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Journal articles on the topic 'Oxidative modulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Janero, D. R., and C. Yarwood. "Oxidative modulation and inactivation of rabbit cardiac adenylate deaminase." Biochemical Journal 306, no. 2 (1995): 421–27. http://dx.doi.org/10.1042/bj3060421.

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Oxidative stress and adenine nucleotide catabolism occur concomitantly in several disease states, such as cardiac ischaemia-reperfusion, and may act as synergistic determinants of tissue injury. However, the mechanisms underlying this potential interaction remain ill-defined. We examined the influence of oxidative stress on the molecular, kinetic and regulatory properties of a ubiquitous AMP-catabolizing enzyme, adenylate deaminase (AMPD) (EC 3.5.4.6). To this intent, rabbit heart AMPD and an H2O2/ascorbate/iron oxidation system were employed. Enzyme exposure to the complete oxidation system a

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2

Santos, Leonardo, Carlos Escande, and Ana Denicola. "Potential Modulation of Sirtuins by Oxidative Stress." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9831825.

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Sirtuins are a conserved family of NAD-dependent protein deacylases. Initially proposed as histone deacetylases, it is now known that they act on a variety of proteins including transcription factors and metabolic enzymes, having a key role in the regulation of cellular homeostasis. Seven isoforms are identified in mammals (SIRT1–7), all of them sharing a conserved catalytic core and showing differential subcellular localization and activities. Oxidative stress can affect the activity of sirtuins at different levels: expression, posttranslational modifications, protein-protein interactions, an

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3

da Palma, Renata K., Ivana C. Moraes-Silva, Danielle da Silva Dias, et al. "Resistance or aerobic training decreases blood pressure and improves cardiovascular autonomic control and oxidative stress in hypertensive menopausal rats." Journal of Applied Physiology 121, no. 4 (2016): 1032–38. http://dx.doi.org/10.1152/japplphysiol.00130.2016.

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We investigated whether resistance training (RT) vs. aerobic training (AT) differentially impacts on arterial pressure and related mechanisms in ovariectomized spontaneously hypertensive rats (SHRs). Female SHRs were ovariectomized and assigned to one of the following groups: sedentary, AT, or RT; sham sedentary SHR were used as control group. AT was performed on a treadmill, whereas RT was performed on a vertical ladder. Both exercise protocols were performed for 8 wk, 5 days/wk. Arterial pressure, baroreflex sensitivity, autonomic modulation, and cardiac oxidative stress parameters (lipid pe

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4

Hondorp, Elise R., and Rowena G. Matthews. "Oxidation of Cysteine 645 of Cobalamin-Independent Methionine Synthase Causes a Methionine Limitation in Escherichia coli." Journal of Bacteriology 191, no. 10 (2009): 3407–10. http://dx.doi.org/10.1128/jb.01722-08.

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ABSTRACT Cobalamin-independent methionine synthase (MetE) catalyzes the final step in Escherichia coli methionine biosynthesis but is inactivated under oxidative conditions, triggering a methionine deficiency. This study demonstrates that the mutation of MetE cysteine 645 to alanine completely eliminates the methionine auxotrophy imposed by diamide treatment, suggesting that modulation of MetE activity via cysteine 645 oxidation has significant physiological consequences for oxidatively stressed cells.

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Lawlor, Susan M., та Nora M. O'brien. "Modulation of oxidative stress by β-carotene in chicken embryo fibroblasts". British Journal of Nutrition 73, № 6 (1995): 841–50. http://dx.doi.org/10.1079/bjn19950089.

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The ability of β-carotene to protect against oxidative stressin vitrowas assessed. Primary cultures of chicken embryo fibroblasts (CEF) were oxidatively stressed by exposure to paraquat (PQ). Activities of the antioxidant enzymes superoxide dismutase (SOD;EC1.15.1.1), catalase (CAT;EC1.11.1.6) and glutathione peroxidase (GSH-Px;EC1.11.1.9) were measured as indices of oxidative stress. CEF incubated with 0·25 mM-PQ for 18 h exhibited increased SOD and CAT activities and decreased GSH-Px activity compared with the control (P< 0·001). Incorporation of added β-carotene (0·1 μM) into 0·25 mM-PQ-

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6

Singh, Prabhakar, and Syed Ibrahim Rizvi. "Modulation Effects of Curcumin on Erythrocyte Ion-Transporter Activity." International Journal of Cell Biology 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/630246.

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Curcumin ((1E,6E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione), the yellow biphenolic pigment isolated from turmeric (Curcuma longa), has various medicinal benefits through antioxidation, anti-inflammation, cardiovascular protection, immunomodulation, enhancing of the apoptotic process, and antiangiogenic property. We explored the effects of curcuminin vitro(10−5 M to 10−8 M) andin vivo(340 and 170 mg/kg b.w., oral) on Na+/K+ATPase (NKA), Na+/H+exchanger (NHE) activity, and membrane lipid hydroperoxides (ROOH) in control and experimental oxidative stress erythrocytes of Wistar

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7

Carlesi, C., E. Caldarazzo Ienco, S. Piazza, et al. "Oxidative stress modulation in neurodegenerative diseases." Mediterranean Journal of Nutrition and Metabolism 4, no. 3 (2011): 219–25. http://dx.doi.org/10.3233/s12349-011-0053-z.

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8

Zima, Tom??&OV0165;, Emanuele Albano, Magnus Ingelman-Sundberg, et al. "Modulation of Oxidative Stress by Alcohol." Alcoholism: Clinical & Experimental Research 29, no. 6 (2005): 1060–65. http://dx.doi.org/10.1097/01.alc.0000168168.43419.54.

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9

Alamdari, Daryoush Hamidi, Malektaj Honarmand, Abdolfattah Sarrafnejad, et al. "Oxidative Stress Modulation Immediately After Hemodialysis." Dialysis & Transplantation 38, no. 9 (2009): 354–58. http://dx.doi.org/10.1002/dat.20345.

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10

Da Costa, Laura A., Alaa Badawi, and Ahmed El-Sohemy. "Nutrigenetics and Modulation of Oxidative Stress." Annals of Nutrition and Metabolism 60, s3 (2012): 27–36. http://dx.doi.org/10.1159/000337311.

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11

Beltowski, Jerzy. "Statins and Modulation of Oxidative Stress." Toxicology Mechanisms and Methods 15, no. 2 (2005): 61–92. http://dx.doi.org/10.1080/15376520590918766.

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12

Carlesi, C., E. Caldarazzo Ienco, S. Piazza, et al. "Oxidative stress modulation in neurodegenerative diseases." Mediterranean Journal of Nutrition and Metabolism 4, no. 3 (2011): 219–25. http://dx.doi.org/10.1007/s12349-011-0053-z.

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13

Čipak Gašparović, Ana, Lidija Milković, Nadia Dandachi, et al. "Chronic Oxidative Stress Promotes Molecular Changes Associated with Epithelial Mesenchymal Transition, NRF2, and Breast Cancer Stem Cell Phenotype." Antioxidants 8, no. 12 (2019): 633. http://dx.doi.org/10.3390/antiox8120633.

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Oxidative stress plays a role in carcinogenesis, but it also contributes to the modulation of tumor cells and microenvironment caused by chemotherapeutics. One of the consequences of oxidative stress is lipid peroxidation, which can, through reactive aldehydes such as 4-hydroxy-2-nonenal (HNE), affect cell signaling pathways. On the other hand, cancer stem cells (CSC) are now recognized as a major factor of malignancy by causing metastasis, relapse, and therapy resistance. Here, we evaluated whether oxidative stress and HNE modulation of the microenvironment can influence CSC growth, modificat

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14

Boccatonda, Andrea, Romina Tripaldi, Giovanni Davì, and Francesca Santilli. "Oxidative Stress Modulation Through Habitual Physical Activity." Current Pharmaceutical Design 22, no. 24 (2016): 3648–80. http://dx.doi.org/10.2174/1381612822666160413123806.

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15

Sahoo, Nirakar, Toshinori Hoshi, and Stefan H. Heinemann. "Oxidative Modulation of Voltage-Gated Potassium Channels." Antioxidants & Redox Signaling 21, no. 6 (2014): 933–52. http://dx.doi.org/10.1089/ars.2013.5614.

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16

Floc'h, Nicolas, Jakub Kolodziejski, Leila Akkari, et al. "Modulation of Oxidative Stress by Twist Oncoproteins." PLoS ONE 8, no. 8 (2013): e72490. http://dx.doi.org/10.1371/journal.pone.0072490.

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17

Larbi, Anis, Juergen Kempf, and Graham Pawelec. "Oxidative stress modulation and T cell activation." Experimental Gerontology 42, no. 9 (2007): 852–58. http://dx.doi.org/10.1016/j.exger.2007.05.004.

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18

Tripathi, Rakshamani, H. Mohan, and J. P. Kamat. "Modulation of oxidative damage by natural products." Food Chemistry 100, no. 1 (2007): 81–90. http://dx.doi.org/10.1016/j.foodchem.2005.09.012.

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19

Carrasco, Rodrigo, Rodrigo L. Castillo, Juan G. Gormaz, Montserrat Carrillo, and Paaladinesh Thavendiranathan. "Role of Oxidative Stress in the Mechanisms of Anthracycline-Induced Cardiotoxicity: Effects of Preventive Strategies." Oxidative Medicine and Cellular Longevity 2021 (January 25, 2021): 1–16. http://dx.doi.org/10.1155/2021/8863789.

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Anthracycline-induced cardiotoxicity (AIC) persists as a significant cause of morbidity and mortality in cancer survivors. Although many protective strategies have been evaluated, cardiotoxicity remains an ongoing threat. The mechanisms of AIC remain unclear; however, several pathways have been proposed, suggesting a multifactorial origin. When the central role of topoisomerase 2β in the pathophysiology of AIC was described some years ago, the classical reactive oxygen species (ROS) hypothesis shifted to a secondary position. However, new insights have reemphasized the importance of the role o

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20

Armengol Lopez, Sandra, Kathleen M. Botham, and Charlotte Lawson. "The Oxidative State of Chylomicron Remnants Influences Their Modulation of Human Monocyte Activation." International Journal of Vascular Medicine 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/942512.

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Chylomicron remnants (CMRs) contribute directly to human monocyte activationin vitro, by increasing reactive oxygen species (ROS) production and cell migration. In this study, the effects of the oxidative state of CMR on the degree of monocyte activation was investigated. CMR-like particles (CRLPs) were prepared in three different oxidative states, normal (CRLPs), protected from oxidation by incorporation of the antioxidant, probucol (pCRLPs), or oxidised with CuSO4(oxCRLPs). Lipid accumulation and ROS production were significantly increased in primary human monocytes incubated with CRLPs, whi

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21

Zhu, Bo, Li-Kai Yan, Yun Geng, Hang Ren, Wei Guan, and Zhong-Min Su. "IrIII/NiII-Metallaphotoredox catalysis: the oxidation state modulation mechanism versus the radical mechanism." Chemical Communications 54, no. 47 (2018): 5968–71. http://dx.doi.org/10.1039/c8cc03550d.

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An oxidation state modulation mechanism, merging oxidative quenching (Ir<sup>III</sup>–*Ir<sup>III</sup>–Ir<sup>IV</sup>–Ir<sup>III</sup>) and nickel catalytic (Ni<sup>II</sup>–Ni<sup>I</sup>–Ni<sup>III</sup>–Ni<sup>I</sup>–Ni<sup>II</sup>) cycles, is disclosed for Ir/Ni-metallaphotoredox catalysis.

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22

Malorni, W., F. Iosi, M. T. Santini, and U. Testa. "Menadione-induced oxidative stress leads to a rapid down-modulation of transferrin receptor recycling." Journal of Cell Science 106, no. 1 (1993): 309–18. http://dx.doi.org/10.1242/jcs.106.1.309.

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It has been demonstrated that perturbation of oxidative balance plays an important role in numerous pathological states as well as in physiological modifications leading to aging. In order to evaluate the role of the oxidative state in cells, biochemical and ultrastructural studies were carried out on K562 and HL-60 cell cultures. Particular attention was given to the transferrin receptor, which plays an important role in cellular iron metabolism. In order to evaluate if oxidative stress influences the transferrin receptor regulation process, the free-radical inducer menadione was used. The re

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23

Seidel, Thorsten, Stefan Scholl, Melanie Krebs, et al. "Regulation of the V-type ATPase by redox modulation." Biochemical Journal 448, no. 2 (2012): 243–51. http://dx.doi.org/10.1042/bj20120976.

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ATP-hydrolysis and proton pumping by the V-ATPase (vacuolar proton-translocating ATPase) are subject to redox regulation in mammals, yeast and plants. Oxidative inhibition of the V-ATPase is ascribed to disulfide-bond formation between conserved cysteine residues at the catalytic site of subunit A. Subunits containing amino acid substitutions of one of three conserved cysteine residues of VHA-A were expressed in a vha-A null mutant background in Arabidopsis. In vitro activity measurements revealed a complete absence of oxidative inhibition in the transgenic line expressing VHA-A C256S, confirm

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24

MOREL, Yannick, and Robert BAROUKI. "Repression of gene expression by oxidative stress." Biochemical Journal 342, no. 3 (1999): 481–96. http://dx.doi.org/10.1042/bj3420481.

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Gene expression is modulated by both physiological signals (hormones, cytokines, etc.) and environmental stimuli (physical parameters, xenobiotics, etc.). Oxidative stress appears to be a key pleiotropic modulator which may be involved in either pathway. Indeed, reactive oxygen species (ROS) have been described as second messengers for several growth factors and cytokines, but have also been shown to rise following cellular insults such as xenobiotic metabolism or enzymic deficiency. Extensive studies on the induction of stress-response genes by oxidative stress have been reported. In contrast

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25

Fernandez-García, Jose, Fernando Cardona, and Francisco Tinahones. "Inflammation, Oxidative Stress and Metabolic Syndrome: Dietary Modulation." Current Vascular Pharmacology 11, no. 6 (2014): 906–19. http://dx.doi.org/10.2174/15701611113116660175.

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26

Chandra, Joya, Afshin Samali, and Sten Orrenius. "Triggering and modulation of apoptosis by oxidative stress." Free Radical Biology and Medicine 29, no. 3-4 (2000): 323–33. http://dx.doi.org/10.1016/s0891-5849(00)00302-6.

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27

Kolodziejski, J., N. Floc'h, L. Akkari, et al. "477 Modulation of Oxidative Stress by Twist Oncoproteins." European Journal of Cancer 48 (July 2012): S115. http://dx.doi.org/10.1016/s0959-8049(12)71150-4.

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28

Dragutan, Ileana, and Rolf J. Mehlhorn. "Modulation of oxidative damage by nitroxide free radicals." Free Radical Research 41, no. 3 (2007): 303–15. http://dx.doi.org/10.1080/10715760601089356.

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29

Kim, You Jung, and Takako Yokozawa. "Modulation of Oxidative Stress and Melanogenesis by Proanthocyanidins." Biological & Pharmaceutical Bulletin 32, no. 7 (2009): 1155–59. http://dx.doi.org/10.1248/bpb.32.1155.

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30

Gorrini, Chiara, Isaac S. Harris, and Tak W. Mak. "Modulation of oxidative stress as an anticancer strategy." Nature Reviews Drug Discovery 12, no. 12 (2013): 931–47. http://dx.doi.org/10.1038/nrd4002.

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31

Choudhary, Gaurav, and Samuel C. Dudley. "Heart Failure, Oxidative Stress, and Ion Channel Modulation." Congestive Heart Failure 8, no. 3 (2002): 148–55. http://dx.doi.org/10.1111/j.1527-5299.2002.00716.x.

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32

Číž, M., and A. Lojek. "Modulation of neutrophil oxidative burst via histamine receptors." British Journal of Pharmacology 170, no. 1 (2013): 17–22. http://dx.doi.org/10.1111/bph.12107.

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33

El-Demerdash, Fatma M., Ehab A. Abbady, and Hoda H. Baghdadi. "Oxidative stress modulation byRosmarinus officinalisin creosote-induced hepatotoxicity." Environmental Toxicology 31, no. 1 (2014): 85–92. http://dx.doi.org/10.1002/tox.22024.

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34

Korkina, Liudmila, Tomris Ozben, and Luciano Saso. "Modulation of Oxidative Stress: Pharmaceutical and Pharmacological Aspects." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/6023417.

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35

Ribeiro, Daniela, Marisa Freitas, Sara M. Tomé, Artur M. S. Silva, Graça Porto, and Eduarda Fernandes. "Modulation of human neutrophils' oxidative burst by flavonoids." European Journal of Medicinal Chemistry 67 (September 2013): 280–92. http://dx.doi.org/10.1016/j.ejmech.2013.06.019.

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36

Yu, Byung Pal. "Aging and oxidative stress: Modulation by dietary restriction." Free Radical Biology and Medicine 21, no. 5 (1996): 651–68. http://dx.doi.org/10.1016/0891-5849(96)00162-1.

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37

Bouton, C. "Nitrosative and oxidative modulation of iron regulatory proteins." Cellular and Molecular Life Sciences 55, no. 9 (1999): 1043. http://dx.doi.org/10.1007/s000180050355.

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38

Abdel-Salam, Omar M. E., Rehab Fawzy Abdel-Rahman, Amany A. Sleem, and Abdel Razik Farrag. "Modulation of lipopolysaccharide-induced oxidative stress by capsaicin." Inflammopharmacology 20, no. 4 (2011): 207–17. http://dx.doi.org/10.1007/s10787-011-0101-9.

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39

Pavlovic, Dusica, Vidosava Djordjevic, and Gordana Kocic. "Signal transduction-free radical modulation." Jugoslovenska medicinska biohemija 21, no. 2 (2002): 69–84. http://dx.doi.org/10.2298/jmh0202069p.

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Signal transduction is the process of signal transmission from cell surface to cell interior. This ubiquitous mechanism enables functioning of general but also specific cell-tissue processes, involved in maintaining of cell homeostasis. Normal transduction processes disturbance represents the most frequent molecular basis in pathogenesis and complications of many diseases. Understanding of all sequences involved in signalling pathway cascades offers a possibility of different modulators application in therapeutic purposes. The activation of phagocyte NADPH oxidase is one of the best studied pa

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40

Chakravarty, Shilpa, and Syed Ibrahim Rizvi. "Day and Night GSH and MDA Levels in Healthy Adults and Effects of Different Doses of Melatonin on These Parameters." International Journal of Cell Biology 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/404591.

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The pineal secretory product melatonin (chemically, N-acetyl-5-methoxytryptamine) acts as an effective antioxidant and free-radical scavenger and plays an important role in several physiological functions such as sleep induction, immunomodulation, cardiovascular protection, thermoregulation, neuroprotection, tumor-suppression and oncostasis. Membrane lipid-peroxidation in terms of malondialdehyde (MDA) and intracellular glutathione (GSH) is considered to be a reliable marker of oxidative stress. The present work was undertaken to study the modulating effect of melatonin on MDA and GSH in human

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41

Lee, Choongho. "Therapeutic Modulation of Virus-Induced Oxidative Stress via the Nrf2-Dependent Antioxidative Pathway." Oxidative Medicine and Cellular Longevity 2018 (October 31, 2018): 1–26. http://dx.doi.org/10.1155/2018/6208067.

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Virus-induced oxidative stress plays a critical role in the viral life cycle as well as the pathogenesis of viral diseases. In response to reactive oxygen species (ROS) generation by a virus, a host cell activates an antioxidative defense system for its own protection. Particularly, a nuclear factor erythroid 2p45-related factor 2 (Nrf2) pathway works in a front-line for cytoprotection and detoxification. Recently, a series of studies suggested that a group of clinically relevant viruses have the capacity for positive and negative regulations of the Nrf2 pathway. This virus-induced modulation

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42

Joshi, Manjunath B., Danila Ivanov, Maria Philippova, Emmanouil Kyriakakis, Paul Erne, and Thérèse J. Resink. "A requirement for thioredoxin in redox-sensitive modulation of T-cadherin expression in endothelial cells." Biochemical Journal 416, no. 2 (2008): 271–80. http://dx.doi.org/10.1042/bj20080765.

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T-cad (T-cadherin), a glycosylphosphatidylinositol-anchored cadherin superfamily member, is expressed widely in the brain and cardiovascular system, and absent, decreased, or even increased, in cancers. Mechanisms controlling T-cad expression are poorly understood. The present study investigated transcriptional regulation of T-cad in ECs (endothelial cells). Conditions of oxidative stress (serum-deprivation or presence of H2O2) elevate T-cad mRNA and protein levels in ECs. Reporter gene analysis, using serially deleted T-cad promoter stretches ranging from −99 to −2304 bp, located the minimal

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Nebbioso, Marcella, Gianfranco Scarsella, Aloisa Librando, and Nicola Pescosolido. "Biomolecular Modulation of Neurodegenerative Events during Ageing." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/978654.

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The objective is to assess the modulation of retinal and optic nerve degenerative events induced by the combination ofα-lipoic acid (ALA) and superoxide dismutase (SOD) in an animal model of ageing. For this study, 24 male Wistar-Harlan strain rats were left to age for up to 24 months. One group of rats was subjected to a diet supplemented with ALA and SOD for 8 weeks, while another group was used as a positive control and not subjected to any dietary treatment. To assess the cytoprotective effects of the antioxidants, a morphological analysis was carried out on sections of retina and optic ne

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Almeida, Teresa, Marta Marques, Dominik Mojzita, et al. "Isc1p Plays a Key Role in Hydrogen Peroxide Resistance and Chronological Lifespan through Modulation of Iron Levels and Apoptosis." Molecular Biology of the Cell 19, no. 3 (2008): 865–76. http://dx.doi.org/10.1091/mbc.e07-06-0604.

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The inositolphosphosphingolipid phospholipase C (Isc1p) of Saccharomyces cerevisiae belongs to the family of neutral sphingomyelinases that generates the bioactive sphingolipid ceramide. In this work the role of Isc1p in oxidative stress resistance and chronological lifespan was investigated. Loss of Isc1p resulted in a higher sensitivity to hydrogen peroxide that was associated with an increase in oxidative stress markers, namely intracellular oxidation, protein carbonylation, and lipid peroxidation. Microarray analysis showed that Isc1p deficiency up-regulated the iron regulon leading to inc

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45

Gatti, Martina, Manuela Zavatti, Francesca Beretti, et al. "Oxidative Stress in Alzheimer’s Disease: In Vitro Therapeutic Effect of Amniotic Fluid Stem Cells Extracellular Vesicles." Oxidative Medicine and Cellular Longevity 2020 (October 24, 2020): 1–13. http://dx.doi.org/10.1155/2020/2785343.

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Alzheimer’s disease (AD) is characterized by abnormal protein aggregation, deposition of extracellular β-amyloid proteins (Aβ), besides an increase of oxidative stress. Amniotic fluid stem cells (AFSCs) should have a therapeutic potential for neurodegenerative disorders, mainly through a paracrine effect mediated by extracellular vesicles (EV). Here, we examined the effect of EV derived from human AFSCs (AFSC-EV) on the disease phenotypes in an AD neuron primary culture. We observed a positive effect of AFSC-EV on neuron morphology, viability, and Aβ and phospho-Tau levels. This could be due t

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46

Csonka, Csaba, Márta Sárközy, Márton Pipicz, László Dux, and Tamás Csont. "Modulation of Hypercholesterolemia-Induced Oxidative/Nitrative Stress in the Heart." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–23. http://dx.doi.org/10.1155/2016/3863726.

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Hypercholesterolemia is a frequent metabolic disorder associated with increased risk for cardiovascular morbidity and mortality. In addition to its well-known proatherogenic effect, hypercholesterolemia may exert direct effects on the myocardium resulting in contractile dysfunction, aggravated ischemia/reperfusion injury, and diminished stress adaptation. Both preclinical and clinical studies suggested that elevated oxidative and/or nitrative stress plays a key role in cardiac complications induced by hypercholesterolemia. Therefore, modulation of hypercholesterolemia-induced myocardial oxidat

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Rodrigues Henriques, Juan Ricardo, and Neira Gamboa de Domínguez. "Modulation of the oxidative stress in malaria infection by clotrimazole." Brazilian Journal of Pharmaceutical Sciences 48, no. 3 (2012): 519–28. http://dx.doi.org/10.1590/s1984-82502012000300019.

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Antimycotic clotrimazole (CTZ) has demonstrated remarkable activity against Plasmodium falciparum in vitro and in vivo. Hemoglobin degradation by Plasmodium parasites makes amino acids available for protein synthesis, inducing oxidative stress in infected cells and producing free heme. These events represent biochemical targets for potential antimalarials. In this study, we have tested the ability of CTZ to modify the oxidative status in Plasmodium berghei-infected erythrocytes. After hemolysis, activities of superoxide dismutase (SOD), catalase (CAT), glutathione cycle and NADPH+H+-producing

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48

Allen, Paige E., and Juan J. Martinez. "Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria." Pathogens 9, no. 8 (2020): 614. http://dx.doi.org/10.3390/pathogens9080614.

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Lipids are a broad group of molecules required for cell maintenance and homeostasis. Various intracellular pathogens have developed mechanisms of modulating and sequestering host lipid processes for a large array of functions for both bacterial and host cell survival. Among the host cell lipid functions that intracellular bacteria exploit for infection are the modulation of host plasma membrane microdomains (lipid rafts) required for efficient bacterial entry; the recruitment of specific lipids for membrane integrity of intracellular vacuoles; and the utilization of host lipid droplets for the

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Denu, Ryan A., and Peiman Hematti. "Effects of Oxidative Stress on Mesenchymal Stem Cell Biology." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2989076.

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Mesenchymal stromal/stem cells (MSCs) are multipotent stem cells present in most fetal and adult tissues.Ex vivoculture-expanded MSCs are being investigated for tissue repair and immune modulation, but their full clinical potential is far from realization. Here we review the role of oxidative stress in MSC biology, as their longevity and functions are affected by oxidative stress. In general, increased reactive oxygen species (ROS) inhibit MSC proliferation, increase senescence, enhance adipogenic but reduce osteogenic differentiation, and inhibit MSC immunomodulation. Furthermore, aging, sene

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Kello, Martin, Peter Takac, Peter Kubatka, Tomas Kuruc, Klaudia Petrova, and Jan Mojzis. "Oxidative Stress-Induced DNA Damage and Apoptosis in Clove Buds-Treated MCF-7 Cells." Biomolecules 10, no. 1 (2020): 139. http://dx.doi.org/10.3390/biom10010139.

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Abstract:

In recent decades, several spices have been studied for their potential in the prevention and treatment of cancer. It is documented that spices have antioxidant, anti-inflammatory, immunomodulatory, and anticancer effects. The main mechanisms of spices action included apoptosis induction, proliferation, migration and invasion of tumour inhibition, and sensitization of tumours to radiotherapy and chemotherapy. In this study, the ability of clove buds extract (CBE) to induce oxidative stress, DNA damage, and stress/survival/apoptotic pathways modulation were analysed in MCF-7 cells. We demonstra

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