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Journal articles on the topic 'Oxidative damage'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Krisko, Anita, and Miroslav Radman. "Protein damage, ageing and age-related diseases." Open Biology 9, no. 3 (2019): 180249. http://dx.doi.org/10.1098/rsob.180249.

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Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortalit

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2

Nunomura, Akihiko, Kazuhiro Honda, Atsushi Takeda, et al. "Oxidative Damage to RNA in Neurodegenerative Diseases." Journal of Biomedicine and Biotechnology 2006 (2006): 1–6. http://dx.doi.org/10.1155/jbb/2006/82323.

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Since 1999, oxidative damage to RNA molecules has been described in several neurological diseases including Alzheimer's disease, Parkinson's disease, Down syndrome, dementia with Lewy bodies, prion disease, subacute sclerosing panencephalitis, and xeroderma pigmentosum. An early involvement of RNA oxidation of vulnerable neuronal population in the neurodegenerative diseases has been demonstrated, which is strongly supported by a recent observation of increased RNA oxidation in brains of subjects with mild cognitive impairment. Until recently, little is known about consequences and cellular han

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Rice-Evans, C., S. C. Omorphos, and E. Baysal. "Sickle cell membranes and oxidative damage." Biochemical Journal 237, no. 1 (1986): 265–69. http://dx.doi.org/10.1042/bj2370265.

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Sickle erythrocytes and their membranes are susceptible to endogenous free-radical-mediated oxidative damage which correlates with the proportion of irreversibly sickled cells. The suppression of incubation-induced oxidative stress by antioxidants, free radical scavengers and an iron chelator suggest that oxidation products of membrane-bound haemoglobin contribute towards the pathology of the disease.

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4

Singh, Abhishek Kumar, Sandeep Singh, Geetika Garg, and Syed Ibrahim Rizvi. "Rapamycin alleviates oxidative stress-induced damage in rat erythrocytes." Biochemistry and Cell Biology 94, no. 5 (2016): 471–79. http://dx.doi.org/10.1139/bcb-2016-0048.

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An imbalanced cellular redox system promotes the production of reactive oxygen species (ROS) that may lead to oxidative stress-mediated cell death. Erythrocytes are the best-studied model of antioxidant defense mechanism. The present study was undertaken to investigate the effect of the immunosuppressant drug rapamycin, an inducer of autophagy, on redox balance of erythrocytes and blood plasma of oxidatively challenged rats. Male Wistar rats were oxidatively challenged with HgCl2 (5 mg/kg body mass (b.m.)). A significant (p < 0.05) induction in ROS production, plasma membrane redox system (

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5

Skrypnyk, N. V., and O. O. Maslova. "Oxidative DNA damage." Biopolymers and Cell 23, no. 3 (2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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6

Davenport, R. J. "Trash Cache: Secret mitochondrial weapon fights oxidative damage (Oxidative damage)." Science of Aging Knowledge Environment 2002, no. 12 (2002): 41nw—41. http://dx.doi.org/10.1126/sageke.2002.12.nw41.

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7

DAS, Nilanjana, Rodney L. LEVINE, William C. ORR, and Rajindar S. SOHAL. "Selectivity of protein oxidative damage during aging in Drosophila melanogaster." Biochemical Journal 360, no. 1 (2001): 209–16. http://dx.doi.org/10.1042/bj3600209.

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The purpose of the present study was to determine whether oxidation of various proteins during the aging process occurs selectively or randomly, and whether the same proteins are damaged in different species. Protein oxidative damage to the proteins, present in the matrix of mitochondria in the flight muscles of Drosophila melanogaster and manifested as carbonyl modifications, was detected immunochemically with anti-dinitrophenyl-group antibodies. Aconitase was found to be the only protein in the mitochondrial matrix that exhibited an age-associated increase in carbonylation. The accrual of ox

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8

Soria-Meneses, Pedro Javier, Alejandro Jurado-Campos, Virgilio Gómez-Rubio, et al. "Determination of Ram (Ovis aries) Sperm DNA Damage Due to Oxidative Stress: 8-OHdG Immunodetection Assay vs. SCSA®." Animals 12, no. 23 (2022): 3286. http://dx.doi.org/10.3390/ani12233286.

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Conventional DNA analysis techniques can hardly detect DNA damage in ruminant spermatozoa due to high DNA compaction in these cells. Furthermore, these techniques cannot discriminate whether the damage is due to oxidative stress. The main purpose of this study was to evaluate the efficacy of two techniques for determining DNA damage in ovine sperm when the source of that damage is oxidative stress. Semen samples from twenty Manchega rams (Ovis aries) were collected and cryopreserved. After thawing, the samples were subjected to different levels of oxidative stress, and DNA oxidation was quanti

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9

Huang, Yue, Zhiling Li, En Lin, Pei He та Gaizhen Ru. "Oxidative damage-induced hyperactive ribosome biogenesis participates in tumorigenesis of offspring by cross-interacting with the Wnt and TGF-β1 pathways in IVF embryos". Experimental & Molecular Medicine 53, № 11 (2021): 1792–806. http://dx.doi.org/10.1038/s12276-021-00700-0.

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AbstractIn vitro fertilization (IVF) increases the risk of tumorigenesis in offspring. The increased oxidative damage during IVF may be involved in tumor formation. However, the molecular mechanisms underlying this phenomenon remain largely unclear. Using a well-established model of oxidatively damaged IVF mouse embryos, we applied the iTRAQ method to identify proteins differentially expressed between control and oxidatively damaged zygotes and explored the possible tumorigenic mechanisms, especially with regard to the effects of oxidative damage on ribosome biogenesis closely related to tumor

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10

Jeshan, Milad, Fatemeh Yousefbeyk, Hiva Rahmati, Amir Hosein Shoormeij, Mitra Rezazadeh, and Ehsan Zamani. "Salvia spinosa L. Protects against Diabetes-Induced Nephropathy by Attenuation of Mitochondrial Oxidative Damage in Mice." Advances in Pharmacological and Pharmaceutical Sciences 2021 (December 26, 2021): 1–10. http://dx.doi.org/10.1155/2021/4657514.

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Mitochondrial oxidative damage is a crucial factor in the pathogenesis of diabetic nephropathy (DN), which is among the most prevalent problems of diabetes, and there hasn’t been an effective treatment for DN yet. This study planned to investigate the effects of Salvia spinosa L. on mitochondrial function along with its protection against streptozotocin-induced nephropathy in diabetic mice. After the injection of streptozotocin (STZ) and verification of the establishment of diabetes, mice (n = 30) were randomly divided into the following groups: control group, diabetic-control, S. spinosa-trea

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11

Lozano-Picazo, Carmen María, and Francisco Fernández-Belda. "Especies reactivas de oxígeno y su implicación en Biomedicina." Anales de Veterinaria de Murcia 34 (December 16, 2020): 17–26. http://dx.doi.org/10.6018/analesvet.332621.

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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 ce

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12

Anderson, Andrew P., Xuemei Luo, William Russell, and Y. Whitney Yin. "Oxidative damage diminishes mitochondrial DNA polymerase replication fidelity." Nucleic Acids Research 48, no. 2 (2019): 817–29. http://dx.doi.org/10.1093/nar/gkz1018.

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Abstract Mitochondrial DNA (mtDNA) resides in a high ROS environment and suffers more mutations than its nuclear counterpart. Increasing evidence suggests that mtDNA mutations are not the results of direct oxidative damage, rather are caused, at least in part, by DNA replication errors. To understand how the mtDNA replicase, Pol γ, can give rise to elevated mutations, we studied the effect of oxidation of Pol γ on replication errors. Pol γ is a high fidelity polymerase with polymerase (pol) and proofreading exonuclease (exo) activities. We show that Pol γ exo domain is far more sensitive to ox

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13

Sherman, Michael. "Oxidative Damage in Neurodegenerative Diseases: Relevance of Dietary Antioxidants." Neuroscience and Neurological Surgery 2, no. 5 (2018): 01–03. http://dx.doi.org/10.31579/2578-8868/040.

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14

Jasenovec, Tomas, Rastislav Vazan, Dominika Radosinska, Roman Gardlik, and Jana Radosinska. "Melatonin Pre-Treatment Protects Erythrocytes Against Subsequent Oxidative Damage." Molecules 30, no. 3 (2025): 658. https://doi.org/10.3390/molecules30030658.

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Research on the effects of melatonin on erythrocyte deformability has yielded mixed results. While some studies reported improvements, others found no effect, and a few even noted a deterioration in deformability. Moreover, the impact of melatonin may vary between healthy erythrocytes and those subjected to oxidative stress. This study investigated the dose-dependent effects of melatonin on erythrocytes under baseline conditions and oxidative stress, using both pre- and post-stress incubation protocols. Oxidative damage was induced with tert-butyl hydroperoxide (TBHP), and its extent was asses

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15

Toomey, Lillian M., Melissa G. Papini, Thomas O. Clarke, et al. "Secondary Degeneration of Oligodendrocyte Precursor Cells Occurs as Early as 24 h after Optic Nerve Injury in Rats." International Journal of Molecular Sciences 24, no. 4 (2023): 3463. http://dx.doi.org/10.3390/ijms24043463.

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Optic nerve injury causes secondary degeneration, a sequela that spreads damage from the primary injury to adjacent tissue, through mechanisms such as oxidative stress, apoptosis, and blood-brain barrier (BBB) dysfunction. Oligodendrocyte precursor cells (OPCs), a key component of the BBB and oligodendrogenesis, are vulnerable to oxidative deoxyribonucleic acid (DNA) damage by 3 days post-injury. However, it is unclear whether oxidative damage in OPCs occurs earlier at 1 day post-injury, or whether a critical ‘window-of-opportunity’ exists for therapeutic intervention. Here, a partial optic ne

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Sumner, Edward R., Anupama Shanmuganathan, Theodora C. Sideri, Sylvia A. Willetts, John E. Houghton, and Simon V. Avery. "Oxidative protein damage causes chromium toxicity in yeast." Microbiology 151, no. 6 (2005): 1939–48. http://dx.doi.org/10.1099/mic.0.27945-0.

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Oxidative damage in microbial cells occurs during exposure to the toxic metal chromium, but it is not certain whether such oxidation accounts for the toxicity of Cr. Here, a Saccharomyces cerevisiae sod1Δ mutant (defective for the Cu,Zn-superoxide dismutase) was found to be hypersensitive to Cr(VI) toxicity under aerobic conditions, but this phenotype was suppressed under anaerobic conditions. Studies with cells expressing a Sod1p variant (Sod1H46C) showed that the superoxide dismutase activity rather than the metal-binding function of Sod1p was required for Cr resistance. To help identify the

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17

Zhang, Weiran, Ranwei Zhong, Xiangping Qu, Yang Xiang, and Ming Ji. "Effect of 8-Hydroxyguanine DNA Glycosylase 1 on the Function of Immune Cells." Antioxidants 12, no. 6 (2023): 1300. http://dx.doi.org/10.3390/antiox12061300.

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Excess reactive oxygen species (ROS) can cause an imbalance between oxidation and anti-oxidation, leading to the occurrence of oxidative stress in the body. The most common product of ROS-induced base damage is 8-hydroxyguanine (8-oxoG). Failure to promptly remove 8-oxoG often causes mutations during DNA replication. 8-oxoG is cleared from cells by the 8-oxoG DNA glycosylase 1 (OGG1)-mediated oxidative damage base excision repair pathway so as to prevent cells from suffering dysfunction due to oxidative stress. Physiological immune homeostasis and, in particular, immune cell function are vulne

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18

Breusing, Nicolle, and Tilman Grune. "Regulation of proteasome-mediated protein degradation during oxidative stress and aging." Biological Chemistry 389, no. 3 (2008): 203–9. http://dx.doi.org/10.1515/bc.2008.029.

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Abstract Protein degradation is a physiological process required to maintain cellular functions. There are distinct proteolytic systems for different physiological tasks under changing environmental and pathophysiological conditions. The proteasome is responsible for the removal of oxidatively damaged proteins in the cytosol and nucleus. It has been demonstrated that proteasomal degradation increases due to mild oxidation, whereas at higher oxidant levels proteasomal degradation decreases. Moreover, the proteasome itself is affected by oxidative stress to varying degrees. The ATP-stimulated 26

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19

Oliveira, Rodrigo Assunção, Ana Paula Rennó Sierra, Marino Benetti, et al. "Impact of Hot Environment on Fluid and Electrolyte Imbalance, Renal Damage, Hemolysis, and Immune Activation Postmarathon." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/9824192.

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Previous studies have demonstrated the physiological changes induced by exercise exposure in hot environments. We investigated the hematological and oxidative changes and tissue damage induced by marathon race in different thermal conditions. Twenty-six male runners completed the São Paulo International Marathon both in hot environment (HE) and in temperate environment (TE). Blood and urine samples were collected 1 day before, immediately after, 1 day after, and 3 days after the marathon to analyze the hematological parameters, electrolytes, markers of tissue damage, and oxidative status. In b

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20

Sun, Yi, Wen-Jia Zhang, Xin Zhao, Ren-Pei Yuan, Hui Jiang, and Xiao-Ping Pu. "PARK7 protein translocating into spermatozoa mitochondria in Chinese asthenozoospermia." REPRODUCTION 148, no. 3 (2014): 249–57. http://dx.doi.org/10.1530/rep-14-0222.

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PARK7 (DJ1) is a multifunctional oxidative stress response protein that protects cells against reactive oxygen species (ROS) and mitochondrial damage. PARK7 defects are known to cause various physiological dysfunctions, including infertility. Asthenozoospermia (AS), i.e. low-motile spermatozoa in the ejaculate, is a common cause of human male infertility. In this study, we found that downregulation of PARK7 resulted in increased levels of lipid peroxide and ROS, decreased mitochondrial membrane potential, and reduced mitochondrial complex I enzyme activity in the spermatozoa from AS patients.

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21

Klaunig, James E., Lisa M. Kamendulis, and Barbara A. Hocevar. "Oxidative Stress and Oxidative Damage in Carcinogenesis." Toxicologic Pathology 38, no. 1 (2009): 96–109. http://dx.doi.org/10.1177/0192623309356453.

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22

Chen, Zhigang, Qiaoling Yuan, Guangren Xu, Huiyu Chen, Hongyu Lei, and Jianming Su. "Effects of Quercetin on Proliferation and H2O2-Induced Apoptosis of Intestinal Porcine Enterocyte Cells." Molecules 23, no. 8 (2018): 2012. http://dx.doi.org/10.3390/molecules23082012.

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Weanling stress and toxicosis, which are harmful to the health of pigs’ intestines, are associated with oxidative stress. Quercetin (Que) is a polyphenolic compound that shows good anti-cancer, anti-inflammation and anti-oxidation effects. This study aimed to elaborate whether or not Que promotes IPEC-J2 (intestinal porcine enterocyte cells) proliferation and protects IPEC-J2 from oxidative damage. Thus, we examined the effects of Que on proliferation and H2O2-induced apoptosis in IPEC-J2. The results showed that Que increased IPEC-J2 viabililty, propelled cells from G1 phase into S phase and

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23

Hanna, Bishoy M. F., Maurice Michel, Thomas Helleday, and Oliver Mortusewicz. "NEIL1 and NEIL2 Are Recruited as Potential Backup for OGG1 upon OGG1 Depletion or Inhibition by TH5487." International Journal of Molecular Sciences 22, no. 9 (2021): 4542. http://dx.doi.org/10.3390/ijms22094542.

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DNA damage caused by reactive oxygen species may result in genetic mutations or cell death. Base excision repair (BER) is the major pathway that repairs DNA oxidative damage in order to maintain genomic integrity. In mammals, eleven DNA glycosylases have been reported to initiate BER, where each recognizes a few related DNA substrate lesions with some degree of overlapping specificity. 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most abundant DNA oxidative lesions, is recognized and excised mainly by 8-oxoguanine DNA glycosylase 1 (OGG1). Further oxidation of 8-oxoG generates hydantoin lesio

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Strzelczyk, Joanna Katarzyna, and Andrzej Wiczkowski. "Oxidative damage and carcinogenesis." Współczesna Onkologia 3 (2012): 230–33. http://dx.doi.org/10.5114/wo.2012.29290.

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25

Yao, Jeffrey K., Ravinder D. Reddy, and Daniel P. van Kammen. "Oxidative Damage and Schizophrenia." CNS Drugs 15, no. 4 (2001): 287–310. http://dx.doi.org/10.2165/00023210-200115040-00004.

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26

Imlay, James A. "Pathways of Oxidative Damage." Annual Review of Microbiology 57, no. 1 (2003): 395–418. http://dx.doi.org/10.1146/annurev.micro.57.030502.090938.

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Smith, M. A., G. Perry, P. L. Richey, et al. "Oxidative damage in Alzheimer's." Nature 382, no. 6587 (1996): 120–21. http://dx.doi.org/10.1038/382120b0.

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28

Jacob, R. A., and B. J. Burri. "Oxidative damage and defense." American Journal of Clinical Nutrition 63, no. 6 (1996): 985S—990S. http://dx.doi.org/10.1093/ajcn/63.6.985.

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29

Poli, Giuseppe, and Maurizio Parola. "Oxidative damage and fibrogenesis." Free Radical Biology and Medicine 22, no. 1-2 (1997): 287–305. http://dx.doi.org/10.1016/s0891-5849(96)00327-9.

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30

Oberley, Terry D. "Oxidative Damage and Cancer." American Journal of Pathology 160, no. 2 (2002): 403–8. http://dx.doi.org/10.1016/s0002-9440(10)64857-2.

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31

Cruz-Guilloty, Fernando, and Victor L. Perez. "Defence against oxidative damage." Nature 478, no. 7367 (2011): 42–43. http://dx.doi.org/10.1038/478042a.

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32

Hayes, Robert C., Lynn A. Petrullo, Haimei Huang, Susan S. Wallace, and J. Eugene LeClerc. "Oxidative damage in DNA." Journal of Molecular Biology 201, no. 2 (1988): 239–46. http://dx.doi.org/10.1016/0022-2836(88)90135-0.

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33

Vissers, Margret C. M., and Christine C. Winterbourn. "Oxidative damage to fibronectin." Archives of Biochemistry and Biophysics 285, no. 1 (1991): 53–59. http://dx.doi.org/10.1016/0003-9861(91)90327-f.

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Vissers, Margret C. M., and Christine C. Winterbourn. "Oxidative damage to fibronectin." Archives of Biochemistry and Biophysics 285, no. 2 (1991): 357–64. http://dx.doi.org/10.1016/0003-9861(91)90372-p.

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35

NAGAKI, M., and H. MORIWAKI. "Hepatoprotection against oxidative damage." Hepatology Research 32, no. 1 (2005): 9–11. http://dx.doi.org/10.1016/j.hepres.2005.03.003.

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36

Perry, G., D. A. Zelasko, L. M. Sayre, and M. A. Smith. "Oxidative Damage to Axonal Cytoskeletal Proteins." Microscopy and Microanalysis 3, S2 (1997): 43–44. http://dx.doi.org/10.1017/s1431927600007108.

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Proteins of the axonal cytoskeleton, particularly neurofilament and microtubule-associated protein τ, should be particularly sensitive to the effects of oxidative modification due to their high content of lysine, an amino acid that is particularly susceptible to direct oxidization as well as adduction by carbonyls produced from lipid and sugar oxidation. To understand the susceptibility of the cytoskeleton to oxidative modification and whether such modification is related to the physiological function of the cytoskeleton, we undertook a cytological analysis of motor neurons isolated from mouse

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Sestili, Piero, Maurizio Brigotti, Cinzia Calcabrini, et al. "Deuterium Incorporation Protects Cells from Oxidative Damage." Oxidative Medicine and Cellular Longevity 2019 (July 18, 2019): 1–13. http://dx.doi.org/10.1155/2019/6528106.

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In the cold environments of the interstellar medium, a variety of molecules in which a hydrogen (H) atom has been replaced by its heavier isotope deuterium (D) can be found. From its emergence, life had to counteract the toxic action of many agents, which posed a constant threat to its development and propagation. Oxygen-reactive species are archaic toxicants that lead to protein damage and genomic instability. Most of the oxidative lesions involve cleavage of C-H bonds and H abstraction. According to free radical chemistry principles, the substitution of D for H in oxidation-sensitive positio

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Ávalos, A., A. I. Haza, and Paloma Morales. "Manufactured Silver Nanoparticles of Different Sizes Induced DNA Strand Breaks and Oxidative DNA Damage in Hepatoma and Leukaemia Cells and in Dermal and Pulmonary Fibroblasts." Folia Biologica 61, no. 1 (2015): 33–42. http://dx.doi.org/10.14712/fb2015061010033.

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Many classes of silver nanoparticles (AgNPs) have been synthesized and widely applied, but no conclusive information on their potential cytotoxicity and genotoxicity mechanisms is available. Therefore, the purpose of this study was to compare the potential genotoxic effects (DNA strand breaks and oxidative DNA damage) of 4.7 nm coated and 42 nm uncoated AgNPs, using the comet assay, in four relevant human cell lines (hepatoma, leukaemia, and dermal and pulmonary fibroblasts) in order to understand the impact of such nanomaterials on cellular DNA. The results indicated that in all cell lines te

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Collins, A. R., and E. Horváthová. "Oxidative DNA damage, antioxidants and DNA repair: applications of the comet assay." Biochemical Society Transactions 29, no. 2 (2001): 337–40. http://dx.doi.org/10.1042/bst0290337.

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Estimates of background levels of oxidative base damage in human white blood cells vary enormously, from 300 down to 0.4 molecules of 8-oxoguanine per 106 guanines. An EC-funded Concerted Action, the European Standards Committee on Oxidative DNA Damage, is currently attempting to resolve the discrepancy and to agree a realistic estimate of basal endogenous oxidation. Oxidation of lymphocyte DNA is a useful marker of oxidative stress, and this can be decreased by supplementation with pure antioxidants or with foods rich in antioxidants. The steady-state level of DNA oxidation is ultimately cont

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Rosenmund, A., C. Kuyas, and A. Haeberli. "Oxidative radioiodination damage to human lactoferrin." Biochemical Journal 240, no. 1 (1986): 239–45. http://dx.doi.org/10.1042/bj2400239.

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Oxidative iodination of human lactoferrin (Lf) as commonly performed by using the chloramine-T, the Iodogen or the lactoperoxidase method produces an unreliable tracer protein because of excessive and heterogeneous polymer formation. Before iodination a minor tetramer fraction may be demonstrable in iron-saturated Lf only. Iodination-induced polymerization of iron-poor as well as iron-saturated Lf occurs independently of the presence or absence of 10 mM-EDTA and the 125I-/Lf molar ratio used for iodination. 125I-Lf polymers are mainly covalently linked, as suggested by the lack of substantial

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Hirota, Yuko, Dongchon Kang, and Tomotake Kanki. "The Physiological Role of Mitophagy: New Insights into Phosphorylation Events." International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/354914.

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Mitochondria play an essential role in oxidative phosphorylation, fatty acid oxidation, and the regulation of apoptosis. However, this organelle also produces reactive oxygen species (ROS) that continually inflict oxidative damage on mitochondrial DNA, proteins, and lipids, which causes further production of ROS. To oppose this oxidative stress, mitochondria possess quality control systems that include antioxidant enzymes and the repair or degradation of damaged mitochondrial DNA and proteins. If the oxidative stress exceeds the capacity of the mitochondrial quality control system, it seems th

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Bruckbauer, Steven T., Benjamin B. Minkoff, Michael R. Sussman, and Michael M. Cox. "Proteome Damage Inflicted by Ionizing Radiation: Advancing a Theme in the Research of Miroslav Radman." Cells 10, no. 4 (2021): 954. http://dx.doi.org/10.3390/cells10040954.

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Oxidative proteome damage has been implicated as a major contributor to cell death and aging. Protein damage and aging has been a particular theme of the recent research of Miroslav Radman. However, the study of how cellular proteins are damaged by oxidative processes is still in its infancy. Here we examine oxidative changes in the proteomes of four bacterial populations—wild type E. coli, two isolates from E. coli populations evolved for high levels of ionizing radiation (IR) resistance, and D. radiodurans—immediately following exposure to 3000 Gy of ionizing radiation. By a substantial marg

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Binek, Aleksandra, Celia Castans, Inmaculada Jorge, et al. "Oxidative Post-translational Protein Modifications upon Ischemia/Reperfusion Injury." Antioxidants 13, no. 1 (2024): 106. http://dx.doi.org/10.3390/antiox13010106.

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While reperfusion, or restoration of coronary blood flow in acute myocardial infarction, is a requisite for myocardial salvage, it can paradoxically induce a specific damage known as ischemia/reperfusion (I/R) injury. Our understanding of the precise pathophysiological molecular alterations leading to I/R remains limited. In this study, we conducted a comprehensive and unbiased time-course analysis of post-translational modifications (PTMs) in the post-reperfused myocardium of two different animal models (pig and mouse) and evaluated the effect of two different cardioprotective therapies (isch

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Kino, Katsuhito, Taishu Kawada, Masayo Hirao-Suzuki, Masayuki Morikawa, and Hiroshi Miyazawa. "Products of Oxidative Guanine Damage Form Base Pairs with Guanine." International Journal of Molecular Sciences 21, no. 20 (2020): 7645. http://dx.doi.org/10.3390/ijms21207645.

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Among the natural bases, guanine is the most oxidizable base. The damage caused by oxidation of guanine, commonly referred to as oxidative guanine damage, results in the formation of several products, including 2,5-diamino-4H-imidazol-4-one (Iz), 2,2,4-triamino-5(2H)-oxazolone (Oz), guanidinoformimine (Gf), guanidinohydantoin/iminoallantoin (Gh/Ia), spiroiminodihydantoin (Sp), 5-carboxamido-5-formamido-2-iminohydantoin (2Ih), urea (Ua), 5-guanidino-4-nitroimidazole (NI), spirodi(iminohydantoin) (5-Si and 8-Si), triazine, the M+7 product, other products by peroxynitrite, alkylated guanines, and

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Shen, Mingyue, Ruixin Cai, Zhedong Li, Xiaodie Chen, and Jianhua Xie. "The Molecular Mechanism of Yam Polysaccharide Protected H2O2-Induced Oxidative Damage in IEC-6 Cells." Foods 12, no. 2 (2023): 262. http://dx.doi.org/10.3390/foods12020262.

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Oxidative stress is involved in maintaining homeostasis of the body, and an in-depth study of its mechanism of action is beneficial for the prevention of chronic illnesses. This study aimed to investigate the protective mechanism of yam polysaccharide (CYP) against H2O2-induced oxidative damage by an RNA-seq technique. The expression of genes and the function of the genome in the process of oxidative damage by H2O2 in IEC-6 cells were explored through transcriptomic analysis. The results illustrated that H2O2 damaged cells by promoting cell differentiation and affecting tight junction proteins

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Fejfer, Katarzyna, Piotr Buczko, Marek Niczyporuk, et al. "Oxidative Modification of Biomolecules in the Nonstimulated and Stimulated Saliva of Patients with Morbid Obesity Treated with Bariatric Surgery." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4923769.

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Morbid obesity leads to progressive failure of many human organs and systems; however, the role of oxidative damage to salivary composition is still unknown in the obese patients. In this study, we assessed the effect of bariatric surgery on oxidative damage in nonstimulated (NS) and stimulated (S) whole saliva. The study included 47 subjects with morbid obesity as well as 47 age- and gender-matched healthy volunteers. Oxidative modifications to lipids (4-hydroxynonenal (4-HNE) and 8-isoprostanes (8-isoP)), proteins (advanced oxidation protein products (AOPP) and protein carbonyl groups (PC)),

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Kong, Qingjun, Qingzhi Zeng, Jia Yu, Hongxi Xiao, Jun Lu, and Xueyan Ren. "Mechanism of Resveratrol Dimers Isolated from Grape Inhibiting 1O2 Induced DNA Damage by UHPLC-QTOF-MS2 and UHPLC-QQQ-MS2 Analyses." Biomedicines 9, no. 3 (2021): 271. http://dx.doi.org/10.3390/biomedicines9030271.

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Resveratrol dimers have been extensively reported on due to their antioxidative activity. Previous studies revealed that resveratrol dimer has been shown to selectively quench singlet oxygen (1O2), and could protect DNA from oxidative damage. The mechanism of resveratrol dimers protecting DNA against oxidative damage is still not clear. Therefore, in this project, the reactants and products of resveratrol dimers protecting guanine from oxidative damage were qualitatively monitored and quantitatively analyzed by UHPLC-QTOF-MS2 and UHPLC-QQQ-MS2. Results showed that when guanine and resveratrol

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Patra, R. C., Amiya K. Rautray, and D. Swarup. "Oxidative Stress in Lead and Cadmium Toxicity and Its Amelioration." Veterinary Medicine International 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/457327.

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Oxidative stress has been implicated to play a role, at least in part, in pathogenesis of many disease conditions and toxicities in animals. Overproduction of reactive oxygen species and free radicals beyond the cells intrinsic capacity to neutralize following xenobiotics exposure leads to a state of oxidative stress and resultant damages of lipids, protein, and DNA. Lead and cadmium are the common environmental heavy metal pollutants and have widespread distribution. Both natural and anthropogenic sources including mining, smelting, and other industrial processes are responsible for human and

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Salimi, Ahmad, Elahe Baghal, Hassan Ghobadi, Niloufar Hashemidanesh, Farzad Khodaparast, and Enayatollah Seydi. "Mitochondrial, lysosomal and DNA damages induced by acrylamide attenuate by ellagic acid in human lymphocyte." PLOS ONE 16, no. 2 (2021): e0247776. http://dx.doi.org/10.1371/journal.pone.0247776.

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Acrylamide (AA), is an important contaminant formed during food processing under high temperature. Due to its potential neurotoxicity, reproductive toxicity, hepatotoxicity, immunotoxicity, genotoxicity and carcinogenicity effects, this food contaminant has been recognized as a human health concern. Previous studies showed that acrylamide-induced toxicity is associated with active metabolite of acrylamide by cytochrome P450 enzyme, oxidative stress, mitochondrial dysfunction and DNA damage. In the current study, we investigated the role of oxidative stress in acrylamide’s genotoxicity and ther

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Qin, Bei, Kuan Yang, and Ruijun Cao. "Synthesis and Antioxidative Activity of Piperine Derivatives Containing Phenolic Hydroxyl." Journal of Chemistry 2020 (July 21, 2020): 1–9. http://dx.doi.org/10.1155/2020/2786359.

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Piperine was used in this study in its raw form, and different steps, such as amide hydrolysis and amidation, were used to synthesize piperine derivatives containing a phenolic hydroxyl group. DPPH and ABTS free radical scavenging assays were used to assess piperine derivative antioxidant activities. We constructed an AAPH oxidative stress erythrocyte model to study the effect of piperine derivatives on the hemolysis rate of oxidatively damaged erythrocytes as well as the hemoglobin oxidation rate. This AAPH model was also used to determine piperine derivative effects on antioxidant enzyme act

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