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1

Pathogenesis of Reactive Oxygen Species: A Review

100%

Olajide P. A., Omowumi O. S., Odine G. O.

World News of Natural Sciences

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2022

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vol. 44

150-164

EN

Oxidative stress is known top-lay an important role in the development and pathogenesis of several chronic diseases such as diabetes, neurodegenerative diseases, and cancer. Exposure to poisons and toxicants results in the generation of pro-oxidant which eventually cause dysfunction in enzymatic activities and defect in the DNA, resulting to alteration in the expression of genes the induction of oxidative stress is by far associated with modern life styles which include the consumption and exposure to chemicals which are used to preserve and process food. Hence, this review provides insight to the relationship between reactive oxygen species and some chronic disorders. That is the contribution of reactive oxygen species to the pathogenesis of some diseases.

2

Changes in the Blood Antioxidant Defense Capacity During a 24 Hour Run

100%

Zbigniew W., Ewa S.-K., Barbara K., Sławomir J., Małgorzata M., Katarzyna K., Stanisław P., Dagmara G.

Journal of Human Kinetics

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2010

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vol. 24

65-74

EN

The objective of this study was to determine whether running a 24-h race would cause oxidative damage and changes in the blood antioxidant defense capacity in endurance-trained athletes. Fourteen male amateur runners (mean age 43.0±10.8 y, body weight 64.3±7.2 kg height 171±5 cm, weekly covered distance 81±43 km, training history 8±9 y) who participated in a 24-hr ultra-marathon and volunteered to give blood samples during the race were enrolled for this study. Blood samples were taken before the run, after completing the marathon distance (42.217 km), after 12 h and at the conclusion of the race.The capacity of erythrocyte antioxidant defense system was evaluated by measuring the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), glutathione reductase (GR), concentrations of non-enzymatic antioxidants (uric acid and glutathione-GSH), and selected biomarkers of oxidative stress (i.e., plasma level of malondialdehyde (MDA) and plasma antioxidant capacity by FRAP ("ferric-reducing ability of plasma")). Moreover, in order to elucidate between-group differences in the total capacity of the blood antioxidant defense system, an index of antioxidant potential (POTAOX) was calculated as a sum of standardized values of activities of antioxidant enzymes (SOD, CAT, GPX, GR) and non-enzymatic antioxidants (uric acid, GSH).A progressive decline was observed in activities of SOD and CAT with the distance covered during the race, while the opposite trend was found in activities of GPX and GR that tended to increase. A significant decrease was recorded in GSH content after completing the marathon distance, which tended toward slightly higher values, without reaching the baseline level, at the finish of the race. Plasma concentration of uric acid (UA) was not significantly affected, except for the value recorded after 12 h of running that was significantly (p<0.05) lower, while both markers of oxidative stress (FRAP and MDA) increased significantly after completing the marathon distance. Comparison of the calculated values of the POTAOX index recorded pre-race and throughout the competition implies that the most drastic decline in the total antioxidant capacity occurred at mid-race (i.e. after 12 h of running).

3

Life with Oxidative Stress

100%

Gurda D., Kietrys A. M., Szopa A., Twardowski T.

Chemical and Process Engineering

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2012

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vol. 33

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issue 4

509-528

EN

Incomplete oxygen reduction gives rise to reactive oxygen species (ROS). For a long time they have been considered unwelcome companions of aerobic metabolism. Organisms using oxygen developed several systems of ROS scavenging with enzymatic and non enzymatic antioxidants, which allow them control the cellular level of oxygen derived from free radicals. It is well established nowadays that ROS are not necessarily negative byproducts, but they also play an important role in cellular mechanisms. They are involved in many regular cellular processes in all aerobic organisms. When the antioxidant system is overcome and the balance between ROS production and scavenging is disrupted, oxidative stress occurs. It has been reported that oxidative stress may be linked to some human diseases and is also involved in biotic and abiotic stress response in plants.

4

Role of mitochondria in carcinogenesis

88%

Tokarz P., Blasiak J.

Acta Biochimica Polonica

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2014

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vol. 61

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issue 4

671-678

EN

Mitochondria play the central role in supplying cells with ATP and are also the major source of reactive oxygen species (ROS) - molecules of both regulatory and destructive nature. Dysfunction of mitochondrial metabolism and/or morphology have been frequently reported in human cancers. This dysfunction can be associated with mitochondrial DNA (mtDNA) damage, which may be changed into mutations in mtDNA coding sequences, or the displacement-loop region, changes in the mtDNA copy number or mtDNA microsatellite instability. All these features are frequently associated with human cancers. Mutations in mtDNA can disturb the functioning of the ROS-producing organelle and further affect the entire cell which may contribute to genomic instability typical for cancer cells. Although the association between some mtDNA mutations and cancer is well established, the causative relationship between these two features is largely unknown. A hint suggesting the driving role of mtDNA mutations in carcinogenesis comes from the observation of tumor promotion after mtDNA depletion. Mitochondria with damaged DNA may alter signaling of the mitochondrial apoptosis pathway promoting cancer cell survival and conferring resistance to anticancer drugs. This resistance may be underlined by mtDNA copy number depletion. Therefore, mitochondria are considered a promising target in anticancer therapy and several mitochondria-targeting drugs are in preclinical and clinical trials. Some other aspects of mitochondrial structure and functions, including morphology and redox potential, can also be associated with cancer transformation and constitute new anticancer targets. Recently, several studies have disclosed new mechanisms underlying the association between mitochondria and cancer, including the protection of mtDNA by telomerase, suggesting new approaches in mitochondria-oriented anti-cancer therapy.

5

THE EFFECTS OF CARVACROL ON OXIDATIVE STRESS PARAMETERS AND APOPTOSIS PROCESS VIA TRPA1 CHANNELS IN NEUROBLASTOMA CELLS

88%

Gunal M. Y., Ovey I. S.

Acta Poloniae Pharmaceutica - Drug Research

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2019

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vol. 76

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issue 3

535-542

EN

Objectives: This study is a preliminary study to investigate the effects of carvacrol (CRV) obtained from thyme on the apoptosis process in neuroblastoma cells. Methods: In this study, seven groups were designed as control, CRV, CRV + AP-18, CRV + melatonin, CRV + melatonin + AP-18, melatonin and melatonin + AP-18. All groups were stimulated using CNM (cinnamaldehyde) which is TRPA1 channel stimulator. Levels of Reactive oxygen species (ROS), caspase-3, caspase-9, mitochondrial depolarization, apoptosis, intracellular free calcium and 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) were measured. Data were evaluated using one way ANOVA analysis. Results: Levels of ROS, mitochondrial depolarisation, caspase-3 and -9 and apoptosis were significantly higher in all groups treated with CRV compared to control (P <0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, ROS and caspase-3 were significantly lower than control (P <0,05). MTT levels were significantly decreased in all groups treated with CRV compared to control (P <0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, MTT was higher than control(P <0,05). Conclusion: It has also been shown that CRV can also exert its effects through TRPA1 channels in neuroblastoma cells, which may accelerate the apoptosis process by acting on these channels, increasing ROS and caspase-3 levels. Changes in MTT levels support this result. However, in order to better evaluate the effects of CRV on the apoptosis process, it would be useful to investigate changes in caspase-9, mitochondrial depolarization, and calcium channels.

6

Life with Oxidative Stress

88%

Twardowski T., Gurda D., Kietrys A. M., Szopa A.

Chemical and Process Engineering

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2012

|

issue 4

7

The production of reactive oxygen species in peripheral blood neutrophils is modulated by airway mucous

88%

Babusyte A., Jeroch J., Stakauskas R., Sakalauskas R.

Open Medicine

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2009

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vol. 4

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issue 2

245-252

EN

Neutrophils are a major source of reactive oxygen species (ROS). The role of airway mucous on ROS production is unknown. The aim of our study was to investigate the direct influence of bronchoalveolar lavage fluid (BALF) and induced sputum (IS) alone or in combination with chemical/biological stimulus on ROS production in peripheral blood neutrophils during chronic obstructive pulmonary disease (COPD). Neutrophils were isolated from peripheral blood of 47 patients with moderate COPD and 14 healthy individuals (HI). BALF/RPMI (1:1) or IS/RPMI (1:1) from COPD patients were used to stimulate neutrophils alone or in combination with phorbolmyristate- acetate (PMA) (0.1–30 nM) or Staphylococcus aureus bacteria (0.7–500 bact/neutrophil). Relative generation of ROS was measured flow cytometrically. BALF/RPMI and in combination with relatively low PMA or all bacteria concentrations stimulated ROS; while, combination with relatively high PMA concentrations suppressed ROS in of COPD patients and HI. IS/RPMI and its combination with PMA inhibited ROS generation in both groups; whereas, IS stimulated or had a tendency to stimulate ROS production with relatively high bacteria concentrations. In conclusion, BALF and IS directly or in combination with chemical/biological factors modulated ROS production. This effect was stronger in neutrophils from COPD patients and depended on chemical/biological stimulus intensity.

8

Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging.

88%

Kirchman P. A., Miceli M. V., West R. L., Jiang J. C., Kim S., Michal Jazwinski S.

Acta Biochimica Polonica

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2003

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vol. 50

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issue 4

1039-1056

EN

The yeast Saccharomyces cerevisiae has a finite replicative life span. Yeasts possess two prohibitins, Phb1p and Phb2p, in similarity to mammalian cells. These proteins are located in the inner mitochondrial membrane, where they are involved in the processing of newly-synthesized membrane proteins. We demonstrate that the elimination of one or both of the prohibitin genes in yeast markedly diminished the replicative life span of cells that lack fully-functional mitochondria, while having no effect on cells with functioning mitochondria. This deleterious effect was suppressed by the deletion of the RAS2 gene. The expression of PHB1 and PHB2 declined gradually up to 5-fold during the life span. Cells in which PHB1 was deleted in conjunction with the absence of a mitochondrial genome displayed remarkable changes in mitochondrial morphology, distribution, and inheritance. This loss of mitochondrial integrity was not seen in cells devoid of PHB1 but possessing an intact mitochondrial genome. In a subset of the cells, the changes in mitochondrial integrity were associated with increased production of reactive oxygen species, which co-localized with the altered mitochondria. The mitochondrial deficits described above were all suppressed by deletion of RAS2. Our data, together with published information, are interpreted to provide a unified view of the role of the prohibitins in yeast aging. This model posits that the key initiating event is a decline in mitochondrial function, which leads to progressive oxidative damage that is exacerbated in the absence of the prohibitins. This aggravation of the initial damage is ameliorated by the suppression of the production of mitochondrial proteins in the absence of Ras2p signaling of mitochondrial biogenesis.

9

Lycopene as a guardian of redox signalling

88%

Palozza P., Catalano A., Simone R., Cittadini A.

Acta Biochimica Polonica

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2012

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vol. 59

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issue 1

21-25

EN

It has been suggested that lycopene, the major carotenoid found in tomato, exhibits health-beneficial effects by virtue of its antioxidant activity. However, recent literature suggests that lycopene can actually "perform" roles independent of such capacity and involving a direct modulation of redox signalling. Reactive oxygen species are known to act as second messengers in the modulation of cellular signalling leading to gene expression changes and pharmacological responses. Lycopene may control redox-sensitive molecular targets, affecting enzyme activities and expressions and modulating the activation of MAPKs and transcription factors, such as NF-κB and AP-1, Nrf2.

10

Plasma humanin as a prognostic biomarker for canine myxomatous mitral valve disease: a comparison with plasma NT-roBNP

75%

Mangkhang K., Punyapornwithaya V., Tankaew P., Pongkan W., Chattipakorn N., Boonyapakorn C., Mangkhang K., Punyapornwithaya V., Tankaew P., Pongkan W., Chattipakorn N., Boonyapakorn C.

Polish Journal of Veterinary Sciences

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2018

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vol. 21

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issue 4

11

Oxidative damage to DNA and antioxidant status in aging and age-related diseases

75%

Olinski R., Siomek A., Rozalski R., Gackowski D., Foksinski M., Guz J., Dziaman T., Szpila A., Tudek B.

Acta Biochimica Polonica

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2007

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vol. 54

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issue 1

11-26

EN

Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.

12

The key role of the redox status in regulation of metabolism in photosynthesizing organisms

75%

Kornas A., Kuźniak E., Ślesak I., Miszalski Z.

Acta Biochimica Polonica

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2010

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vol. 57

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issue 2

143-151

EN

The redox status of the cell is described by the ratio of reduced to non-reduced compounds. Redox reactions which determine the redox state are an essential feature of all living beings on Earth. However, the first life forms evolved under strongly anoxic conditions of the young Earth, and the redox status probably was based on iron and sulphur compounds. Nowadays, redox reactions in cells have developed in strict connection to molecular oxygen and its derivatives i.e. reactive oxygen species (ROS). Oxygen has started to accumulate on the Earth due to oxygenic photosynthesis. All aspects of aerobic life involve ROS, reactive nitrogen species (RNS), antioxidants and redox regulation. Many different redox-active compounds are involved in the complex of redox processes, including pyridine nucleotides, thioredoxins, glutaredoxins and other thiol/disulphide-containing proteins. Redox regulation is integrated with the redox-reactions in photosynthesis and respiration to achieve an overall energy balance and to maintain a reduced state necessary for the biosynthetic pathways that are reductive in nature. It underlies the physiological and developmental flexibility in plant response to environmental signals.

13

Female headstart in resistance to hyperoxia-induced oxidative stress in mice

63%

Šarić A., Sobočanec S., Šafranko Ž., Popović-Hadžija M., Aralica G., Korolija M., Kušić B., Balog T.

Acta Biochimica Polonica

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2014

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vol. 61

|

issue 4

801-807

EN

Increased oxygen concentration (hyperoxia) induces oxidative damage of tissues and organs. Oxygen toxicity in hyperoxia is controlled by factors such as sex, age, tissue, strain and hormones. In most species females show lower incidence of some age-related pathologies linked with oxidative stress, which has been attributed to a beneficial effect of ovarian hormones. In this study we found that hyperoxia induced hepatic oxidative damage exclusively in male CBA/H mice, followed by their decreased survival. Histopathological examination revealed that the observed differences in survival were not the consequence of acute lung injury induced by hyperoxia. Next, we observed that an increased Sirt1 protein level in hyperoxia-exposed female CBA/H mice correlated with their lower PPAR-γ and higher eNOS and Sod2 protein levels. In males, higher PPAR-γ and lower Sod2 protein levels were associated with unchanged Sirt1 expression. Although these results are of a correlative nature only, they clearly show that females show better survival, increased resistance to hyperoxia and have generally more efficient defense systems, which suggests that their headstart in resistance to hyperoxia could be a consequence of the beneficial effect of ovarian hormones.

14

Anticancer Activities of Ferrous and Ferric Ions in Progression, Proliferation, Angiogenesis, Invasion and Metastasis against Cancer and Tumor Cells

63%

Ishida T.

World News of Natural Sciences

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2018

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vol. 17

111-129

EN

The process of ferroptotic death is characterized by the overwhelming, iron-depending accumulation of lethal lipid ROS. Unlike other forms of apoptotic and non-apoptotic death, this requirement for ROS accumulation appears to be universal. Redox cycling is a characteristic of transition metals such as iron (Ferritin Fe3+ ⇄ Ferrous Fe2+). Iron via the Fenton reaction can exacerbate the consequences of hydrogen peroxide (H2O2) production, leading to the generation of hydroxyl radicals. The superoxide ion can participate in regenerating ferrous iron that is required for the Fenton reaction. An excess of iron is toxic due to its ability to engage in redox cycling and promote free radical formation. Super oxide anion generation; O2 → ･O2－. Hydrogen peroxide production; ･O2－ + 2H+ + e- → H2O2. Haber-Weiss reaction; H2O2 + O2－ → ･OH + OH－ + O2. Fenton reaction; Fe2+ + H2O2 → Fe3+ + OH－ + ･OH. Reduction to Fe(Ⅱ); Fe3+ ＋･O2－ → Fe2+ + O2. Ferritin is stable in iron-rich conditions, whereas it is rapidly degraded under conditions of iron starvation and ferritin degradation can be led. New blood vessel formation in angiogenesis is fundamental to tumor growth, invasion, and metastatic dissemination. Iron deficiency will lead to the dysfunction of immune system, metabolic disorders, myasthenia and anemia, whereas, excess iron also damages several vital organs. Thus, iron is essential for multiple cell functions, but is also potentially deleterious reasons of its ability to generate free oxygen radicals, iron balance by continuously recycling and reusing cellular iron, storage in ferritin, and export through ferroportin protecting cells from free iron toxicity. However. the exact molecular mechanism involved on iron imbalance in development for tumor cells and the iron overload-mediated induction of apoptosis are required to be explored in future.

15

Molecules released by helminth parasites involved in host colonization

51%

Dzik J. M.

Acta Biochimica Polonica

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2006

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vol. 53

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issue 1

33-64

EN

Parasites are designed by evolution to invade the host and survive in its organism until they are ready to reproduce. Parasites release a variety of molecules that help them to penetrate the defensive barriers and avoid the immune attack of the host. In this respect, particularly interesting are enzymes and their inhibitors secreted by the parasites. Serine-, aspartic-, cysteine-, and metalloproteinases are involved in tissue invasion and extracellular protein digestion. Helminths secrete inhibitors of these enzymes (serpins, aspins, and cystatins) to inhibit proteinases, both of the host and their own. Proteinases and their inhibitors, as well as helminth homologues of cytokines and molecules containing phosphorylcholine, influence the immune response of the host biasing it towards the anti-inflammatory Th2 type. Nucleotide-metabolizing enzymes and cholinesterase are secreted by worms to reduce inflammation and expel the parasites from the gastrointestinal tract. An intracellular metazoan parasite, Trichinella spiralis, secretes, among others, protein kinases and phosphatases, endonucleases, and DNA-binding proteins, which are all thought to interfere with the host cellular signals for muscle cell differentiation. Secretion of antioxidant enzymes is believed to protect the parasite from reactive oxygen species which arise from the infection-stimulated host phagocytes. Aside from superoxide dismutase, catalase (rarely found in helminths), and glutathione peroxidase (selenium-independent, thus having a poor activity with H2O2), peroxiredoxins are probably the major H2O2-detoxifying enzymes in helminths. Secretion of antioxidant enzymes is stage-specific and there are examples of regulation of their expression by the concentration of reactive oxygen species surrounding the parasite. The majority of parasite-secreted molecules are commonly found in free-living organisms, thus parasites have only adapted them to use in their way of life.

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Pathogenesis of Reactive Oxygen Species: A Review

Changes in the Blood Antioxidant Defense Capacity During a 24 Hour Run

Life with Oxidative Stress

Role of mitochondria in carcinogenesis

THE EFFECTS OF CARVACROL ON OXIDATIVE STRESS PARAMETERS AND APOPTOSIS PROCESS VIA TRPA1 CHANNELS IN NEUROBLASTOMA CELLS

Life with Oxidative Stress

The production of reactive oxygen species in peripheral blood neutrophils is modulated by airway mucous

Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging.

Lycopene as a guardian of redox signalling

Plasma humanin as a prognostic biomarker for canine myxomatous mitral valve disease: a comparison with plasma NT-roBNP

Oxidative damage to DNA and antioxidant status in aging and age-related diseases

The key role of the redox status in regulation of metabolism in photosynthesizing organisms

Female headstart in resistance to hyperoxia-induced oxidative stress in mice

Anticancer Activities of Ferrous and Ferric Ions in Progression, Proliferation, Angiogenesis, Invasion and Metastasis against Cancer and Tumor Cells

Molecules released by helminth parasites involved in host colonization