesis course, transcription factors, and epigenetic changes. On the other hand, microRNAs may in turn modulate the redox signaling pathways, altering their integrity, stability, and functionality, thus contributing to the pathogenesis of multiple diseases.

However, the information about the interplay between oxidative stress and microRNA regulation is still limited. The present review is aimed at summarizing the current understanding of molecular crosstalk between microRNAs and the generation of ROS in the pathogenesis of cancer. Usually, a moderate increase level of ROS can promote cell differentiation and proliferation, whereas overproduction of ROS may result in oxidative damage to lipids, DNA, and proteins [ 4 ].

Therefore, maintaining ROS homeostasis has a crucial role for normal cell growth and survival. Generally, the cellular levels of ROS are cautiously monitored by the natural antioxidant defense network so that the redox homeostasis could be maintained. Disruption of normal redox state a condition termed as oxidative stresseither because of excessive amounts of ROS or dysfunction of antioxidant defense system, would result in toxic damages through the production of free radicals and peroxides, thus give rise to pathophysiological situation that lead to multiple diseases, including cancer [ 35 ].

Compared to normal cells, cancer cells usually have elevated levels of ROS, reflecting a disturbance in redox hemostasis. This may attribute to enhanced metabolic activity and disrupted cellular signaling [ 167 ].

It is believed that ROS changes in cancer cells are very complicated due to the multiple factors that modulate the ROS hemostasis and stress response [ 189 ]. Under persistent oxidative stress circumstances, cancer cells may evolve a particular set of adaptive mechanisms, which not only enhance ROS scavenging systems to deal with the stress but also suppress cell apoptosis.

On the other hand, cancer cells with increased ROS level are more likely to be susceptible to damage due to excessive amounts of exogenous agents [ 1011 ]. Several studies have indicated that, to efficiently kill cancer cells and reduce drug resistance related to oxidative damage, it is pivotal to understand the complicated ROS alternations in cancer cells and the underlying regulation mechanisms [ 12 ]. MicroRNAs are small noncoding RNA molecules with a length of 19 to 25 nt that play an essential role in posttranscriptional regulation by binding to the 3 - untranslated regions UTRs of target gene and regulating various cellular processes, such as cell proliferation, apoptosis, and stress response [ 1314 ].

Previous studies have found that the regulation of microRNAs was cell type- and tissue-specific. Therefore, microRNAs can regulate different groups of mRNAs involved in diverse pathological conditions and the pathogenesis of various human diseases, such as immune system disorders and malignancies [ 15 ].

On the other hand, the relative stability of microRNA made it has the possibility to be novel diagnostic biomarkers and potential therapeutic targets for various types of cancers [ 16 ]. Mounting evidence from previous studies has implied that the expression of microRNA altered in response to ROS accumulation [ 17 ].

It is principal to understand the interplay between ROS production and microRNAs in carcinogenesis, since both of them have been demonstrated to be dysregulated and have great potential to be novel therapeutic targets in cancer. The present review focused on the comprehensive summarization of the current understanding of molecular crosstalk between ROS production and microRNAs in the pathogenesis of cancer.

Several studies have revealed that ROS production could be modulated by microRNAs through regulating several redox signaling pathways. This alternation enhances the expression and activity of several antioxidant genes that inhibit cell apoptosis, at the same time promote cancer cell survival and tumorigenesis [ 2021 ]. Karihtala and colleagues observed that upregulation of miR in pancreatic cancer was negatively associated with Nrf2 expression and predicted better cell differentiation [ 22 ].

Free radical damage - causes, symptoms, diagnosis, treatment, pathology

On the other hand, Singh et al. Silencing of miR could promote cell apoptosis and inhibit colony formation, mammosphere formation, and cell migration [ 23 ]. Eades et al. Moreover, Gu and colleagues reported that the upregulation of miR in lung cancer cells could promote tumor cell colony formation and migration, as well as repressing cell death. Downregulation of miR would significantly decrease the cellular levels of Nrf2, NAD P H quinone oxidoreductase 1, and heme oxygenase-1 HO-1thus suppressing cancer cell survival and migration and facilitating cell apoptosis [ 26 ].

Chen and colleagues reported that miRb was the upregulator of peroxiredoxin-like 2A PRXL2Aan antioxidant molecule that protects cells from oxidative damage.Javascript is currently disabled in your browser.

Several features of this site will not function whilst javascript is disabled. Received 30 November Published 26 April Volume Pages — Review by Single-blind. Editor who approved publication: Dr Richard Walker. Oxidative stress occurs from the imbalance between RONS production and these antioxidant defenses.

Aging is a process characterized by the progressive loss of tissue and organ function. The oxidative stress theory of aging is based on the hypothesis that age-associated functional losses are due to the accumulation of RONS-induced damages. At the same time, oxidative stress is involved in several age-related conditions ie, cardiovascular diseases [CVDs], chronic obstructive pulmonary disease, chronic kidney disease, neurodegenerative diseases, and cancerincluding sarcopenia and frailty.

Given the important role of oxidative stress in the pathogenesis of many clinical conditions and aging, antioxidant therapy could positively affect the natural history of several diseases, but further investigation is needed to evaluate the real efficacy of these therapeutic interventions. The purpose of this paper is to provide a review of literature on this complex topic of ever increasing interest.

Keywords: elderly, reactive oxygen species, reactive nitrogen species, antioxidants. Free radicals are highly reactive atoms or molecules with one or more unpaired electron s in their external shell and can be formed when oxygen interacts with certain molecules.

RONS, whether they are endogenous or exogenous, cause oxidative modification of each of the major cellular macromolecules carbohydrates, lipids, proteins, and DNA6 which can also be used as markers of oxidative stress. Protein carbonyl PC is formed by Fenton reaction of oxidants with lysine, arginine, proline, and threonine residues of the protein side chains. The oxidation of LDL is a complex process during which both the protein and the lipids undergo oxidative changes that can cause cholesterol accumulation.

Antioxidant defense protects biological systems from free radical toxicity and includes both endogenous and exogenous molecules. Additionally, GSH-Px converts peroxides and hydroxyl radicals into nontoxic forms by the oxidation of reduced glutathione GSH into glutathione disulfide and then reduced to GSH by glutathione reductase. Other antioxidant enzymes are glutathione-S-transferase and glucosephosphate dehydrogenase. Aging is the progressive loss of tissue and organ function over time.

Oxidative stress, cellular senescence, and consequently, SASP factors are involved in several acute and chronic pathological processes, such as CVDs, acute and chronic kidney disease CKDneurodegenerative diseases NDsmacular degeneration MDbiliary diseases, and cancer. The consequent activation of the immune system induces an inflammatory state that creates a vicious circle in which chronic oxidative stress and inflammation feed each other, and consequently, increases the age-related morbidity and mortality.

The connection between oxidative stress and the main age-related diseases is described in the following sections Figure 1. Figure 1 Oxidative stress, age-related diseases, and relative biomarkers.

CVDs are a leading cause of morbidity and mortality in the elderly, and atherosclerosis plays a crucial role as main causal event. The evidence currently available links atherosclerosis with oxidized LDL-cholesterol oxLDL as the compound mainly responsible for its production, also in elderly. In healthy adults varying in age, brachial artery flow-mediated dilation is inversely related to NT in vascular endothelial cells.

Diabetes mellitus type 1 and 2 is a metabolic disease associated with increased formation of free radicals and decreased antioxidant potential, leading to macro- and microvascular complications. Oxidant stress in type 2 diabetes T2D promotes prothrombotic reactions, leading to CV complications.

Increased intracellular glucose leads to an increased RONS production, which exceeds the antioxidant capability of the cell to neutralize them. These results suggest that there is an increased oxidative stress in the elderly T2D patients, which can be partly balanced by increased antioxidant defense system in subjects with IGT. COPD is a major cause of morbidity and mortality worldwide 39 and its prevalence increases with age. Environmental oxidants from cigarette smoke activate macrophage and epithelial cells triggering proinflammatory cytokine and chemokine generation, which induce immune response.

Released proteases break down connective tissues in the lung, potentially resulting in chronic bronchitis or emphysema. Moreover, excessive RONS released via oxidative bursts of polymorphonuclear leukocytes PMNs and alveolar macrophages have been shown to inhibit antiprotease processes and accelerate the degradation of lung tissue.Exposure to a variety of environmental factors such as salinity, drought, metal toxicity, extreme temperature, air pollutants, ultraviolet-B UV-B radiation, pesticides, and pathogen infection leads to subject oxidative stress in plants, which in turn affects multiple biological processes via reactive oxygen species ROS generation.

ROS include hydroxyl radicals, singlet oxygen, and hydrogen peroxide in the plant cells and activates signaling pathways leading to some changes of physiological, biochemical, and molecular mechanisms in cellular metabolism. Excessive ROS, however, cause oxidative stress, a state of imbalance between the production of ROS and the neutralization of free radicals by antioxidants, resulting in damage of cellular components including lipids, nucleic acids, metabolites, and proteins, which finally leads to the death of cells in plants.

Thus, maintaining a physiological level of ROS is crucial for aerobic organisms, which relies on the combined operation of enzymatic and nonenzymatic antioxidants. In this review, recent findings on the metabolism of ROS as well as the antioxidative defense machinery are briefly updated. The latest findings on differential regulation of antioxidants at multiple levels under adverse environment are also discussed here. The environment consists of a set of relationships between livings and nonliving things and is perfectly balanced by various natural processes.

Each species influences its environment and, in turn, gets influenced by it.

distribution of aerobic and oxidative stress related

In general, numerous environmental factors including salinity, drought, extreme temperature, metal toxicity, air pollutants, ultraviolet light [ 1 ], and high doses of pesticides as well as pathogen infection can lead to subject oxidative stress in plants [ 2 — 6 ]. The oxidative stress is caused either by the direct effects of environmental stress or by indirect reactive oxygen species ROS generation and accumulation, which damage a cell before elimination.

In order to evade stressors, animals are able to move and escape. Plants as sessile organisms, however, have developed complex strategies to release stressors.

It then exhibits growth retardation under oxidative stress, including flower and leaf abscission [ 78 ], root gravitropism [ 9 ], seed germination [ 10 ], polar cell growth [ 11 ], lignin biosynthesis in cell wall [ 12 ], and cell senescence [ 13 ].

They are regarded as natural byproducts of the aerobic way of life and are generated in different cellular compartments like chloroplasts, peroxisomes, mitochondria, and plasma membrane [ 16 ]. It is significant that the increase of ROS level is highly reactive and affects a large variety of cellular, physiological, and biochemical functions, such as the disruption of plasma membrane via carbohydrate deoxidation, lipid peroxidation, protein denaturation, and the destruction of DNA, RNA, enzymes, and pigments [ 17 — 20 ].

All of those result in the loss of crop yield and quality [ 621 — 27 ]. For example, in potatoes Solanum tuberosum L. Similarly, in rice Oryza sativa L. Besides, in sweet oranges Citrus sinensis L. Osbeckoverexpression of CitERF13 in citrus fruit peel resulted in rapid chlorophyll degradation and led to the accumulation of ROS [ 2930 ]. Moreover, in Arabidopsis Arabidopsis thalianamutants of the singlet oxygen 1 O 2 overproducing flu and chlorina1 ch1 have shown that 1 O 2 -induced changes in gene expression can lead to either PCD or acclimation [ 31 ].

In conclusion, all of those observations demonstrate that ROS have a significant impact on crop yield and quality. In the past several decades, research on oxidative stress was mainly focused on Escherichia coli.

In the past ten years, however, it has moved beyond animals e. It has substantially increased the understanding of the role and action of oxidative stress in general development-defense and environment-related responses [ 32 — 35 ].

Plants evolved their own antioxidant protection mechanism to maintain a dynamic balance of ROS, since the overcounteraction of ROS leads to the loss of an important intracellular signaling molecule [ 36 ].

This review primarily deals with the metabolism of ROS in plants and gives a brief introduction to the types, generation sites, and induced oxidative stresses of ROS. Then, we will focus on the antioxidative defense machinery in resisting the risk of overproduced ROS under disadvantageous environments and summarize recent researches on different environmental factors in regulating oxidative stress in plants. The environment of molecular oxygen O 2 is generally inactive due to its electron configuration [ 37 ].This study examined the effect of a yearlong exercise intervention on F 2 -isoprostane, a specific marker of lipid peroxidation and a general marker of oxidative stress.

Baseline and month measures included: urinary F 2 -isoprostane, maximal O 2 uptake, body weight, body fat percentage, waist circumference, and intra-abdominal fat surface area.

Urine samples were available from and women at baseline and months, respectively. Similar subgroup analyses by month changes in body fat percentage, weight, and intra-abdominal fat were not statistically significant. These findings suggest that aerobic exercise, when accompanied by relatively marked gains in aerobic fitness, decreases oxidative stress among previously sedentary older women, and that these effects occur with minimal change in mass or body composition.

Oxidative stress occurs when the production of reactive species, derived largely from oxygen and nitrogen, exceeds degradation by the antioxidant defense system.

The ensuing damage to DNA, protein, and lipid has been implicated in cardiovascular and pulmonary diseases, diabetes, neurodegenerative disorders, and some cancers 3 Such efforts with human study subjects have been hindered by difficulties in the measurement of oxidative damage.

Recently, however, sensitive and stable methods have become available to measure F 2 -isoprostanes 7. F 2 -isoprostanes are a family of isomeric F 2 -prostaglandin-like compounds, derived from free radical-catalyzed peroxidation of arachidonic acid, independent of the cyclooxygenase enzyme. A recent multi-institutional study concluded that F 2 -isoprostane was the most accurate method to assess oxidative stress in vivo from urine or plasma samples 9.

Given the lack of data on this topic, we investigated the effect of a yearlong aerobic exercise intervention compared to a stretching control program on F 2 -isoprostane concentrations in postmenopausal women. This work was conducted with ancillary funding, using previously collected urine specimens and data from the Physical Activity for Total Health study ClinicalTrials.

Participants were women who resided in the Seattle, WA area. All women provided written, informed consent and all procedures were approved by the Fred Hutchinson Cancer Research Center Institutional Review Board. For months 1—3, the intervention participants attended 3 mandatory exercise sessions at a study facility University of Washington or a commercial gym and exercised twice per week at home.

For months 4—12, the intervention group attended at least 1 session per week at a study facility and conducted the remaining sessions at home or at a study facility. Exercise logs were reviewed weekly by study staff to monitor adherence with the study protocol and to intervene when needed. Women in the control group attended once-weekly 45 minute stretching and relaxation sessions and were asked to not otherwise change exercise habits for the duration of the trial.

All women were asked to not change their dietary habits for the duration of the trial. At baseline immediately prior to randomization3-months, and months, participants completed self-reported questionnaires on diet item food frequency questionnairealcohol consumption, medications, and dietary supplement usage, as described previously At baseline and months, all women had a clinic visit for spot urine collection after a 12h fast.

distribution of aerobic and oxidative stress related

All samples were processed within one hour of collection, aliquoted into 1. Date and time of collection and time since last meal were recorded, as well as medications used, vigorous activities in the past eight hours, and consumption of alcoholic beverages in the previous 48 hours.Metrics details. Obesity-related oxidative stress, the imbalance between pro-oxidants and antioxidants e.

Reactive oxygen species ROS are essential for physiological functions including gene expression, cellular growth, infection defense, and modulating endothelial function. Physical activity also results in an acute state of oxidative stress. However, it is likely that chronic physical activity provides a stimulus for favorable oxidative adaptations and enhanced physiological performance and physical health, although distinct responses between aerobic and anaerobic activities warrant further investigation.

Studies support the benefits of dietary modification as well as exercise interventions in alleviating oxidative stress susceptibility. Since obese individuals tend to demonstrate elevated markers of oxidative stress, the implications for this population are significant. Therefore, in this review our aim is to discuss i the role of oxidative stress and inflammation as associated with obesity-related diseases, ii the potential concerns and benefits of exercise-mediated oxidative stress, and iii the advantageous role of dietary modification, including acute or chronic caloric restriction and vitamin D supplementation.

Acute exercise is a small source of oxidative stress, while chronic exercise elicits protective adaptations against oxidative damage. Chronic ingestion of energy-rich foods may contribute to obesity, while acute ingestion may also elicit potentially adverse metabolic responses including oxidative stress. Caloric restriction may attenuate oxidative stress and serve as a beneficial weight loss intervention for obese individuals.

The prevalence of obesity continues to increase in the USA, with recent reports indicating over Obese individuals have demonstrated markers indicative of oxidative stress, including elevated measures of reactive oxygen species ROS [ 2 ] and diminished antioxidant defense, which is associated with lower antioxidant enzymes [ 3 ].

Effect of Exercise on Oxidative Stress: A 12-Month Randomized, Controlled Trial

Oxidative stress is associated with systemic inflammation, endothelial cell proliferation and apoptosis, and increased vasoconstriction, and thus a noteworthy contributing factor to endothelial dysfunction. In concert, this evidence supports the relationship between oxidative stress, endothelial dysfunction, atherosclerosis, and cardiovascular disease CVD [ 4 ].

ROS are oxidizing agents generated during cellular metabolism when the chemical reduction of oxygen forms unstable free radicals, characterized by an unpaired electron [ 4 ]. ROS are essential for physiological functions such as gene expression, cellular growth, infection defense, and modulating endothelial function [ 4 — 6 ].

However, to maintain a physiologically beneficial level of ROS within cells, antioxidants are necessary. Antioxidants are enzymatic and nonenzymatic molecules which significantly delay or prevent the oxidizing damage of ROS through the inhibition of ROS formation and action or by repairing cells which have been damaged by ROS [ 5 ].

Furthermore, obesity-induced inflammation is frequently associated with increased oxidative stress Fig. Specifically, leptin, an adipocyte-derived hormone, is elevated in obese individuals and can induce oxidative stress [ 7 ] and plays a key role in mediating a pro-inflammatory state in obesity [ 8 ]; and Korda et al.

Additionally, the chronic ingestion of lipid-rich meals can also enhance oxidative stress, lead to weight gain, and facilitate the development of insulin resistance [ 9 ].

distribution of aerobic and oxidative stress related

These negative effects can be attenuated with specific nutrient intake strategies including caloric restriction CR and the consumption of exogenous antioxidants. Finally, oxidative stress is elevated during physical activity, but likely serves to instigate a positive antioxidant adaptation [ 1011 ].

Therefore, in this review our aim is to discuss i the role of oxidative stress and inflammation as associated with obesity-related diseases, ii the potential concerns and benefits of exercise-mediated oxidative stress, and iii the advantageous role of dietary modification, including acute or chronic CR and vitamin D supplementation. The link between obesity-induced inflammation and oxidative stress. Increased pro-inflammatory response and leukocyte infiltration in obese populations promote the formation of ROS, resulting in oxidative stress.

One of the earliest subclinical stages in the atherosclerotic process is an impairment of endothelium-dependent vasodilation, also known as endothelial dysfunction [ 12 ]. A mediator of obesity-induced endothelial dysfunction is the level of oxidative stress.Free radicals are associated with speeding up the aging process, and degenerative diseases.

They are unstable and highly reactive. An analogy of a single unpaired electron: a boy who goes stag to the prom and keeps bumping into girls trying to find a date! Too many free radicals can cause propagation of cell injury autocatalytic reaction.

It is an internal part of the cell that acts as a sort of generator that produces the energy to power the cell. The mitochondria turn the energy from food into a substance that cells can utilize. When you have too much oxidation oxidative stressyou need an ANTI-oxidant to repair it. The good news is that the cells in our bodies actually make a natural antioxidant — a substance called, glutathione.

Glutathoine is comprised of three amino acids called glycine, cystine, and glutamine. Individuals who are on the autism spectrum, as well as individuals who have ADHD have been shown to have low red blood cell glutathione. There are studies that suggest their bodies do not regenerate glutathione in a normal way, causing a cellular shortage of glutathione and therefore more likelihood of damage from toxins to which they may be exposed.

People who have this enzyme mutation cannot process B vitamins B12 and folic acid normally, which can affect many jobs the cell has to do. One of these jobs is to regenerate glutathoine. Glutathoine is made of three amino acids: cystine, glycine, and glutamine. In order to regenerate gluathione, a cell must be able to automatically generate these amino acids. When a mutation of the MTHFR gene is present, the cell cannot change homocysteine into cystathionene which is then used to regenerate glutathione.

However, unless tested for the mutation, it is impossible to know if one has it. Do not take if you are pregnant or nursing. The Doctor Emi Team. Share This Story!

Related Posts. Confused About Magnesium Compounds? High Blood Pressure Hypertension. Turmeric, Curcumin, and Your Health.Regular physical activity is an effective non-pharmacological therapy for prevention and control of hypertension. We investigated the effects of aerobic exercise training in vascular remodelling and in the mechanical and functional alterations of coronary and small mesenteric arteries from spontaneously hypertensive rats SHR.

Exercise also reduced collagen deposition and normalized altered internal elastic lamina organization and expression of MMP-9 in mesenteric arteries from SHR. Exercise did not affect contractile responses of coronary arteries but improved the endothelium-dependent relaxation in SHR.

In mesenteric arteries, training normalized the increased contractile responses induced by U and by high concentrations of acetylcholine.

Obesity-Related Oxidative Stress: the Impact of Physical Activity and Diet Manipulation

Exercise training of SHR improves endothelial function and vascular stiffness in coronary and small mesenteric arteries.

This might be related to the concomitant decrease of oxidative stress and increase of NO bioavailability. Such effects demonstrate the beneficial effects of exercise on the vascular system and could contribute to a reduction in blood pressure.

Hypertension is associated with vascular structural, mechanical and functional alterations such as increased wall-to-lumen ratio and vascular stiffness, impairment of endothelium-dependent vasodilator responses and enhancement of vasoconstrictor responses to different agonists. Reactive oxygen species ROS seem to play a major role in these alterations through their effects on cellular function such as inactivation of NO, regulation of cell growth and differentiation, modulation of synthesis and degradation of extracellular matrix ECM proteins and activation of many kinases and of pro-inflammatory genes Lee and Griendling, ; Briones and Touyz, ; Drummond et al.

A sedentary lifestyle has been identified as a risk factor for development of cardiovascular disease, and aerobic activity is considered to be an effective component of prevention of cardiovascular events Mitchell et al. In terms of hypertension, aerobic exercise is a well-recommended non-pharmacological measure that is effective for prevention and control of high blood pressure levels Fagard and Cornelissen, Exercise training is known to change the morphology of vessels from spontaneously hypertensive rats SHR Amaral et al.

In addition, improved endothelium-dependent responses after exercise training have been demonstrated in hypertensive humans Higashi and Yoshizumi, ; Yung et al. Hypertension appears to be responsible for increased coronary resistance, impaired autoregulation and left ventricular dysfunction Harrison et al. On the other hand, resistance arteries are mainly involved in the regulation of blood pressure. In addition, the exact mechanisms whereby exercise contributes to improve cardiovascular health need to be better understood and amelioration of oxidative stress is emerging as a strong candidate.

Growing evidence indicates that exercise increases antioxidant capacity Gomez-Cabrera et al. The purpose of the present study was to investigate the effects of aerobic exercise training in the vascular remodelling and in the mechanical and functional alterations of coronary and small mesenteric arteries from SHR and to elucidate the underlying mechanisms. We would propose that aerobic exercise training improves the hypertension-associated vascular alterations by modulating oxidative stress and NO bioavailability, and this in turn could contribute to the observed effects of exercise on blood pressure.


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