EPR Technology Spectroscopic Investigation of Generation of Reactive Oxygen Species Free Radicals in Laccase-Activated Jute Fiber

2014 ◽  
Vol 45 (5) ◽  
pp. 505-515 ◽  
Author(s):  
Chunxiao Zhou ◽  
Aixue Dong ◽  
Qiang Wang ◽  
Xuerong Fan ◽  
Yuanlin Cao
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Spectroscopic Investigation ◽  
Reactive Oxygen ◽  
Jute Fiber ◽  
Oxygen Species

scholarly journals Environmentally persistent free radicals are ubiquitous in wildfire charcoals and remain stable for years

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Gabriel Sigmund ◽  
Cristina Santín ◽  
Marc Pignitter ◽  
Nathalie Tepe ◽  
Stefan H. Doerr ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Reactive Oxygen ◽  
Resonance Spectroscopy ◽  
Oxygen Species ◽  
Pyrogenic Carbon ◽  
Spin Resonance ◽  
Long Time ◽  
High Concentrations

AbstractGlobally landscape fires produce about 256 Tg of pyrogenic carbon or charcoal each year. The role of charcoal as a source of environmentally persistent free radicals, which are precursors of potentially harmful reactive oxygen species, is poorly constrained. Here, we analyse 60 charcoal samples collected from 10 wildfires, that include crown as well as surface fires in forest, shrubland and grassland spanning different boreal, temperate, subtropical and tropical climate. Using electron spin resonance spectroscopy, we measure high concentrations of environmentally persistent free radicals in charcoal samples, much higher than those found in soils. Concentrations increased with degree of carbonization and woody fuels favoured higher concentrations. Moreover, environmentally persistent free radicals remained stable for an unexpectedly long time of at least 5 years. We suggest that wildfire charcoal is an important global source of environmentally persistent free radicals, and therefore potentially of harmful reactive oxygen species.

Diagnostic Range Ionizing Radiation and Reactive Oxygen Species Production: an Initial Experience

2021 ◽  
Vol 11 (5) ◽  
Author(s):  
Sirohi Shikha ◽  
Tandon Prof. Anupama ◽  
Banerjee Prof. B.D. ◽  
Kumar Ranjeet
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Ionizing Radiation ◽  
Venous Blood ◽  
Radiation Detection ◽  
Control Sample ◽  
Reactive Oxygen ◽  
P Value ◽  
Oxygen Species ◽  
Mdct Examination

Radiation is a common occurrence in our daily lives that comes from both natural and man-made sources. Ionizing Radiation (IR) causes damage either directly or indirectly through the generation of reactive oxygen species (ROS). Oxidative damage to DNA, lipids, proteins, and many metabolites occurs through a complex series of processes that are enhanced by endogenous signalling which is activated by free radicals. Though literature is abundant on ROS and antioxidants at high doses, no study to the best of our knowledge has assessed the ROS levels after Multi Detector Computed Tomography (MDCT) examination (i.e. in diagnostic range radiation). The aim of the present study was to assess the production of ROS after diagnostic level radiation by MDCT examination and at 24 hour follow up. The study involved fifty patients posted for clinically indicated MDCT which were recruited. The average radiation dose was 2-9 mGy. Three blood samples were drawn, one prior to CT (control sample), within half an hour of CT (post CT) and 24 hrs after CT. 3 ml venous blood was withdrawn in aseptic conditions and immediately serum was isolated for ROS assessment. The blood examination results were compared in immediate and post 24 hour after MDCT and both were compared with control values and correlated with radiation parameters. Our results have shown a significant increase in ROS level in immediate post CT samples compared to prior CT scan samples (control) (p value <0.0001). The ROS levels reduced at 24 hours compared to immediate post CT, however they were still higher than control values. Our findings reflect that there is a rapid increase in free radicals production in the mitochondria after diagnostic level radiation. Detection of higher ROS levels at 24 hours suggests incomplete repair with the presence of some residual oxidative species at 24 hours.

Extremely enhanced contaminant decomposition catalyzed by hemin via the coupling of persistent free radicals and ascorbic acid

2015 ◽  
Vol 51 (89) ◽  
pp. 16139-16142 ◽  
Author(s):  
Yuyuan Yao ◽  
Bin Jiang ◽  
Yajun Mao ◽  
Juan Chen ◽  
Zhenfu Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Free Radicals ◽  
Reactive Oxygen ◽  
Environmental Pollutant ◽  
Ros Generation ◽  
Oxygen Species ◽  
Positive Role ◽  
Rate Enhancement

A positive role of PFRs in enhancing reactive oxygen species (ROS) generation for an extreme rate enhancement in environmental pollutant decomposition is reported.

scholarly journals Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration

Life ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 101 ◽  
Author(s):  
Andrey Y. Abramov ◽  
Elena V. Potapova ◽  
Viktor V. Dremin ◽  
Andrey V. Dunaev
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disorders ◽  
Structural Changes ◽  
Wide Spectrum ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Misfolded Proteins ◽  
Oxygen Species

Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones—Alzheimer’s and Parkinson’s disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.

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