Relevant bibliographies by topics / Endogenous ROS

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'Endogenous ROS'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Endogenous ROS"

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Supruniuk, Elżbieta, Jan Górski, and Adrian Chabowski. "Endogenous and Exogenous Antioxidants in Skeletal Muscle Fatigue Development during Exercise." Antioxidants 12, no. 2 (February 16, 2023): 501. http://dx.doi.org/10.3390/antiox12020501.

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Muscle fatigue is defined as a decrease in maximal force or power generated in response to contractile activity, and it is a risk factor for the development of musculoskeletal injuries. One of the many stressors imposed on skeletal muscle through exercise is the increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which intensifies as a function of exercise intensity and duration. Exposure to ROS/RNS can affect Na+/K+-ATPase activity, intramyofibrillar calcium turnover and sensitivity, and actin–myosin kinetics to reduce muscle force production. On the other hand, low ROS/RNS concentrations can likely upregulate an array of cellular adaptative responses related to mitochondrial biogenesis, glucose transport and muscle hypertrophy. Consequently, growing evidence suggests that exogenous antioxidant supplementation might hamper exercise-engendering upregulation in the signaling pathways of mitogen-activated protein kinases (MAPKs), peroxisome-proliferator activated co-activator 1α (PGC-1α), or mammalian target of rapamycin (mTOR). Ultimately, both high (exercise-induced) and low (antioxidant intervention) ROS concentrations can trigger beneficial responses as long as they do not override the threshold range for redox balance. The mechanisms underlying the two faces of ROS/RNS in exercise, as well as the role of antioxidants in muscle fatigue, are presented in detail in this review.
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Lu, Qing-Bin. "Reaction Cycles of Halogen Species in the Immune Defense: Implications for Human Health and Diseases and the Pathology and Treatment of COVID-19." Cells 9, no. 6 (June 13, 2020): 1461. http://dx.doi.org/10.3390/cells9061461.

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There is no vaccine or specific antiviral treatment for COVID-19, which is causing a global pandemic. One current focus is drug repurposing research, but those drugs have limited therapeutic efficacies and known adverse effects. The pathology of COVID-19 is essentially unknown. Without this understanding, it is challenging to discover a successful treatment to be approved for clinical use. This paper addresses several key biological processes of reactive oxygen, halogen and nitrogen species (ROS, RHS and RNS) that play crucial physiological roles in organisms from plants to humans. These include why superoxide dismutases, the enzymes to catalyze the formation of H2O2, are required for protecting ROS-induced injury in cell metabolism, why the amount of ROS/RNS produced by ionizing radiation at clinically relevant doses is ~1000 fold lower than the endogenous ROS/RNS level routinely produced in the cell and why a low level of endogenous RHS plays a crucial role in phagocytosis for immune defense. Herein we propose a plausible amplification mechanism in immune defense: ozone-depleting-like halogen cyclic reactions enhancing RHS effects are responsible for all the mentioned physiological functions, which are activated by H2O2 and deactivated by NO signaling molecule. Our results show that the reaction cycles can be repeated thousands of times and amplify the RHS pathogen-killing (defense) effects by 100,000 fold in phagocytosis, resembling the cyclic ozone-depleting reactions in the stratosphere. It is unraveled that H2O2 is a required protective signaling molecule (angel) in the defense system for human health and its dysfunction can cause many diseases or conditions such as autoimmune disorders, aging and cancer. We also identify a class of potent drugs for effective treatment of invading pathogens such as HIV and SARS-CoV-2 (COVID-19), cancer and other diseases, and provide a molecular mechanism of action of the drugs or candidates.
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Sharma, Ajay Kumar, Harshit Singh, and Harinath Chakrapani. "Photocontrolled endogenous reactive oxygen species (ROS) generation." Chemical Communications 55, no. 36 (2019): 5259–62. http://dx.doi.org/10.1039/c9cc01747j.

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Pan, Zhixiang, Jun Zhang, Kaili Ji, Vayou Chittavong, Xingyue Ji, and Binghe Wang. "Organic CO Prodrugs Activated by Endogenous ROS." Organic Letters 20, no. 1 (November 7, 2017): 8–11. http://dx.doi.org/10.1021/acs.orglett.7b02775.

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Hole, Paul S., Lorna Pearn, Amanda J. Tonks, Philip E. James, Alan K. Burnett, Richard L. Darley, and Alex Tonks. "Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells." Blood 115, no. 6 (February 11, 2010): 1238–46. http://dx.doi.org/10.1182/blood-2009-06-222869.

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Abstract Excessive production of reactive oxygen species (ROS) is a feature of human malignancy and is often triggered by activation of oncogenes such as activated Ras. ROS act as second messengers and can influence a variety of cellular process including growth factor responses and cell survival. We have examined the contribution of ROS production to the effects of N-RasG12D and H-RasG12V on normal human CD34+ progenitor cells. Activated Ras strongly up-regulated the production of both superoxide and hydrogen peroxide through the stimulation of NADPH oxidase (NOX) activity, without affecting the expression of endogenous antioxidants or the production of mitochondrially derived ROS. Activated Ras also promoted both the survival and the growth factor–independent proliferation of CD34+ cells. Using oxidase inhibitors and antioxidants, we found that excessive ROS production by these cells did not contribute to their enhanced survival; rather, ROS promoted their growth factor–independent proliferation. Although Ras-induced ROS production specifically activated the p38MAPK oxidative stress response, this failed to induce expression of the cell-cycle inhibitor, p16INK4A; instead, ROS promoted the expression of D cyclins. These data are the first to show that excessive ROS production in the context of oncogene activation can promote proliferative responses in normal human hematopoietic progenitor cells.
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Koval, M., S. T. Geist, E. M. Westphale, A. E. Kemendy, R. Civitelli, E. C. Beyer, and T. H. Steinberg. "Transfected connexin45 alters gap junction permeability in cells expressing endogenous connexin43." Journal of Cell Biology 130, no. 4 (August 15, 1995): 987–95. http://dx.doi.org/10.1083/jcb.130.4.987.

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Many cells express multiple connexins, the gap junction proteins that interconnect the cytosol of adjacent cells. Connexin43 (Cx43) channels allow intercellular transfer of Lucifer Yellow (LY, MW = 443 D), while connexin45 (Cx45) channels do not. We transfected full-length or truncated chicken Cx45 into a rat osteosarcoma cell line ROS-17/2.8, which expresses endogenous Cx43. Both forms of Cx45 were expressed at high levels and colocalized with Cx43 at plasma membrane junctions. Cells transfected with full-length Cx45 (ROS/Cx45) and cells transfected with Cx45 missing the 37 carboxyl-terminal amino acids (ROS/Cx45tr) showed 30-60% of the gap junctional conductance exhibited by ROS cells. Intercellular transfer of three negatively charged fluorescent reporter molecules was examined. In ROS cells, microinjected LY was transferred to an average of 11.2 cells/injected cell, while dye transfer between ROS/Cx45 cells was reduced to 3.9 transfer between ROS/Cx45 cells was reduced to 3.9 cells. In contrast, ROS/Cx45tr cells transferred LY to > 20 cells. Transfer of calcein (MW = 623 D) was also reduced by approximately 50% in ROS/Cx45 cells, but passage of hydroxycoumarin carboxylic acid (HCCA; MW = 206 D) was only reduced by 35% as compared to ROS cells. Thus, introduction of Cx45 altered intercellular coupling between cells expressing Cx43, most likely the result of direct interaction between Cx43 and Cx45. Transfection of Cx45tr and Cx45 had different effects in ROS cells, consistent with a role of the carboxyl-terminal domain of Cx45 in determining gap junction permeability or interactions between connexins. These data suggest that coexpression of multiple connexins may enable cells to achieve forms of intercellular communication that cannot be attained by expression of a single connexin.
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Sarniak, Agata, Joanna Lipińska, Karol Tytman, and Stanisława Lipińska. "Endogenous mechanisms of reactive oxygen species (ROS) generation." Postępy Higieny i Medycyny Doświadczalnej 70 (November 14, 2016): 1150–65. http://dx.doi.org/10.5604/17322693.1224259.

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HALVEY, Patrick J., Walter H. WATSON, Jason M. HANSEN, Young-Mi GO, Afshin SAMALI, and Dean P. JONES. "Compartmental oxidation of thiol–disulphide redox couples during epidermal growth factor signalling." Biochemical Journal 386, no. 2 (February 22, 2005): 215–19. http://dx.doi.org/10.1042/bj20041829.

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Exogenously added ROS (reactive oxygen species) cause generalized oxidation of cellular components, whereas endogenously generated ROS induced by physiological stimuli activate discrete signal transduction pathways. Compartmentation is an important aspect of such pathways, but little is known about its role in redox signalling. We measured the redox states of cytosolic and nuclear Trx1 (thioredoxin-1) and mitochondrial Trx2 (thioredoxin-2) using redox Western blot methodologies during endogenous ROS production induced by EGF (epidermal growth factor) signalling. The glutathione redox state was measured by HPLC. Results showed that only cytosolic Trx1 undergoes significant oxidation. Thus EGF signalling involves subcellular compartmental oxidation of Trx1 in the absence of a generalized cellular oxidation.
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Leuti, Alessandro, Mauro Maccarrone, and Valerio Chiurchiù. "Proresolving Lipid Mediators: Endogenous Modulators of Oxidative Stress." Oxidative Medicine and Cellular Longevity 2019 (June 18, 2019): 1–12. http://dx.doi.org/10.1155/2019/8107265.

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Specialized proresolving mediators (SPMs) are a novel class of endogenous lipids, derived byω-6 andω-3 essential polyunsaturated fatty acids such as arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) that trigger and orchestrate the resolution of inflammation, which is the series of cellular and molecular events that leads to spontaneous regression of inflammatory processes and restoring of tissue homeostasis. These lipids are emerging as highly effective therapeutic agents that exert their immunoregulatory activity by activating the proresolving pathway, as reported by a consistent bulk of evidences gathered in the last two decades since their discovery. The production of reactive oxygen (ROS) and nitrogen (RNS) species by immune cells plays indeed an important role in the inflammatory mechanisms of host defence, and it is now clear that oxidative stress, viewed as an imbalance between such species and their elimination, can lead to many chronic inflammatory diseases. This review, the first of its kind, is aimed at exploring the manifold effects of SPMs on modulation of reactive species production, along with the mechanisms through which they either inhibit molecular signalling pathways that are activated by oxidative stress or induce the expression of endogenous antioxidant systems. Furthermore, the possible role of SPMs in oxidative stress-mediated chronic disorders is also summarized, suggesting not only that their anti-inflammatory and proresolving properties are strictly associated with their antioxidant role but also that these endogenous lipids might be exploited in the treatment of several pathologies in which uncontrolled production of ROS and RNS or impairment of the antioxidant machinery represents a main pathogenetic mechanism.
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Kobayashi, Daisuke, Kei Kondo, Nobuyuki Uehara, Seiko Otokozawa, Naoki Tsuji, Atsuhito Yagihashi, and Naoki Watanabe. "Endogenous Reactive Oxygen Species Is an Important Mediator of Miconazole Antifungal Effect." Antimicrobial Agents and Chemotherapy 46, no. 10 (October 2002): 3113–17. http://dx.doi.org/10.1128/aac.46.10.3113-3117.2002.

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ABSTRACT We investigated the significance of endogenous reactive oxygen species (ROS) produced by fungi treated with miconazole. ROS production in Candida albicans was measured by a real-time fluorogenic assay. The level of ROS production was increased by miconazole at the MIC (0.125 μg/ml) and was enhanced further in a dose-dependent manner, with a fourfold increase detected when miconazole was used at 12.5 μg/ml. This increase in the level of ROS production was completely inhibited by pyrrolidinedithiocarbamate (PDTC), an antioxidant, at 10 μM. In a colony formation assay, the decrease in cell viability associated with miconazole treatment was significantly prevented by addition of PDTC. Moreover, the level of ROS production by 10 clinical isolates of Candida species was inversely correlated with the miconazole MIC (r = −0.8818; P < 0.01). These results indicate that ROS production is important to the antifungal activity of miconazole.
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Dissertations / Theses on the topic "Endogenous ROS"

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Singhapol, Chatchawan. "Mitochondrial localisation of hTERT protects against nuclear DNA damage and mitochondrial ROS production after endogenous and exogenous stress." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2216.

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Under oxidative stress condition, telomerase catalytic subunit can shuttle from the nucleus and localises within mitochondria. hTERT can improve mitochondrial functions and contribute to a decreased oxidative stress suggesting an entirely new function of telomerase in protecting mitochondria and cells under stress. However, there are still many questions about the mechanism and what factors influence the protective function of telomerase. In this study we investigated the kinetic exclusion of hTERT, the catalytic subunit of telomerase, in various cell lines under different oxidative stress conditions. We also used organelle specific hTERT localisation vectors to model hTERT localisation and investigated a correlation between hTERT location, nuclear DNA damage and ROS production. We found that cells excluded endogenous hTERT from the nucleus in a heterogeneous fashion independently of the cell types. Importantly, nuclear DNA damage showed a significant correlation with the localisation of hTERT. Cells where hTERT remained in the nucleus displayed high DNA damage while cells which excluded hTERT from the nucleus displayed no or very low DNA damage. Our results from specific hTERT localisation vectors specified that mitochondrial localisation of hTERT protects the nucleus from DNA damage and did not showed any sign of apoptosis induction while nuclear localisation of hTERT correlated with higher amounts of DNA damage and apoptosis. Moreover, mitochondrial localisation of hTERT decreased mitochondrial ROS generation levels directly after both endogenous and exogenous stress which we interpret as the reason for the prevention of nuclear DNA damage. Additionally, we analysed whether p53 status might influence the protective function of telomerase. Our results in an isogenic cell pair of glioblastoma cells showed that p53 status does not prominently influence the protective function of mitochondrial hTERT under low stress condition. However, nuclear hTERT of cells which contained inactive p53 displayed a significantly higher nuclear DNA damage than cells which contained an active p53 and this became more pronounced when stress levels were increased. We hypothesise that telomerase localisation might possibly interact with p53 when a cancer cell is under stress condition. However, the molecular mechanism for that is unknown. Our results demonstrate a novel link between mitochondrial localisation of hTERT, decrease of mitochondrial ROS generation and the protective capacity of hTERT to nuclear DNA from damage after stress treatments.
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Mutneja, Manpreet S. "Endogenous RGS proteins modulate acute desensitization of GIRK currents /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3099926.

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Garzon, D. "HIGH RESOLUTION MASS SPECTROMETRIC STRATEGIES FOR DETECTION OF PROTEINS AND PEPTIDES COVALENTLY MODIFIED BY ELECTROPHILIC XENOBIOTICS AND ENDOGENOUS INTERMEDIATES." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/250677.

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Non enzymatic protein covalent modifications are involved in the toxic effects induced by electrophilic xenobiotics as well as by endogenous cytotoxic oxidation by-products. Aim of my Ph.D work was to set-up MS methods for the identification, characterization and quantification of non-enzymatic covalently modified proteins and peptides in biological matrices. To reach this goal both tandem MS and high resolution approaches were employed due to the wealth of structural and molecular information that these techniques can provide. As a first step the MS methods were applied for understanding in both in vitro and ex vivo conditions the mechanism of protein haptenation induced by amoxicillin (AX). The MS approach was then focused to study in ex vivo condition the covalent reaction between histidine dipeptides, such as carnosine, and toxic endogenous intermediates like reactive carbonyl species (RCS). .
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Mourão, Carlos Manuel Pombo Martins. "Enzimas antioxidantes e patologias neurodegenerativas: estado da arte." Master's thesis, 2013. http://hdl.handle.net/10284/7043.

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A literatura apresenta uma evidência crescente de que o stress oxidativo promovido pelas espécies oxigénio-reativas (ROS) pode ter um papel vital na etiologia das doenças neurodegenerativas como a doença de Alzheimer, a doença de Parkinson ou a esquizofrenia, entre outras. As ROS possuem um papel duplo, tanto benéfico quanto prejudicial, no organismo humano. Estas são geralmente reguladas por enzimas antioxidantes endógenas para que o balanço oxidativo seja mantido mas, por factores endógenos e exógenos, pode ocorrer uma alteração com produção excessiva que resulta em stress oxidativo. Este stress oxidativo constante promove danos nos componentes celulares, como nas proteínas, nos lípidos ou nas bases do ADN. O mecanismo de oxidação é particularmente importante no cérebro, uma vez que este está exposto a grandes quantidades de oxigénio, promotor do aparecimento de radicais livres e de ROS. O mecanismo adaptativo de defesa antioxidante apresenta, também ele, uma importância acrescida neste órgão na tentativa de evitar que os componentes cerebrais sejam afetados e, consequentemente, o desenvolvimento de doenças neurodegenerativas. Este trabalho pretende permitir um melhor conhecimento sobre a natureza bioquímica das ROS, as fontes dos radicais livres, o dano proteico, lipídico e no ADN promovido por estes, o papel das enzimas antioxidantes endógenas na regulação das funções fisiológicas e a implicação do stress oxidativo na etiologia das doenças neurodegenerativas. Para tal foi realizada uma revisão bibliográfica da literatura existente sobre o tema.
The evidence in the literature that the oxidative stress promoted by reactive oxygen species have a vital role in the etiology of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and schizophrenia, among other, is growing. ROS are generally governed by endogenous antioxidant enzymes to maintain the oxidative balance in the organism but, because endogenous or exogenous oxidative factors may occur, this balance can be corrupted and lead to oxidative stress. Constant oxidative stress can result in damage in the cellular components such as proteins, lipids or DNA bases. The oxidation mechanism is particularly important in the brain since it is exposed to large quantities of oxygen promoting the appearance of free radicals and ROS. The adaptive antioxidant defense mechanism is also important in this organ in the attempt to prevent the components of the brain from being affected and then developing neurodegenerative diseases. This paper aims to provide a better understanding of the biochemical nature of ROS, the sources of free radicals, damage protein, lipid and DNA promoted by these, the role of endogenous antioxidant enzymes in the regulation of physiological functions and the involvement of oxidative stress in the etiology neurodegenerative diseases. For this we conducted a literature review of the existing literature on the subject.
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Shee, Somnath. "Manipulating Bacterial and Host Reactive Oxygen Species (ROS)- based mechanisms to potentiate killing of Mycobacterium tuberculosis (Mtb)." Thesis, 2021. https://etd.iisc.ac.in/handle/2005/5680.

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Mycobacterium tuberculosis (Mtb) is evolutionarily equipped to resist exogenous reactive oxygen species but shows vulnerability to an increase in endogenous ROS (eROS). Since eROS is an unavoidable consequence of aerobic metabolism, understanding how eROS levels are controlled is essential yet remains uncharacterized. By combining the Mrx1-roGFP2 redox biosensor with transposon mutagenesis, we identified 368 genes (redoxosome) responsible for maintaining non-toxic levels of eROS in Mtb. Integrating redoxosome with a global network of protein-protein interactions and transcriptional regulators revealed a hypothetical protein (rv0158) as a top node managing eROS and redox homeostasis in Mtb. RNA sequencing, seahorse XF flux measurements, and lipid analysis indicate that rv0158 is required to balance the deployment of fatty acid substrates between lipid anabolism and oxidation. Disruption of rv0158 perturbed redox balance in a carbon-source-specific manner, promoted killing in response to anti-TB drugs, reduced survival in macrophages, and lowered persistence in mice. We describe a novel pathogen response to moxifloxacin. Mtb, unlike Escherichia coli, decreases respiration in response to moxifloxacin. Nevertheless, cells were killed, as ROS increased due to NADH-dependent reductive stress. Moxifloxacin lethality was mitigated by supplementing bacterial cultures with a ROS scavenger (thiourea), and an iron chelator (bipyridyl), indicating ROS is part and not a consequence of death processes. Treatment with N-acetyl cysteine (NAC) accelerated respiration and ROS production, increased moxifloxacin lethality, and lowered the mutant prevention concentration. Thus, redox and bioenergetic imbalance contribute to the moxifloxacin-mediated killing of Mtb. These results provide a way to make fluoroquinolones more effective anti-tuberculosis agents. We have previously reported that Mtb H37Rv sets up a gradient of mycothiol redox potential: EMSH-oxidized (-240 mV) to EMSH-reduced (-320 mV) inside macrophages, where the EMSH -reduced Mtb subpopulation are significantly more tolerant to anti-TB drugs. Therefore, one of the keys to subverting drug-tolerance is to impede the emergence of EMSH -reduced subpopulation by inducing overwhelming oxidative stress. In this study, we exposed THP1-macrophages infected with Mtb H37Rv expressing Mrx1-roGFP2-biosensor, to a library of FDA-approved drugs (Enzo Life Sciences; BML-2842) and scored for the oxidative shift in the Mtb- EMSH at 24 hours post infection. Based on their activity to trigger oxidative stress inside the bacterium, non-cytotoxicity to host, and inhibition of bacterial growth inside macrophages, C5 molecule emerged as the top hit. Pre-treatment with C5 potentiated killing of Mtb by all tested antibiotics (isoniazid, rifampicin, and moxifloxacin) and reduced drug-tolerance.
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Lin, Xu Hong, and 林旭宏. "Effects of endogenous carotenoids and hemoglobin on lipid oxidation and browning of dried mullet roe." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/52511642557435067505.

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Book chapters on the topic "Endogenous ROS"

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Elliott, Michael H., and Abboud J. Ghalayini. "Phosphorylation of Caveolin-1 in Bovine Rod Outer Segments in vitro by an Endogenous Tyrosine Kinase." In Advances in Experimental Medicine and Biology, 335–41. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-74904-4_39.

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Sempéré, Antoine J., Robert Mauget, and André Lacroix. "Seasonal Regulation of the Sexual Cycle and Antler Growth in Roe Deer: Evidence for an Endogenous Rhythm." In The Biology of Deer, 499–504. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2782-3_119.

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Di Girolamo, M., T. Cacciamani, M. Pallas, and D. Corda. "Activities Involved in the Modulation of the G Protein Endogenous ADP-Ribosylation in Normal and K-ras-Transformed Thyroid Cells." In Molecular Oncology and Clinical Applications, 173–80. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-5663-8_20.

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Ahsan, Haseeb, Mohammad Yusuf Hasan, and Rizwan Ahmad. "Reactive Oxygen Species (ROS) in the Pathophysiology of Rheumatoid Arthritis (RA)." In Reactive Oxygen Species [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101333.

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Free radicals are highly reactive molecules that are unstable and have extremely short-short half-life. They are derived from either oxygen (reactive oxygen species, ROS) or nitrogen (reactive nitrogen species, RNS) in mitochondria, plasma membrane and endoplasmic reticulum due to oxidative stress and damage. ROS/RNS are physiologically useful at low concentrations and are responsible for the activation of redox-sensitive signaling pathways, phagocytosis of infected cells and removal of abnormal and aging cells. The endogenous sources of ROS are the electron transport chain, the respiratory burst of phagocytes and oxidation of lipids. These radicals react with biomolecules such as DNA, proteins and lipids and may cause pathophysiological conditions such as autoimmunity, carcinogenesis, and neurodegenerative diseases. The role of ROS in autoimmune response remains complex and they have been implicated in the initiation, generation and amplification of novel epitopes. ROS also appears to play a critical role in rheumatoid arthritis (RA), a systemic autoimmune disease of the joints also known as inflammatory arthritis (IA). ROS are involved in the initiation of various signaling pathways and have a significant role in the pathophysiology of RA.
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Kageyama, Hakuto. "Biological Activities of MAAs and their Applications 2: Antioxidative Properties." In An Introduction to Mycosporine-Like Amino Acids, 77–87. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815136081123010008.

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It is known that the generation of reactive oxygen species (ROS) caused by UV irradiation and oxidative reactions accelerate skin aging. Substances that suppress or eliminate the generation of ROS are called antioxidants. So far, various mycosporine-like amino acids (MAAs) have been reported to have antioxidative activities. To prevent damage to the skin caused by ROS and maintain the homeostasis of the epidermis, skin cells have an endogenous antioxidant system consisting of enzymatic reactions. Although many points are unclear about the regulatory mechanisms, it has been suggested that MAAs are involved in the regulation of genes encoding enzymes that are involved in this system. This chapter provides a comprehensive overview of the antioxidant activities of MAAs.
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Eddaikra, Atika, and Naouel Eddaikra. "Endogenous Enzymatic Antioxidant Defense and Pathologies." In Antioxidants - Benefits, Sources, Mechanisms of Action. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95504.

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Oxidative stress is an important component of various diseases. It manifests as an imbalance caused by an excessive production of reactive oxygen species (ROS) which are associated with a deficit of antioxidant activity. This deficit can be the consequence of genetic factors, environmental ones, metabolic imbalance, toxicity or direct attacks by the accumulation of free radicals. These can induce metabolic dysfunction affecting biological macromolecules in their structures or activities. From a physiological perspective, the neutralization of free radicals is ensured by enzymatic, antioxidant and non-enzymatic defense systems. In the present chapter, we will focus on the endogenous enzymatic antioxidant defense system such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPxs), thioredoxin (Trx) and paraxonase which play an important role in homeostatic redox balance. Also, we will review this set of antioxidants enzymes within different pathological states such as diabetes, cancer, autoimmune diseases, cardiovascular, Alzheimer’s, Parkinson’s or parasitic diseases such as Leishmaniasis and Malaria.
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Mbemba Fundu, Théophile, Paulin Mutwale Kapepula, Jean Paul Nzundu Mbo, Justin Mboloko Esimo, and Nadège Ngombe Kabamba. "Congolese Traditional Foods as Sources of Antioxidant Nutrients for Disease Prevention." In Recent Developments in Antioxidants From Natural Sources [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109319.

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Oxidative stress, characterized by excessive production of reactive species, is involved in several chronic diseases such as cardiovascular, chronic obstructive pulmonary, sickle cell, chronic kidney, neurodegenerative, and cancer. The negative impact of ROS and RNS, produced by endogenous and exogenous processes, is neutralized by antioxidant defenses. Given the importance of oxidative stress to human health, the use of antioxidants as therapy directs medical research toward the specificity of antioxidants causing each disease. Fruits and vegetables contain antioxidants, such as nutraceuticals, pharmaceuticals, and phytoceuticals, the consumption of which reduces the risk of developing chronic diseases. Flora of African countries is endowed with plant species that would make a putative source for new antioxidants. This article reports antioxidant activities of traditional foods from Democratic Republic of the Congo. Further studies are needed to ensure mechanisms of their functionality in the human body.
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Diksha, Sumit Singh, Evani Mahajan, Satwinder Kaur Sohal, and Shallina Gupta. "Antioxidants and Oxidative Stress as Foe and Friends in Prevention of Cancer." In Functional Foods for Health Maintenance: Understanding their Role in Cancer Prevention, 135–78. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815179217123010009.

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Cancer has become a major public health problem and is one of the leading causes of death among humans worldwide. It is characterized by the abnormal proliferation of cells due to failed normal regulatory mechanisms. Oxidative stress plays a crucial role in the pathology of many cancers and is characterized by an imbalance between the production and removal of reactive oxygen species (ROS). Under normal physiological conditions, the intracellular levels of ROS are steadily maintained to prevent cell damage, and detoxification of ROS is facilitated by various non-enzymatic and enzymatic antioxidants. These antioxidants have a widespread application in the prevention of cancer, as many endogenous and exogenous antioxidants can prevent and repair damage caused by disrupted redox status of cells during carcinogenesis. Our body can produce some of the antioxidants, but to obtain the rest of the antioxidants, it relies on external sources, primarily the diet of an individual. Also, there are certain health issues reported with the long-term usage of synthetic antioxidants. Therefore, nowadays, many nutritionists and dieticians suggest consuming food and natural products that are either rich sources of antioxidants or are supplemented with various nature-based antioxidants. This chapter seeks to explain the role of ROS in oncogenesis, understand the dynamics between oxidative damage and the antioxidants, types of antioxidants, natural sources of antioxidants, mode of action of antioxidants and the role of antioxidants in cancer prevention and treatment along with their disputable effects in cancer therapy.
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Rajashekaraiah, Vani, Carl Hsieh, and Masannagari Pallavi. "Modulations in Oxidative Stress of Erythrocytes during Bacterial and Viral Infections." In Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98236.

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Oxidative stress (OS) occurs when the generation of free radicals and reactive oxygen species (ROS) overwhelms the antioxidant capacity. OS causes storage lesions which can be defined as a series of biochemical and biomechanical changes. Erythrocytes are constantly exposed to OS due to the presence of ROS, which are countered by the endogenous antioxidant system. Various irreversible changes that occur include fragmentation and aggregation of proteins and lipids. The changes in proteins, lipids and antioxidant capacity are used as OS biomarkers to assess the efficacy of the erythrocytes, post oxidative insult. Aging of erythrocytes is also associated with the changes in its physical, biochemical and physiological properties and OS causes its rapid aging. Bacterial and viral infections also cause OS which alters the erythrocytes’ antioxidant capacity. These modulations in its microenvironment are both beneficial in terms of protection against invading microorganisms as well as harmful to the erythrocytes, causing damage to surrounding cells and tissues. Thus, OS biomarkers can be used to gain insights into the effects of bacterial and viral infections on the erythrocyte microenvironment.
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Malankar, Gauri S., Beatriz S. Cugnasca, Felipe Wodtke, João L. Petrarca de Albuquerque, Pratiksha P. Deshmukh, Divyesh S. Shelar, Alcindo A. Dos Santos, and Sudesh T. Manjare. "Chalcogen-based Probes." In Chalcogen Chemistry: Fundamentals and Applications, 384–418. The Royal Society of Chemistry, 2023. http://dx.doi.org/10.1039/bk9781839167386-00384.

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Recently, selenium and tellurium atoms have been incorporated in various fluorophores such as rhodamine, cyanine, fluorescein, BODIPY, coumarin, and BOPHY for the detection and quantification of different analytes of biochemical and environmental interest by fluorescence measurements. The relevance of the insertion of chalcogen atoms in fluorescent compounds refers to their excellent redox characteristics, conferring unique properties to the resulting compounds, as analytical/biochemical probes. Additionally, selenium plays pivotal roles in biochemical events interacting selectively with endogenous sulfur-based biomolecules. About tellurium, there are only rare reports of its occurrence in certain fungi when exposed to tellurium-rich environments. Besides that, contrary to certain comments, generically, tellurium (and many organic tellurides) present low or no toxicity. This chapter provides a summary of all reported organic chalcogenated (Se and Te) fluorescent sensors, focusing on those containing selenium or tellurium in their structure, used in the detection of important analytes from a biological and environmental point of view, including metallic ions, reactive oxygen species (ROS), reactive nitrogen species (RNS), and biothiols.
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Conference papers on the topic "Endogenous ROS"

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Filippova, Maria. "Abstract 3766: The response of cervical cancer cells to chemotherapeutic agents depends on endogenous ROS levels as well as the drug-induced ROS profile." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3766.

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Rabbani, Naila, Paul John Thornalley, Maryam Al-Motawa, and Mingzhan Xue. "Vulnerabilities of the SARS-Cov-2 Virus to Proteotoxicity – Opportunity for Repurposed Chemotherapy of COVID-19 Infection." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0291.

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The global pandemic of COVID-19 disease caused by infection with the SARS-CoV-2 Coronavirus, has produced an urgent requirement and search for improved treatments whilst effective vaccines are developed. A strategy for improved drug therapy is to increase levels of endogenous reactive metabolites for selective toxicity to SARS-CoV-2 by preferential damage to the viral proteome. Key reactive metabolites producing major quantitative damage to the proteome in physiological systems are: Reactive oxygen species (ROS) and the reactive glycating agent methylglyoxal (MG); cysteine residues and arginine residues are their most susceptible targets, respectively. From sequenced-based prediction of the SARS-CoV-2 proteome, we found 0.8-fold enrichment or depletion of cysteine residues in functional domains of the viral proteome; whereas there was a 4.6-fold enrichment of arginine residues, suggesting SARS-CoV-2 is resistant to oxidative agents and sensitive to MG. We examined activated arginine residues in functional domain with predicted low pKa by neighboring group interaction in the SARS-CoV-2. We found 25 such arginine residues, including 2 in the spike protein and 10 in the nucleoprotein. These sites were partially conserved in related coronaviridae: SARS-COV and MERS. We also screened and identified drugs, which increase cellular MG concentration to virucidal levels and found two antitumor drugs with historical antiviral activity, doxorubicin and paclitaxel were the best candidate for repurposing. Our findings provide evidence of potential vulnerability of SARS-CoV2 to inactivation by MG and a scientific rationale for repurposing of doxorubicin and paclitaxel for treatment of COVID-19 disease, providing efficacy and adequate therapeutic index may be established.
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Hermán, F., P. Hadházy, and K. Magyar. "QUANTITATIVE DETERMINATION OF ENDOGENOUS PGI2 RELEASE IN ANAESTHETIZED BEAGLE DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643184.

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A 30μm diameter pore size screen was inserted into an arteriovenous bypass system in anaesthetized, heparin-treated beagle dogs. The arterial blood was directed through the screen by a roller pump at a constant rate. As a result, the pressure proximal to the filter continuously increased (F.Hermdn et al.Thromb. Res.44 /1986/,575). The concentration of proximally infused PGI2 that stabilized the filtration pressure curve (pressure stabilizing concentration= PSC) was determined. If it was low enough (between 0.4 and 1.5 nmol/1) we administered the PGI2-releaser bradykinin (1/ug/kg), angiotensin II (0.5/ug/kg) or ADP (20/ug/kg) in bolus dose intravenously. Together with the cnanges in blood pressure, we observed a transient decrease in filtration pressure. From the pressure changes, based on the previously determined PGI2 concentration-res-ponse relationship, we estimated the amounts of released PGI2 as well as the time course of this release. Indomethacin (2 mg/kg i.v.) significantly decreased the PSC for exogenous PGI2 thereby increasing the sensitivity of the method; the release of PGI2 was abolished. The sensitivity of the method could also be increased by infusing BM.13.177 - an endoperoxide, thromboxane receptor antagonist - proximal to the filter (final concentration: 1-10/ug/ml). This substance did not affect the release of PGI2.We conclude that by using this technique the endogenous release of prostacyclin can be continuously determined provided that PGI2 level exceeds 50 pg/ml.
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Roth, Sascha O. M., Thomas J. Macartney, Agnieszka Konopacka, Markus Queisser, and Gopal P. Sapkota. "Abstract B34: Targeted destruction of endogenous K-RAS using an Affinity directed PROtein Missile (AdPROM)." In Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-b34.

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Chi, Xin-Zi, You-Soub Lee, and Suk-Chul Bae. "Abstract B35: Runx3 contributes for the defense against endogenous level of oncogenic K-Ras-induced tumorigenesis." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b35.

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Mohammed, Altaf, Naveena B. Janakiram, Misty Brewer, Ashley Duff, Stan Lightfoot, Richard S. Brush, Robert E. Anderson, and Chinthalapally V. Rao. "Abstract A111: Endogenous conversion of n-6 PUFAs to n-3 PUFAs prevents progression of K-Ras activated pancreatic lesion development to pancreatic ductal carcinoma in Fat-1 transgenic mice." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a111.

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Carvalho, Tamyres MIngorance, Tayana Schultz Jukoski, Guillermo Ortiz Brasil, Flavia Kuroda, and Enilze M. S. F. Ribeiro. "EXPRESSION OF miRNAS SUGGESTS A POTENTIAL ROLE IN BREAST CANCER." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1050.

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Introduction: MicroRNAs (miRNAs) are regulators of gene expression in biological processes, mainly repressing translation or degrading messenger RNA (mRNA) from their target genes. Their deregulation is associated with a wide variety of diseases, including cancer. Breast cancer (BC) is the most common cancer among women worldwide. Understanding the mechanisms involved in this pathology is essential for the discovery of new diagnostic and prognostic markers. Objectives: Investigate the differential expression of selected miRNAs in luminal A (LA) and triple-negative breast cancer (TNBC). Methods: We evaluated the expression of miR-320a, miR-4433b-5p, miR-142-5p, and miR-150-5p in 31 BC samples (19 LA and 12 TNBC) and 29 adjacent non-tumor breast cancer (NT). The miRNAs were selected after in silico study. RT-qPCR was the method of choice, using RNU48 as endogenous control, and the BT-474 cell line was used as a calibrator between plates. The 2−ΔΔCt method was used to estimate miRNA expression level. Individual receiver operating characteristic (ROC) curves were calculated based on RQ values to investigate the diagnostic value of miRNAs. Results: miR-142-5p, miR-150-5p, miR-320a, and miR-4433b-5p were downregulated in BC compared to NT samples. All studied miRNAs were able to discriminate between BC and NT samples with sensitivity and sensibility (AUC – Area under curve >0.7 and p <0.05). A panel including all miRNAs improved the AUC to identify TNBC patients compared to NT (AUC=0.9240, sensitivity 94.44%, specificity 100%). We found no difference comparing miRNAs between LA and TNBC BC subtypes. There was no association between expression levels and prognostic parameters (age, histological grade, size of the tumor, axillary lymph node status). Conclusions: Our data suggest that downregulation of miR-142-5p, miR-150-5p, miR-320a, and miR-4433b-5p can be involved in BC for not repressing the expression of target genes. Functional studies will contribute to elucidate their involvement in BC.
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Miguel Marques, Fernando. "“ALImentáRIO” - Holder for the Supplementary Feeding of Wild Birds." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001397.

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This is an animal design project (design thinking to meet the needs of animals) which aims to bring birds into contact with humans and - through this solution - to bring the sound and movement produced by them into our lives (whether in the countryside, whether in the urban landscape), which can be translated into joy and peace achieved by the harmony of natural wildlife in our domestic environment.Starting question Knowing that birds are elusive and fearful animals, but also can bring joy and movement to our daily lives, how can we attract them to our coexistence? Supplementary feeding can be a good solution, and there are already some versions available on the international market, especially in countries where winter is more extreme. In southern Europe, feeding birds is still not a very common practice. Depending on the type of food the birds eat in their natural habitat and, depending on the endogenous birds, there are variations in the diet, and only a test of placing food available to the birds will determine the type of food to be placed in the supplementary feeder.The "AlimentáRIO" (feeder) is a ceramic supplementary feeding stand/holder that can contain various types of food, in order to test if birds can be attracted close to your home.There are several types of bird food: nectar, seeds, worms, fruit, tallow/lard... And, for each of these types of food, there is a specific type of feeder. The "AlimentáRIO" is a versatile feeder intended to cover all types. Nectar is more suitable for birds that can pollinate during late winter and early spring, when insects are less active. For these reasons, nectar should only be placed in feeders as a food supplement in the winter and autumn.In Portugal, there are some birds that drink nectar, according to Luís Pascoal da Silva , a researcher at CIBIO-inBIO. The scientist states that there are several pollinating birds in Portugal, but the study of the contribution of these birds to pollination is scarce. Seeds - besides the traditional canary seed - can contain sunflower seeds or nuts, such as walnuts and peanuts, depending on the endogenous birds. Fruit is also sought after by some species of birds, namely apples and pears, in addition to other exotic fruits. However, in general, birds can be drawn to any type of fruit. Fat balls are usually tallow/lard balls with seeds and fruits to reinforce supplementary feeding during cold seasons. The "AlimentáRIO" is a suspended wild bird feeder that can be hung in more or less sheltered places, made with materials resistant to the elements, without the need for maintenance. However, its cleaning must be done according to the recommendations referred to in the full article. As already mentioned, the construction materials are low maintenance, and the food container and the deflecting bell jar are made with stoneware - the type of ceramics more resistant to both bumps and thermal variations. The junction of the two parts is made with a nickel-plated threaded rod, covered with an aluminium tube, and all components are joined by manual screw threads, which allows to assemble and disassemble it without the use of any tools, thus facilitating an in-depth cleaning at the end of the supplementary feeding season.The "AlimentáRIO" has a lower part with four concavities for placing food, which allows the possible placement of different types of food at the same time, thus drawing different species. As it is a feeder consisting of a protective and deflecting bell jar, the birds are protected from possible direct attacks from predators and from falling leaves in the autumn. The fact that it is a supplementary feeder that can be hung with a rope makes it difficult for rats and squirrels to get close to the food, given that, if by chance these animals manage to descend on the rope, they must also overcome the challenge of getting through the bell jar (which is a spherical cap) to get to the place where the food is. The results of the placement tests of this supplementary feeder have been reassuring, which show that the feeders foster the approximation of wild birds in relatively short periods of time - between 3 weeks and one month.
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Reports on the topic "Endogenous ROS"

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Friedman, Haya, Chris Watkins, Susan Lurie, and Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7613883.bard.

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Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.
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Sands, Ronald, and Man-Keun Kim. Modeling the Competition for Land: Methods and Application to Climate Policy. GTAP Working Paper, April 2008. http://dx.doi.org/10.21642/gtap.wp45.

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*Chapter 7 of the forthcoming book "Economic Analysis of Land Use in Global Climate Change Policy," edited by Thomas W. Hertel, Steven Rose, and Richard S.J. Tol The Agriculture and Land Use (AgLU) model was developed at Pacific Northwest National Laboratory to assess the impact of a changed climate or a climate policy on land use, carbon emissions from land use change, production of field crops, and production of biofuels. The level of analysis to date is relatively aggregate, at the global or national scale, but the model captures important interactions such as endogenous land use change in response to a climate policy and international trade in agricultural and forest products. This paper describes exploratory efforts to extend the conceptual framework, including geographical disaggregation of land within the United States, improving the dynamics of the forestry sector, valuing carbon in forests, and land requirements for biofuel crops. Conceptual development is done within a single-country, steady-state version of AgLU. Land use is simulated with carbon prices from zero to $200 per t-C, with forests, biofuels, and food crops competing simultaneously for land.
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