scholarly journals Especies reactivas de oxígeno y su implicación en Biomedicina

2020 ◽  
Vol 34 ◽  
pp. 17-26
Author(s):  
Carmen María Lozano-Picazo ◽  
Francisco Fernández-Belda
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Damage ◽  
Ionic Channels ◽  
Stress Generation ◽  
Specific Cell ◽  
Oxygen Species ◽  
Estrés Oxidativo ◽  
Intracellular Ros ◽  
Antioxidant Mechanisms

Las especies reactivas de oxígeno (ROS) actúan como regulador intracelular cuando se generan de forma controlada en puntos concretos de la célula. Modifican la función de proteínas mediante la oxidación reversible de cisteínas. Hay quinasas y fosfatasas de proteínas, factores de transcripción y canales iónicos que están regulados por ROS. Estrés oxidativo y daño celular aparecen cuando los mecanismos antioxidantes de protección son incapaces de mantener bajo el nivel intracelular de ROS. En estas condiciones, ROS inducen pérdida de viabilidad celular en patologías degenerativas de corazón y cerebro y promueven proliferación celular ilimitada en procesos tumorales. La alteración de la función mitocondrial juega un papel clave en la generación del estrés oxidativo y por tanto es una diana terapéutica preferente para evitar o aminorar los daños oxidativos producidos por ROS. Reactive oxygen species (ROS) act as intracellular regulator when they are generated under control in specific cell spots. They modify proteins function by cysteine reversible oxidation. There are protein kinases and phosphatases, transcription factors and ionic channels that are regulated by ROS. Oxidative stress and cell damage arise when the protection antioxidant mechanisms are unable to keep low the intracellular ROS level. Under these conditions, ROS induce cell viability loss in heart and brain degenerative pathologies and promote unlimited cell proliferation in tumor processes. Alteration of the mitochondrial function is a key player in the oxidative stress generation and therefore it is preferential therapeutic target for prevention or attenuation of the ROS-induced oxidative damage.

Failure of Implantation in IVF due to oxidative stress

2021 ◽  
Vol 20 (2) ◽  
pp. 45-52
Author(s):  
Sofoklis Stavros ◽  
Antonios Koutras ◽  
Thomas Ntounis ◽  
Konstantinos Koukoubanis ◽  
Theodoros Papalios ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reproductive Tract ◽  
Sperm Quality ◽  
Reactive Oxygen ◽  
Female Reproductive Tract ◽  
Oxygen Species ◽  
Stress Markers ◽  
Multiple Levels ◽  
Antioxidant Mechanisms

Oxidative stress may play a role in implantation failure on multiple levels. Oxidative stress is found widely in several biological systems, as well as it acts on various molecular levels with different mechanisms. It has been shown that it is rather the disequilibrium between reactive oxygen species causing oxidative stress and antioxidant mechanisms counteracting their effects, than reactive oxygen species levels themselves. Reactive oxygen species play a role in implantation and fertilisation by acting on different levels of embryo-formation and endometrial changes. Additionally, it is widely abundant in the female reproductive tract including ovaries, oocytes, tubal as well as follicular fluid. Moreover, it has been shown that male fertility is affected by reactive oxygen species by determining sperm quality. Last but not least, oxidative stress may affect IVF indirectly through its actions on peritoneal fluid. As long as research studies on elucidating the development of oxidative stress markers on patients undergoing IVF continue, ever more new possibilities emerge on predicting the pregnancy outcome.

scholarly journals Effects of salinity and temperature on in vitro cell cycle and proliferation of Perkinsus marinus from Brazil

Parasitology ◽  
2016 ◽  
Vol 143 (4) ◽  
pp. 475-487 ◽  
Author(s):  
FERNANDO RAMOS QUEIROGA ◽  
LUIS FERNANDO MARQUES-SANTOS ◽  
ISAC ALMEIDA DE MEDEIROS ◽  
PATRÍCIA MIRELLA DA SILVA
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Prolonged Exposure ◽  
Cell Damage ◽  
Oxygen Species ◽  
Perkinsus Marinus ◽  
Tropical Regions ◽  
High Prevalence ◽  
Crassostrea Rhizophorae

SUMMARYField and in vitro studies have shown that high salinities and temperatures promote the proliferation and dissemination of Perkinsus marinus in several environments. In Brazil, the parasite infects native oysters Crassostrea gasar and Crassostrea rhizophorae in the Northeast (NE), where the temperature is high throughout the year. Despite the high prevalence of Perkinsus spp. infection in oysters from the NE of Brazil, no mortality events were reported by oyster farmers to date. The present study evaluated the effects of salinity (5, 20 and 35 psu) and temperature (15, 25 and 35 °C) on in vitro proliferation of P. marinus isolated from a host (C. rhizophorae) in Brazil, for a period of up to 15 days and after the return to the control conditions (22 days; recovery). Different cellular parameters (changes of cell phase's composition, cell density, viability and production of reactive oxygen species) were analysed using flow cytometry. The results indicate that the P. marinus isolate was sensitive to the extreme salinities and temperatures analysed. Only the highest temperature caused lasting cell damage under prolonged exposure, impairing P. marinus recovery, which is likely to be associated with oxidative stress. These findings will contribute to the understanding of the dynamics of perkinsiosis in tropical regions.

scholarly journals Role of Melanin in Melanocyte Dysregulation of Reactive Oxygen Species

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Noah C. Jenkins ◽  
Douglas Grossman
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Potential Alternative ◽  
Oxidative Insult ◽  
Increased Susceptibility

We have recently reported a potential alternative tumor suppressor function for p16 relating to its capacity to regulate oxidative stress and observed that oxidative dysregulation in p16-depleted cells was most profound in melanocytes, compared to keratinocytes or fibroblasts. Moreover, in the absence of p16 depletion or exogenous oxidative insult, melanocytes exhibited significantly higher basal levels of reactive oxygen species (ROS) than these other epidermal cell types. Given the role of oxidative stress in melanoma development, we speculated that this increased susceptibility of melanocytes to oxidative stress (and greater reliance on p16 for suppression of ROS) may explain why genetic compromise of p16 is more commonly associated with predisposition to melanoma rather than other cancers. Here we show that the presence of melanin accounts for this differential oxidative stress in normal and p16-depleted melanocytes. Thus the presence of melanin in the skin appears to be a double-edged sword: it protects melanocytes as well as neighboring keratinocytes in the skin through its capacity to absorb UV radiation, but its synthesis in melanocytes results in higher levels of intracellular ROS that may increase melanoma susceptibility.

scholarly journals Protective effect of esculetin against oxidative stress-induced cell damage via scavenging reactive oxygen species

2008 ◽  
Vol 29 (11) ◽  
pp. 1319-1326 ◽  
Author(s):  
So-hyung Kim ◽  
Kyoung-ah Kang ◽  
Rui Zhang ◽  
Mei-jing Piao ◽  
Dong-ok Ko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Protective Effect ◽  
Cell Damage ◽  
Reactive Oxygen ◽  
Oxygen Species

90 INTRACELLULAR REACTIVE OXYGEN SPECIES IN BOVINE EMBRYOS CULTURED IN VITRO WITH CATALASE UNDER VARIOUS OXYGEN TENSIONS

2012 ◽  
Vol 24 (1) ◽  
pp. 157 ◽  
Author(s):  
N. A. S. Rocha ◽  
B. C. S. Leão ◽  
M. F. Accorsi ◽  
G. Z. Mingoti
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Embryonic Development ◽  
Embryo Development ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bovine Embryos ◽  
Intracellular Ros ◽  
Oxygen Tensions

The production of reactive oxygen species (ROS), such as superoxide anion (O2–), hydroxyl radical (OH–) hydrogen peroxide (H2O2) and organic peroxides, is a normal process that occurs in the cellular mitochondrial respiratory chain. The high oxygen tension in in vitro culture (IVC) conditions is believed to induce oxidative stress, as a result of increase in ROS intracellular production, that can be correlated with embryonic developmental failure. Supplementation with antioxidants during IVC appears to increase the resistance of bovine embryos to the oxidative stress and consequently improve embryo development. The aim of this study was to evaluate the effects of antioxidant (catalase) and oxygen tensions during IVC on the embryonic development and quantification of intracellular ROS. Cumulus–oocyte complexes (COC; n = 337) were in vitro matured (IVM) in TCM-199 supplemented with 0.2 mM pyruvate, 25 mM sodium bicarbonate, 75 μg mL–1 gentamicin, 10% FCS and hormones for 24 h at 38.5°C and 5% CO2 in air. Then they were fertilized and the presumptive zygotes were cultured in SOFaa medium without (control) or with 100 UI catalase (CAT) for 7 days at 38.5°C in one of 2 types of humified atmosphere: 5% CO2 in air (≈20% O2) or in gaseous mixture (7% O2, 5% CO2 and 88% N2). The cleavage rate was evaluated at 72 hours post-insemination (hpi) and the embryonic development at 168 hpi. At this time, the level of intracellular ROS was measured using the fluorescent probe 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA; Molecular Probes, Invitrogen, Oakville, Canada), at 5 μM (Bain et al. 2011 Reprod. Fertil. Dev. 23, 561–575). Stained embryos were imaged immediately using an inverted microscope and analysed by Q-Capture Pro image software (QImaging, Surrey, BC, Canada). The signal intensity values of embryos were subtracted by the average of backgrounds in the images. Embryo development was analysed by chi-squared test and means of the intensity of fluorescence were compared by ANOVA followed by Tukey's test (P < 0.05). The cleavage rates were 84.04%a (control 20% O2), 77.55%a (CAT 20% O2), 77.03%a (control 7% O2) and 71.83%a (CAT 7% O2). The embryonic development rates were 40.43%a (control 20% O2), 33.67%a (CAT 20% O2), 20.27%b (control 7% O2) and 16.90%b (CAT 7% O2). The fluorescent intensity were 3.9 ± 0.4a (control 20% O2), 1.8 ± 0.2b (CAT 20% O2), 2.7 ± 0.2ab (control 7% O2) and 2.8 ± 0.2ab (CAT 7% O2). Although catalase did not significantly affect blastocyst frequencies (P > 0.05), embryo development was adversely affected by reduced O2 tension (P < 0.05). H2DCFDA staining indicated a significant (P < 0.05) reduction in the levels of intracellular ROS within embryos cultured with catalase under 20% O2 compared with the control group in the same O2 tension. Additionally, a consistent but insignificant reduction in intracellular ROS within embryos cultured under 7% O2 was found. We can conclude that supplementation with catalase to IVC medium at 20% O2 is suitable for lowering intracellular ROS levels in IVP bovine embryos, without lowering the rates of blastocysts production. This finding corroborates with theory that antioxidants are beneficial to embryo quality. Alta Genetics Brazil, Deoxi Biotecnologia.

Reactive Oxygen Species Control Hematopoietic Stem Cell-Niche Interaction through the Regulation of N-Cadherin.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 86-86
Author(s):  
Kentaro Hosokawa ◽  
Fumio Arai ◽  
Hiroki Yoshihara ◽  
Keiyo Takubo ◽  
Keisuke Ito ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Stem Cell ◽  
Cell Adhesion ◽  
Oxygen Species ◽  
Self Renewal ◽  
Cell Cycle Activation ◽  
Intracellular Ros ◽  
Quiescent Hscs

Abstract Interaction of tissue stem cells with their particular microenvironments, known as stem cell niches, is critical for maintaining the stem cell properties, including self-renewal capacity and the ability of differentiation into single or multiple lineages. We previously reported that the regulation of reactive oxygen species (ROS) is critical for the self-renewal activity of HSCs (Ito et al., Nature 2004, Ito et al., Nat Med 2006). Accumulation of ROS in HSCs induced defects in repopulating ability and in maintenance of quiescence through the activation of p38MAPK and p16Ink4a, indicating that the oxidative stress contributes to exhaustion of the stem cell population. From these findings, we hypothesized that loss of quiescence was associated with the impaired HSC-niche interaction. Oxidative stress may affect not only intrinsic function of HSC but the interaction between HSCs and their niche. In this study, we investigated the effects of ROS in the interaction of HSC with osteoblastic niche. We have found that the side-population (SP) in c-Kit+Sca-1+ Lin− (KSL) fraction was the quiescent HSCs in the osteoblastic niche and KSL-SP cells expressed N-cadherin (NCAD) (Arai et al., Cell 2004), and NCAD mediated cell adhesion induced quiescence of HSCs. Then we analyzed the role of ROS in the maintenance of NCAD-mediated cell-cell adhesion and detachment of HSCs from the niche under the myelosuppressive condition. Administration of 5-FU to mice decreases the dividing cells (non-SP fraction), but not quiescent cells (SP fraction) in BM on day 2. On day 6, HSC population was shifted from SP to non-SP fraction. This event might be associated with the cell cycle activation and detachment of HSCs from the niche. We found that 5-FU treatment transiently increased a level of intracellular ROS in HSCs and downregulated the expression of NCAD in HSCs. Administration of anti-oxidant, N-Acetyl Cysteine (NAC), in 5-FU treated mice maintained NCAD expression in HSCs, suggesting that increased ROS suppressed the expression of NCAD in HSCs. In addition, NAC treatment inhibited the transition of HSCs from SP to non-SP fraction on day 6. Moreover, 5-FU induced upregulation of G-CSFR and Flt3 expression in HSCs on day 2, while NAC treatment inhibited the expressions of growth factor receptors. These data indicated that intracellular ROS was a trigger for the detachment of HSCs from the niche, and inhibition of oxidative stress in HSCs by ant-oxidant preserved NCAD-mediated cell adhesion and blocked cell cycle activation after myelosuppression. Furthermore, these data led us the possibility that normal quiescent HSCs maintains low oxidative stress by existing in the low oxygen environment. To confirm this hypothesis, we evaluated the redox status of fractionated hematopoietic cells (Lin+, Lin−, KSL-non SP, and KSL-SP) by hypoxic marker pimonidazole. And we confirmed that &gt;80 % of KSL-SP cells were pimonidazole positive, suggesting that quiescent HSCs resided in the hypoxic niche. Altogether, our data suggest that regulation of oxidative stress is critical for the interaction between HSCs and BM niche. And osteoblastic niche maintains HSCs in low oxidative stress.

scholarly journals Pathological and Pharmacological Roles of Mitochondrial Reactive Oxygen Species in Malignant Neoplasms: Therapies Involving Chemical Compounds, Natural Products, and Photosensitizers

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5252
Author(s):  
Yasuyoshi Miyata ◽  
Yuta Mukae ◽  
Junki Harada ◽  
Tsuyoshi Matsuda ◽  
Kensuke Mitsunari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Reactive Oxygen ◽  
Chemotherapeutic Agents ◽  
Malignant Neoplasms ◽  
Oxygen Species ◽  
Efficient Treatment ◽  
Intracellular Ros

Oxidative stress plays an important role in cellular processes. Consequently, oxidative stress also affects etiology, progression, and response to therapeutics in various pathological conditions including malignant tumors. Oxidative stress and associated outcomes are often brought about by excessive generation of reactive oxygen species (ROS). Accumulation of ROS occurs due to dysregulation of homeostasis in an otherwise strictly controlled physiological condition. In fact, intracellular ROS levels are closely associated with the pathological status and outcome of numerous diseases. Notably, mitochondria are recognized as the critical regulator and primary source of ROS. Damage to mitochondria increases mitochondrial ROS (mROS) production, which leads to an increased level of total intracellular ROS. However, intracellular ROS level may not always reflect mROS levels, as ROS is not only produced by mitochondria but also by other organelles such as endoplasmic reticulum and peroxisomes. Thus, an evaluation of mROS would help us to recognize the biological and pathological characteristics and predictive markers of malignant tumors and develop efficient treatment strategies. In this review, we describe the pathological significance of mROS in malignant neoplasms. In particular, we show the association of mROS-related signaling in the molecular mechanisms of chemically synthesized and natural chemotherapeutic agents and photodynamic therapy.

scholarly journals The Role of N-Acetylcysteine Supplementation on the Oxidative Stress Levels, Genotoxicity and Lineage Commitment Potential of Ex Vivo Murine Haematopoietic Stem/Progenitor Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 130 ◽  
Author(s):  
Zariyantey A. Hamid ◽  
Hui Y. Tan ◽  
Paik W. Chow ◽  
Khairul A. W. Harto ◽  
Chin Y. Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Cell Viability ◽  
Progenitor Cells ◽  
Ex Vivo ◽  
Lineage Commitment ◽  
Oxygen Species ◽  
Intracellular Ros

Objectives: The ex vivo maintenance of haematopoietic stem/progenitor cells (HSPCs) is crucial to ensure a sufficient supply of functional cells for research or therapeutic applications. However, when exposed to reactive oxygen species (ROS) in a normoxic microenvironment, HSPCs exhibit genomic instability which may diminish their quantity and quality. This study aimed to investigate the role of N-acetylcysteine (NAC) supplementation on the oxidative stress levels, genotoxicity and lineage commitment potential of murine haematopoietic stem/progenitor cells (HSPCs). Methods: This study was carried out at the Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia, between June 2016 and July 2017. Bone marrow cells were isolated from nine mice and cultured in a growth medium. Various concentrations of NAC between 0.125–2 μM were added to the culture for 48 hours; these cells were then compared to non-supplemented cells harvested from the remaining three mice as the control group. A trypan blue exclusion test was performed to determine cell viability, while intracellular ROS levels and genotoxicity were determined by hydroethidine staining and comet assay, respectively. The lineage commitment potential of erythroid, myeloid and pre-B-lymphoid progenitor cells was evaluated via colony-forming cell assay. Results: NAC supplementation at 0.25, 0.5 and 2 μM significantly increased cell viability (P <0.050), while intracellular ROS levels significantly decreased at 0.25 and 0.5 μM (P <0.050). Moreover, DNA damage was significantly reduced at all NAC concentrations (P <0.050). Finally, the potential lineage commitment of the cells was not significantly affected by NAC supplementation (P >0.050). Conclusion: The findings of this study indicate that NAC supplementation may potentially overcome the therapeutic limitations of ex vivo-maintained HSPCs.Keywords: Hematopoietic Stem Cells; N-acetylcysteine; Reactive Oxygen Species; DNA Damage; Cell Lineage.

MRP1 Plays a Role in Regulating Hematopoietic Stem Cell Oxidative Stress and Differentiation Via MRP1-Dependent Gsh Efflux

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1223-1223
Author(s):  
Cassandra J Reiling ◽  
Dianna Howard ◽  
Christian M Paumi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cell ◽  
Oxygen Species ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Intracellular Ros ◽  
Intracellular Oxidative Stress

Abstract Abstract 1223 Hematopoietic stem cells (HSCs) are currently used therapeutically to treat diseases such as leukemia; however, a greater understanding in both the molecular and environmental requirements for HSCs self-renewal will hopefully increase the success rate of these therapeutic uses. It is increasingly evident that reactive oxygen species (ROS) and cellular oxidative stress play an important role in HSC self-renewal and differentiation. Therefore a better understanding of intracellular oxidative stress regulation is critical to increasing transplant success and increasing successful treatment of Leukemia. Our studies take aim at determining the role of multidrug resistance-associated protein 1 (MRP1) in regulating intracellular ROS in HSC's. MRP1 is expressed at slightly higher levels in HSCs than in mature blood cells. The expression pattern of MRP1 in HSCs suggests a possible role in hematopoietic stem cell integrity and differentiation. A major function of MRP1 is to help maintain the oxidative balance of the cell by transporting reduced glutathione (GSH), oxidized glutathione (GSSG), and glutathione-4-hydroxy-nonenal (HNE-SG) conjugates out of the cell. We have hypothesized that MRP1-dependent efflux of GSH and GSSG in HSC increases intracellular reactive oxygen species (ROS) resulting in a loss of self-renewing and increased differentiation of HSCs. In our current studies we have used C57BL/6 FVB and Mrp1-disrupted FVB [Mrp1 (−/−)] mice to investigate the role of MRP1 in HSC differentiation. Our experiments have revealed an increase in LT-HSC and ST-HSC and a corresponding decrease in MPP's in the MRP1 −/− mice as compared to WT matched controls. To determine if MRP1 plays a role in regulating HSC intracellular oxidative stress levels via GSH and GSSG efflux, we measured cellular oxidative stress as a function of DCF-DA and relative GSH levels as a function of glutathione-monochlorobimane (GS-MCB) conjugate fluorescence by flow cytometry. Our studies revealed higher intracellular ROS in WT mice as compared to MRP1 −/− mice and decreased GS-MCB in our WT mice as compared to the MRP1 −/− mice. Taken together the DCF-DA and MCB assays support our hypothesis that MRP1-dependent efflux of GSH/GSSG decreases cellular GSH resulting in higher level of ROS. Our hypothesis is further supported by analysis of lineage marked cells (Lin+), which showed a distinct differentiation pattern between the cells derived from WT and MRP1−/− bone marrow (BM). These studies are supported by results from colony forming cell (CFC) assays. Interestingly, analysis of whole blood did not result in a robust phenotype with regards to leukocytes; however, we found an increase in the number of platelets in MRP1−/− mice when compared to the WT. The increase in platelets is an intriguing result under further investigation. In light of our recent results we have initiated long-term transplant assays to determine if MRP1 does indeed play a role in HSC differentiation and self-renewal. If our hypothesis is true as suggested by our current studies then we expect that expression of MRP1 will negatively effect the ability of HSC's to successfully transplant in the long-term. Overall our data supports our hypothesis that MRP1-dependent efflux of GSH and GSSG in HSC increases intracellular ROS thereby decreasing HSC self-renewing potential and increasing HSC differentiation. Disclosures: No relevant conflicts of interest to declare.

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