scholarly journals Expression of the Melatonin-Associated Genes in Fibroblasts That Have Been Co-Exposed to Fluoride and a Moderate-Strength Static Magnetic Field

2021 ◽  
Vol 11 (19) ◽  
pp. 8810
Author(s):  
Celina Kruszniewska-Rajs ◽  
Agnieszka Synowiec-Wojtarowicz ◽  
Joanna Gola ◽  
Magdalena Kimsa-Dudek
Keyword(s):  
Magnetic Field ◽  
Oxidative Damage ◽  
Static Magnetic Field ◽  
Human Fibroblasts ◽  
Physical Factor ◽  
Protective Role ◽  
Dermal Fibroblasts ◽  
Cellular Damage ◽  
Negative Effect

Fluoride can weaken the protective role of melatonin in reducing cellular damage. A static magnetic field is a physical factor that can counteract the negative effect of fluoride. Hence, the main objective of the study was to analyze the transcriptional activity of the genes that are associated with the activity of melatonin in human skin fibroblasts that have been co-exposed to fluoride and a moderate-strength static magnetic field. The expression of the melatonin-associated genes in human fibroblasts that had simultaneously been exposed to F− and a static magnetic field was determined using an oligonucleotide microarray and RT-qPCR techniques. The concentration of oxidative damage markers was also measured. In NaF and static magnetic field-treated cells, there was a tendency to compensate for the expression of the differentiating genes (IL27RA, NR1D1, RRP7A, YIPF1, HIST1H2BD) that had been modified by the presence of fluoride. It has been also shown that the oxidative damage marker concentration was statistically lower in the cells that had simultaneously been exposed to fluoride and a static magnetic field compared to the F-treated cells. In conclusion, the protective role of a moderate-strength static magnetic field on human dermal fibroblasts that had been exposed to fluoride was demonstrated, and its mechanism of action is associated with the melatonin-dependent pathways.

The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats

2014 ◽  
Vol 38 (3) ◽  
pp. 774-782 ◽  
Author(s):  
Merve Bacanlı ◽  
Sevtap Aydın ◽  
Gökçe Taner ◽  
Hatice Gül Göktaş ◽  
Tolga Şahin ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Ferulic Acid ◽  
Protective Role ◽  
Albino Rats ◽  
Wistar Albino Rats

scholarly journals Effects of Caloric Restriction on Cardiac Oxidative Stress and Mitochondrial Bioenergetics: Potential Role of Cardiac Sirtuins

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ken Shinmura
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Caloric Restriction ◽  
Functional Decline ◽  
Cellular Damage ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Stress Theory

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.

NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of α-tocopherol

2010 ◽  
Vol 31 (6) ◽  
pp. 579-588 ◽  
Author(s):  
Jeannett A. Izquierdo-Vega ◽  
Manuel Sánchez-Gutiérrez ◽  
Luz María Del Razo
Keyword(s):  
Oxidative Damage ◽  
Nadph Oxidase ◽  
Protective Role

scholarly journals Mapping hole hopping escape routes in proteins

2019 ◽  
Vol 116 (32) ◽  
pp. 15811-15816 ◽  
Author(s):  
Ruijie D. Teo ◽  
Ruobing Wang ◽  
Elizabeth R. Smithwick ◽  
Agostino Migliore ◽  
Michael J. Therien ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Residence Times ◽  
P450 Monooxygenase ◽  
Protection Mechanism ◽  
Biologically Relevant ◽  
Redox Active ◽  
Catalytic Sites ◽  
Benzylsuccinate Synthase

A recently proposed oxidative damage protection mechanism in proteins relies on hole hopping escape routes formed by redox-active amino acids. We present a computational tool to identify the dominant charge hopping pathways through these residues based on the mean residence times of the transferring charge along these hopping pathways. The residence times are estimated by combining a kinetic model with well-known rate expressions for the charge-transfer steps in the pathways. We identify the most rapid hole hopping escape routes in cytochrome P450 monooxygenase, cytochrome c peroxidase, and benzylsuccinate synthase (BSS). This theoretical analysis supports the existence of hole hopping chains as a mechanism capable of providing hole escape from protein catalytic sites on biologically relevant timescales. Furthermore, we find that pathways involving the [4Fe4S] cluster as the terminal hole acceptor in BSS are accessible on the millisecond timescale, suggesting a potential protective role of redox-active cofactors for preventing protein oxidative damage.

scholarly journals Selenium and vascular health

2011 ◽  
Vol 84 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Alan A. Sneddon
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
The Body ◽  
Vascular Health ◽  
Vascular Cells ◽  
Optimal Health ◽  
Oxidative Challenge ◽  
Se Status

Selenium (Se) is an important dietary micronutrient required for sustaining optimal health. Se is incorporated into proteins, many of which are antioxidants that protect the body against oxidative damage. As oxidative damage may contribute to the development of chronic diseases including cardiovascular disease (CVD), Se has been proposed to provide a protective role against this disease. Studies in vitro and in animals continue to provide increasing insight into the role of Se in promoting vascular health and ameliorating CVD. Se within vascular cells limits the adhesion together of such cells, an important early step in the development of vascular disease. Organic forms of Se may also afford vascular cells greater protection against oxidative challenge compared to inorganic forms. Nevertheless, current studies in humans investigating the relationship between Se and CVD have so far proved equivocal; larger randomized trials with different Se exposures in populations spanning the broad physiological Se status are needed to determine the criteria whereby Se may influence CVD outcome within different populations. Further studies are also needed to explore the effects of different Se species and the role of different selenoprotein genotypes in modifying Se status and their resultant impact on cardiovascular function.

scholarly journals The Protective Role of Sulfated Polysaccharides from Green Seaweed Udotea flabellum in Cells Exposed to Oxidative Damage

Marine Drugs ◽  
2018 ◽  
Vol 16 (4) ◽  
pp. 135 ◽  
Author(s):  
Fernando Presa ◽  
Maxsuell Marques ◽  
Rony Viana ◽  
Leonardo Nobre ◽  
Leandro Costa ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Sulfated Polysaccharides ◽  
Green Seaweed ◽  
In Cells
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