Alteration of murine duodenal morphology and redox signalling events by reactive oxygen species generated after whole body γ-irradiation and its prevention by ferulic acid

2017 ◽  
Vol 51 (11-12) ◽  
pp. 886-910 ◽  
Author(s):  
Ujjal Das ◽  
Aaveri Sengupta ◽  
Sushobhan Biswas ◽  
Arghya Adhikary ◽  
Rakhi Dey Sharma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ferulic Acid ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Oxygen Species ◽  
Γ Irradiation ◽  
Redox Signalling

scholarly journals Vesicular Formation of Trans-Ferulic Acid: an Efficient Approach to Improve the Radical Scavenging and Antimicrobial Properties

2021 ◽  
Author(s):  
Anahita Rezaeiroshan ◽  
Majid Saeedi ◽  
Katayoun Morteza-Semnani ◽  
Jafar Akbari ◽  
Akbar Hedayatizadeh-Omran ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Ferulic Acid ◽  
Reactive Oxygen Species Production ◽  
Radical Scavenging ◽  
Reactive Oxygen ◽  
Entrapment Efficiency ◽  
The Body ◽  
Oxygen Species ◽  
Species Production

Abstract Purposes Reactive oxygen species production is harmful to human’s health. The presence of antioxidants in the body may help to diminish reactive oxygen species. Trans-ferulic acid is a good antioxidant, but its low water solubility excludes its utilization. The study aims to explore whether a vesicular drug delivery could be a way to overcome the poor absorption of trans-ferulic acid hence improving its antimicrobial efficiency and antioxidant effect. Methods Niosomal vesicles containing the drug were prepared by film hydration method. The obtained vesicles were investigated in terms of morphology, size, entrapment efficiency, release behavior, cellular cytotoxicity, antioxidant, cellular protection study, and antimicrobial evaluations. Results The optimized niosomal formulation had a particle size of 158.7 nm and entrapment efficiency of 21.64%. The results showed that the optimized formulation containing 25 μM of trans-ferulic acid could enhance the viability of human foreskin fibroblast HFF cell line against reactive oxygen species production. The minimum effective dose of the plain drug and the niosomal formulation against Staphylococcus aurous (ATCC 29213) was 750 µg/mL and 375 µg/mL, respectively, and for Escherichia coli (ATCC 25922), it was 750 µg/mL and 187/5 µg/mL, respectively. The formulation could also improve the minimum bactericidal concentration of the drug in Staphylococcus aurous, Escherichia coli, and Acinobacter baumannii (ATCC 19606). Conclusion These results revealed an improvement in both antibacterial and antioxidant effects of the drug in the niosomal formulation.

Regulatory mechanism of ulinastatin on autophagy of macrophages and renal tubular epithelial cells

2018 ◽  
Vol 16 (1) ◽  
pp. 298-305
Author(s):  
Ming Wu ◽  
Min Hu ◽  
Huansheng Tong ◽  
Junying Liu ◽  
Hui Jiang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Renal Cell ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Inflammatory Factors ◽  
Oxygen Species ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

AbstractKidney ischemia and hypoxia can cause renal cell apoptosis and activation of inflammatory cells, which lead to the release of inflammatory factors and ultimately result in the damage of kidney tissue and the whole body. Renal tubular cell and macrophage autophagy can reduce the production of reactive oxygen species (ROS), thereby reducing the activation of inflammatory cytoplasm and its key effector protein, caspase-1, which reduces the expression of IL-1β and IL-18 and other inflammatory factors. Ulinastatin (UTI), as a glycoprotein drug, inhibits the activity of multiple proteases and reduces myocardial damage caused by ischemia-reperfusion by upregulating autophagy. However, it can be raised by macrophage autophagy, reduce the production of ROS, and ultimately reduce the expression of inflammatory mediators, thereby reducing renal cell injury, promote renal function recovery is not clear. In this study, a series of cell experiments have shown that ulinastatin is reduced by regulating the autophagy of renal tubular epithelial cells and macrophages to reduce the production of reactive oxygen species and inflammatory factors (TNF-α, IL-1β and IL-1), and then, increase the activity of the cells under the sugar oxygen deprivation model. The simultaneous use of cellular autophagy agonists Rapamycin (RAPA) and ulinastatin has a synergistic effect on the production of reactive oxygen species and the expression of inflammatory factors.

Redox signalling involving NADPH oxidase-derived reactive oxygen species

2006 ◽  
Vol 34 (5) ◽  
pp. 960-964 ◽  
Author(s):  
R. Dworakowski ◽  
N. Anilkumar ◽  
M. Zhang ◽  
A.M. Shah
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Second Messengers ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Cell Phenotype ◽  
Oxygen Species ◽  
Mechanical Stimuli ◽  
Nadph Oxidases ◽  
Redox Signalling

Increased oxidative stress plays an important role in the pathophysiology of many diseases such as atherosclerosis, diabetes mellitus, myocardial infarction and heart failure. In addition to the well-known damaging effects of oxygen-free radicals, ROS (reactive oxygen species) also have signalling roles, acting as second messengers that modulate the activity of diverse intracellular signalling pathways and transcription factors, thereby inducing changes in cell phenotype. NADPH oxidases appear to be especially important sources of ROS involved in redox signalling. Seven NADPH oxidase isoforms, known as Noxs (NAPDH oxidases), are expressed in a cell- and tissue-specific fashion. These oxidases are thought to subserve distinct functions as a result of their tightly regulated activation (e.g. by neurohormonal and growth factors and mechanical stimuli) and their specific coupling with distinct downstream signalling pathways. In the present paper, we review the structure and mechanisms of activation of NADPH oxidases and consider their involvement in redox signalling, focusing mainly on the cardiovascular system.

Mitochondrial [dys]function; culprit in pre-eclampsia?

2016 ◽  
Vol 130 (14) ◽  
pp. 1179-1184 ◽  
Author(s):  
Cathal Michael McCarthy ◽  
Louise Clare Kenny
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Redox Signalling ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Ros ◽  
Signalling Systems

Mitochondria are extensively identified for their bioenergetic capacities; however, recently these metabolic hubs are increasingly being appreciated as critical regulators of numerous cellular signalling systems. Mitochondrial reactive oxygen species have evolved as a mode of cross-talk between mitochondrial function and physiological systems, to sustain equipoise and foster adaption to cellular stress. Redox signalling mediated by exaggerated mitochondrial-ROS (reactive oxygen species) has been incriminated in a plethora of disease pathologies. Excessive production of mitochondrial ROS is intrinsically linked to mitochondrial dysfunction. Furthermore, mitochondrial dysfunction is a key facilitator of oxidative stress, inflammation, apoptosis and metabolism. These are key pathogenic intermediaries of pre-eclampsia, hence we hypothesize that mitochondrial dysfunction is a pathogenic mediator of oxidative stress in the pathophysiology of pre-eclampsia. We hypothesize that mitochondrial-targeted antioxidants may restrain production of ROS-mediated deleterious redox signalling pathways. If our hypothesis proves correct, therapeutic strategies directly targeting mitochondrial superoxide scavenging should be actively pursued as they may alleviate maternal vascular dysfunction and dramatically improve maternal and fetal health worldwide.

scholarly journals The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

2016 ◽  
Vol 397 (8) ◽  
pp. 709-724 ◽  
Author(s):  
José Pedro Castro ◽  
Tilman Grune ◽  
Bodo Speckmann
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Oxygen Species ◽  
Body Energy

Abstract White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

scholarly journals In Vivo Imaging of Reactive Oxygen Species in Mouse Brain by using [3H]Hydromethidine as a Potential Radical Trapping Radiotracer

2014 ◽  
Vol 34 (12) ◽  
pp. 1907-1913 ◽  
Author(s):  
Kohji Abe ◽  
Nozomi Takai ◽  
Kazumi Fukumoto ◽  
Natsumi Imamoto ◽  
Misato Tonomura ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Production Model ◽  
Whole Body ◽  
Ros Production ◽  
Oxygen Species ◽  
Radical Trapping ◽  
The Brain

To assess reactive oxygen species (ROS) production by detecting the fluorescent oxidation product, hydroethidine has been used extensively. The present study was undertaken to evaluate the potential of the hydroethidine derivative as a radiotracer to measure in vivo brain ROS production. [3H]-labeled N-methyl-2,3-diamino-6-phenyl-dihydrophenanthridine ([3H]Hydromethidine) was synthesized, and evaluated using in vitro radical-induced oxidization and in vivo brain ROS production model. In vitro studies have indicated that [3H]Hydromethidine is converted to oxidized products by a superoxide radical (O2• -) and a hydroxyl radical (OH• -) but not hydrogen peroxide (H2O2). In vivo whole-body distribution study showed that [3H]Hydromethidine rapidly penetrated the brain and then was washed out in normal mice. Microinjection of sodium nitroprusside (SNP) into the brain was performed to produce ROS such as OH• - via Fenton reaction. A significant accumulation of radioactivity immediately after [3H]Hydromethidine injection was seen in the side of the brain treated with SNP (5 and 20 nmol) compared with that in the contralateral side. These results indicated that [3H]Hydromethidine freely penetrated into the brain where it was rapidly converted to oxidized forms, which were trapped there in response to the production of ROS. Thus, [3H]Hydromethidine should be useful as a radical trapping radiotracer in the brain.

Long-term caloric restriction increases UCP3 content but decreases proton leak and reactive oxygen species production in rat skeletal muscle mitochondria

2005 ◽  
Vol 289 (3) ◽  
pp. E429-E438 ◽  
Author(s):  
Lisa Bevilacqua ◽  
Jon J. Ramsey ◽  
Kevork Hagopian ◽  
Richard Weindruch ◽  
Mary-Ellen Harper
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Proton Leak ◽  
Protonmotive Force ◽  
Ros Production ◽  
Oxygen Species ◽  
Wide Range ◽  
Species Production

Calorie restriction (CR) without malnutrition increases life span and delays the onset of a variety of diseases in a wide range of animal species. However, the mechanisms responsible for the retardation of aging with CR are poorly understood. We proposed that CR may act, in part, by inducing a hypometabolic state characterized by decreased reactive oxygen species (ROS) production and mitochondrial proton leak. Here, we examine the effects of long-term CR on whole animal energetics as well as muscle mitochondrial energetics, ROS production, and ROS damage. CR was initiated in male FBNF1 rats at 6 mo of age and continued for 12 or 18 mo. Mean whole body V̇o2 was 34.6 ( P < 0.01) and 35.6% ( P < 0.001) lower in CR rats than in controls after 12 and 18 mo of CR, respectively. Body mass-adjusted V̇o2 was 11.1 and 29.5% lower (both P < 0.05) in CR rats than in controls after 12 and 18 mo of CR. Muscle mitochondrial leak-dependent (State 4) respiration was decreased after 12 mo compared with controls; however, after 18 mo of CR, there were slight but not statistically significant differences. Proton leak kinetics were affected by 12 mo of CR such that leak-dependent respiration was lower in CR mitochondria only at protonmotive force values exceeding 170 mV. Mitochondrial H2O2 production and oxidative damage were decreased by CR at both time points and increased with age. Muscle UCP3 protein content increased with long-term CR, consistent with a role in protection from ROS but inconsistent with the observed decrease or no change in proton leak.

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