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1.
Trace Element Levels and Oxidant/Antioxidant Status in Patients with Alcohol Abuse.
Saribal, D, Hocaoglu-Emre, FS, Karaman, F, Mırsal, H, Akyolcu, MC
Biological trace element research. 2020;(1):7-13
Abstract
Alcohol abuse is a well-known cause of imbalance in trace element levels and oxidant/antioxidant status of individuals with long time consumption. However, the levels of these parameters in the patients on the early stages of alcohol dependence without liver damage differ on various studies. The aim of our study was to measure the levels of trace elements in the serum and oxidative/antioxidative system members in the red blood cells (RBC) of early-stage alcoholic individuals and compare with control subjects. Our study included 21 male patients recently hospitalized for alcohol abuse and 25 healthy non-abusing male controls. Levels of Fe, Zn, and Cu in the serum and MDA, SOD, CAT, and GSH in the red blood cells (RBC) of the subjects were measured. Fe, Zn, and Cu levels were lower in the study group when compared to the controls. Levels of lipid peroxidation marker MDA was high, whereas the activities of antioxidant enzymes SOD and CAT were decreased in our study group. However, levels of GSH, an antioxidant compound were higher in the alcohol abuse group. RBC SOD levels were positively correlated with Fe, Cu, Zn, and CAT. There was a positive correlation between Fe-Cu, Zn-Fe, Zn-Cu, CAT-Zn, and CAT-SOD. MDA was negatively correlated with Fe, Zn, SOD, and CAT. The results obtained from present study indicate that high levels of alcohol intake are related with increased oxidative damage and decreased levels of antioxidant enzymes and trace elements. Additionally, antioxidant compensation mechanisms are still on process in the early stages of chronic alcohol exposure.
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2.
In vitro bleaching effect of hydrogen peroxide with different time of exposition and concentration on shear bond strength of orthodontic brackets to human enamel: A meta-analysis of in vitro studies.
Imani, MM, Azizi, F, Bahrami, K, Golshah, A, Safari-Faramani, R
International orthodontics. 2020;(1):22-31
Abstract
INTRODUCTION Controversy exists regarding the effect of bleaching on shear bond strength (SBS) of orthodontic brackets to enamel. This study aims to do a review and meta-analysis on the effect of bleaching with hydrogen peroxide on SBS according to the interval between bleaching and bonding to human enamel and the concentration of Hydrogen Peroxide. METHODS An electronic search of the literature was performed in Scopus, PubMed and Cochrane databases including CENTRAL and Cochrane library for relevant in vitro studies on the effect of bleaching with hydrogen peroxide on shear bond strength of human enamel, published until June 2018. Modified Cochrane Risk of Bias tool was used to assess the quality of the individual studies. AMSTAR tool was used for assessing the quality of the study. RESULTS Nineteen studies were included in the qualitative analysis. Regardless of the interval between bleaching and bonding, reduction in SBS was not statistically significant when the hydrogen peroxide of less than 35% is used. Bleaching with 35% hydrogen reduces SBS when the bonding is conducted immediately (P<0.0001) or the time interval was shorter than one day (P<0.0005). On the other hand, use of high dose hydrogen peroxide resulted in a statistically significant reduction in SBS irrespective of the time interval between the procedures (P<0.05 for all categories of time interval). CONCLUSION Bleaching with hydrogen peroxide decreases the SBS of brackets in patients undergoing orthodontic treatment especially if the time interval between bleaching and bonding procedures is short and a high concentration of hydrogen peroxide is used.
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3.
Bacterial Defense Systems against the Neutrophilic Oxidant Hypochlorous Acid.
Sultana, S, Foti, A, Dahl, JU
Infection and immunity. 2020;(7)
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Abstract
Neutrophils kill invading microbes and therefore represent the first line of defense of the innate immune response. Activated neutrophils assemble NADPH oxidase to convert substantial amounts of molecular oxygen into superoxide, which, after dismutation into peroxide, serves as the substrate for the generation of the potent antimicrobial hypochlorous acid (HOCl) in the phagosomal space. In this minireview, we explore the most recent insights into physiological consequences of HOCl stress. Not surprisingly, Gram-negative bacteria have evolved diverse posttranslational defense mechanisms to protect their proteins, the main targets of HOCl, from HOCl-mediated damage. We discuss the idea that oxidation of conserved cysteine residues and partial unfolding of its structure convert the heat shock protein Hsp33 into a highly active chaperone holdase that binds unfolded proteins and prevents their aggregation. We examine two novel members of the Escherichia coli chaperone holdase family, RidA and CnoX, whose thiol-independent activation mechanism differs from that of Hsp33 and requires N-chlorination of positively charged amino acids during HOCl exposure. Furthermore, we summarize the latest findings with respect to another bacterial defense strategy employed in response to HOCl stress, which involves the accumulation of the universally conserved biopolymer inorganic polyphosphate. We then discuss sophisticated adaptive strategies that bacteria have developed to enhance their survival during HOCl stress. Understanding bacterial defense and survival strategies against one of the most powerful neutrophilic oxidants may provide novel insights into treatment options that potentially compromise the ability of pathogens to resist HOCl stress and therefore may increase the efficacy of the innate immune response.
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4.
The interaction of reactive oxygen species and antioxidants at the metabolic interface in salicylic acid-induced adventitious root formation in mung bean [Vigna radiata (L.) R. Wilczek].
Kora, D, Bhattacharjee, S
Journal of plant physiology. 2020;:153152
Abstract
Implications of the role of antioxidant buffering in reactive oxygen species (ROS)-antioxidant interactions and associated redox regulation during adventitious root formation (ARF) were assessed in redox-manipulated salicylic acid (SA)-treated hypocotyl explants of mung bean [Vigna radiata (L.) R. Wilczek]. Application of pro-oxidant H2O2 (500 μM) followed by SA (600 μM) was shown to stimulate ARF, whereas treatments combining 600 μM SA and 10 × 10-4 M DPI (diphenyleneiodonium, an inhibitor of NADPH-oxidase) and 600 μM and SA 10 × 10-4 M (dimethylthiourea, a free radical scavenger) were found to prevent ARF. The redox status of the experimental explants monitored under such treatment conditions (in terms of accumulation of pro-oxidants, in situ localization of O2- and H2O2, radical scavenging property and total thiol content) revealed significant changes in ROS-antioxidant interactions at the metabolic interface, causing alterations in the pattern of ARF. Further, the assessment of activities and transcript abundance of the enzymes of the H2O2 turnover pathway (mainly the ascorbate-glutathione system) supported the transcriptional regulation of genes such as vrrboh, vrAPX, vrGR, vrSOD, and vrCAT and the activities of the relevant enzymes necessary for the generation of endogenous redox cues during ARF. The present work provides an inventory in support of the importance of antioxidant buffering associated with redox regulation for the origin of the metabolic redox cue (redox signal) necessary for SA-induced ARF in mung bean.
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Impairment between Oxidant and Antioxidant Systems: Short- and Long-term Implications for Athletes' Health.
Nocella, C, Cammisotto, V, Pigozzi, F, Borrione, P, Fossati, C, D'Amico, A, Cangemi, R, Peruzzi, M, Gobbi, G, Ettorre, E, et al
Nutrients. 2019;(6)
Abstract
The role of oxidative stress, an imbalance between reactive oxygen species production (ROS) and antioxidants, has been described in several patho-physiological conditions, including cardiovascular, neurological diseases and cancer, thus impacting on individuals' lifelong health. Diet, environmental pollution, and physical activity can play a significant role in the oxidative balance of an organism. Even if physical training has proved to be able to counteract the negative effects caused by free radicals and to provide many health benefits, it is also known that intensive physical activity induces oxidative stress, inflammation, and free radical-mediated muscle damage. Indeed, variations in type, intensity, and duration of exercise training can activate different patterns of oxidant-antioxidant balance leading to different responses in terms of molecular and cellular damage. The aim of the present review is to discuss (1) the role of oxidative status in athletes in relation to exercise training practice, (2) the implications for muscle damage, (3) the long-term effect for neurodegenerative disease manifestations, (4) the role of antioxidant supplementations in preventing oxidative damages.
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6.
Diminishing Inflammation by Reducing Oxidant Generation: Nitrated Fatty Acid-Mediated Inactivation of Xanthine Oxidoreductase.
Kelley, EE
Advances in experimental medicine and biology. 2019;:59-65
Abstract
Inhibition of xanthine oxidoreductase (XOR) has proven beneficial in a plethora of inflammatory disease processes due to a net reduction in pro-inflammatory oxidants and secondary nitrating species. Electrophilic nitrated fatty acid derivatives, such as nitro-oleic acid (OA-NO2) are also noted to display a broad spectrum of anti-inflammatory effects via interaction with critical signaling pathways. An alternative process in which nitrated fatty acids may extend anti-inflammatory actions is via inactivation of XOR, a process that is more effective than allo/oxypurinol-mediated inhibition. Herein, we describe the molecular aspects of nitrated fatty acid-associated inactivation of XOR, identify specificity via structure function relationships and discuss XOR as a crucial component of the anti-inflammatory portfolio of nitrated fatty acids.
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7.
Effect of phototherapy on oxidant/antioxidant status: a randomized controlled trial.
El-Farrash, RA, El-Shimy, MS, Tawfik, S, Nada, AS, Salem, DAD, M Gallo, MS, Abd-Elmohsen, EW
Free radical research. 2019;(2):179-186
Abstract
In order to evaluate the effect of different types of phototherapy on oxidant/antioxidant status in hyperbilirubinemic neonates, an interventional randomized control trial was conducted on 120 neonates ≥35 weeks' gestational age with indirect hyperbilirubinemia reaching phototherapy level. This study is registered with ClinicalTrials.gov as NCT03074292. Neonates were assigned to three groups; 40 neonates received conventional phototherapy, 40 received intensive phototherapy and 40 received blue light-emitting diodes (LED) phototherapy. Complete blood count (CBC), total serum bilirubin (TSB), total antioxidant capacity (TAC), malondialdehyde (MDA), nitric oxide (NO), copper (Cu), zinc (Zn), and iron (Fe) levels were measured before and 24 hours after phototherapy. TSB decreased postphototherapy in all three groups (p < .05 for all), with significantly lower levels following intensive and LED phototherapy compared to conventional phototherapy (p < .05 for both). TAC decreased postphototherapy in the three groups (p < .05 for all). MDA and NO increased postphototherapy (p < .05 for all), with the intensive phototherapy group having the highest levels followed by the conventional while LED phototherapy group showed the lowest levels in comparison to the other groups (p < .05). Cu, Zn and Fe increased postphototherapy in all three groups (p < .05 for all). Positive correlations were found between postphototherapy TSB with TAC, Cu and Zn (p < .05) and negative correlations with MDA, NO and Fe (p < .05) among neonates of the 3 studied groups. In conclusion, different photo therapies have an impact on oxidant/antioxidant balance and are associated with increased oxidative stress markers with the LED phototherapy being the safest.
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8.
Kinetic and stoichiometric constraints determine the pathway of H2O2 consumption by red blood cells.
Orrico, F, Möller, MN, Cassina, A, Denicola, A, Thomson, L
Free radical biology & medicine. 2018;:231-239
Abstract
Red blood cells (RBC) are considered as a circulating sink of H2O2, but a significant debate remains over the role of the different intraerythocyte peroxidases. Herein we examined the kinetic of decomposition of exogenous H2O2 by human RBC at different cell densities, using fluorescent and oxymetric methods, contrasting the results against a mathematical model. Fluorescent measurements as well as oxygen production experiments showed that catalase was responsible for most of the decomposition of H2O2 at cell densities suitable for both experimental settings (0.1-10 × 1010 cell L-1), since sodium azide but not N-ethylmaleimide (NEM) inhibited H2O2 consumption. Oxygen production decreased at high cell densities until none was detected above 1.1 × 1012 cell L-1, being recovered after inhibition of the thiol dependent systems by NEM. This result underlined that the consumption of H2O2 by catalase prevail at RBC densities regularly used for research, while the thiol dependent systems predominate when the cell density increases, approaching the normal number in blood (5 × 1012 cell L-1). The mathematical model successfully reproduced experimental results and at low cell number it showed a time sequence involving Prx as the first line of defense, followed by catalase, with a minor role by Gpx. The turning points were given by the total consumption of reduced Prx in first place and reduced GSH after that. However, Prx alone was able to account for the added H2O2 (50 µM) at physiological RBC density, calling attention to the importance of cell density in defining the pathway of H2O2 consumption and offering an explanation to current apparently conflicting results in the literature.
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9.
The role of operating parameters and oxidative damage mechanisms of advanced chemical oxidation processes in the combat against antibiotic-resistant bacteria and resistance genes present in urban wastewater.
Michael-Kordatou, I, Karaolia, P, Fatta-Kassinos, D
Water research. 2018;:208-230
Abstract
An upsurge in the study of antibiotic resistance in the environment has been observed in the last decade. Nowadays, it is becoming increasingly clear that urban wastewater is a key source of antibiotic resistance determinants, i.e. antibiotic-resistant bacteria and antibiotic resistance genes (ARB&ARGs). Urban wastewater reuse has arisen as an important component of water resources management in the European Union and worldwide to address prolonged water scarcity issues. Especially, biological wastewater treatment processes (i.e. conventional activated sludge), which are widely applied in urban wastewater treatment plants, have been shown to provide an ideal environment for the evolution and spread of antibiotic resistance. The ability of advanced chemical oxidation processes (AOPs), e.g. light-driven oxidation in the presence of H2O2, ozonation, homogeneous and heterogeneous photocatalysis, to inactivate ARB and remove ARGs in wastewater effluents has not been yet evaluated through a systematic and integrated approach. Consequently, this review seeks to provide an extensive and critical appraisal on the assessment of the efficiency of these processes in inactivating ARB and removing ARGs in wastewater effluents, based on recent available scientific literature. It tries to elucidate how the key operating conditions may affect the process efficiency, while pinpointing potential areas for further research and major knowledge gaps which need to be addressed. Also, this review aims at shedding light on the main oxidative damage pathways involved in the inactivation of ARB and removal of ARGs by these processes. In general, the lack and/or heterogeneity of the available scientific data, as well as the different methodological approaches applied in the various studies, make difficult the accurate evaluation of the efficiency of the processes applied. Besides the operating conditions, the variable behavior observed by the various examined genetic constituents of the microbial community, may be directed by the process distinct oxidative damage mechanisms in place during the application of each treatment technology. For example, it was shown in various studies that the majority of cellular damage by advanced chemical oxidation may be on cell wall and membrane structures of the targeted bacteria, leaving the internal components of the cells relatively intact/able to repair damage. As a result, further in-depth mechanistic studies are required, to establish the optimum operating conditions under which oxidative mechanisms target internal cell components such as genetic material and ribosomal structures more intensively, thus conferring permanent damage and/or death and preventing potential post-treatment re-growth.
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10.
Is maternal microbial metabolism an early-life determinant of health?
Romano, KA, Rey, FE
Lab animal. 2018;(9):239-243
Abstract
Mounting evidence suggests that environmental stress experienced in utero (for example, maternal nutritional deficits) establishes a predisposition in the newborn to the development of chronic diseases later in life. This concept is often referred to as the "fetal origins hypothesis" or "developmental origins of health and disease". Since its first proposal, epigenetics has emerged as an underlying mechanism explaining how environmental cues become gestationally "encoded". Many of the enzymes that impart and maintain epigenetic modifications are highly sensitive to nutrient availability, which can be influenced by the metabolic activities of the intestinal microbiota. Therefore, the maternal microbiome has the potential to influence epigenetics in utero and modulate offspring's long-term health trajectories. Here we summarize the current understanding of the interactions that occur between the maternal gut microbiome and the essential nutrient choline, that is not only required for fetal development and epigenetic regulation but is also a growth substrate for some microbes. Bacteria able to metabolize choline benefit from the presence of this nutrient and compete with the host for its access, which under extreme conditions may elicit signatures of choline deficiency. Another consequence of bacterial choline metabolism is the accumulation of the pro-inflammatory, pro-thrombotic metabolite trimethylamine-N-oxide (TMAO). Finally, we discuss how these different facets of microbial choline metabolism may influence infant development and health trajectories via epigenetic mechanisms and more broadly place a call to action to better understand how maternal microbial metabolism can shape their offspring's propensity to chronic disease development later in life.