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

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 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

scholarly journals The Protective Role of Prenatal Alpha Lipoic Acid Supplementation against Pancreatic Oxidative Damage in Offspring of Valproic Acid-Treated Rats: Histological and Molecular Study

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 239
Author(s):  
Fatma M. Ghoneim ◽  
Hani Alrefai ◽  
Ayman Z. Elsamanoudy ◽  
Salwa M. Abo El-khair ◽  
Hanaa A. Khalaf
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Lipoic Acid ◽  
Caspase 3 ◽  
Protective Role ◽  
Alpha Lipoic Acid ◽  
Group Iii ◽  
Rat Offspring ◽  
Group I

Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and β cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

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