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 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.

scholarly journals A Novel Tetrapeptide Derivative Exhibits In Vitro Inhibition of Neutrophil-Derived Reactive Oxygen Species and Lysosomal Enzymes Release

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
Meera Ramanujam ◽  
Rengarajulu Puvanakrishnan
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Anion ◽  
Lysosomal Enzymes ◽  
Reactive Oxygen ◽  
Peptide Sequence ◽  
Ros Generation ◽  
Oxygen Species ◽  
Complement Factors

Neutrophil infiltration plays a major role in the pathogenesis of myocardial injury. Oxidative injury is suggested to be a central mechanism of the cellular damage after acute myocardial infarction. This study is pertained to the prognostic role of a tetrapeptide derivative PEP1261 (BOC-Lys(BOC)-Arg-Asp-Ser(tBu)-OtBU), a peptide sequence (39–42) of lactoferrin, studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation, lysosomal enzymes release, and enhanced expression of C proteins. The groundwork experimentation was concerned with the isolation of neutrophils from the normal and acute myocardial infarct rats to find out the efficacy of PEP1261 in the presence of a powerful neutrophil stimulant, phorbol 12-myristate 13 acetate (PMA). Stimulation of neutrophils with PMA resulted in an oxidative burst of superoxide anion and enhanced release of lysosomal enzymes and expression of complement proteins. The present study further demonstrated that the free radicals increase the complement factors in the neutrophils confirming the role of ROS. PEP1261 treatment significantly reduced the levels of superoxide anion and inhibited the release of lysosomal enzymes in the stimulated control and infarct rat neutrophils. This study demonstrated that PEP1261 significantly inhibited the effect on the ROS generation as well as the mRNA synthesis and expression of the complement factors in neutrophils isolated from infarct heart.

Ascorbic acid improves mitochondrial function in liver of arsenic-treated rat

2010 ◽  
Vol 26 (5) ◽  
pp. 265-272 ◽  
Author(s):  
Sohini Singh ◽  
Suresh Vir Singh Rana
Keyword(s):  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Mitochondrial Function ◽  
Caspase 3 ◽  
Succinic Dehydrogenase ◽  
Reactive Oxygen ◽  
Ultrastructural Changes ◽  
Arsenic Toxicity ◽  
Oxygen Species

Arsenic is an ubiquitous and well-documented carcinogenic metalloid. The most common source of arsenic is drinking water. The mechanism of arsenic toxicity in a cell has historically been centered around its inhibitory effects on cellular respiration and mitochondrial injury. Ascorbic acid, a low molecular weight, water-soluble antioxidant, improves the reduced glutathione (GSH) status by recycling oxidized glutathione. Ascorbic acid can improve mitochondrial function by improving the thiol status; thereby preventing reactive oxygen species— mediated damage to liver as well as kidney. Ascorbic acid has been shown to protect membrane and other cellular compartments by regenerating vitamin E. Therefore, ascorbic acid seems to be a suitable protective factor against arsenic toxicity. Present reports describe the effect of ascorbic acid on oxidative phosphorylation, adenosine triphosphatase (ATPase), succinic dehydrogenase, caspase-3 and apoptosis in the liver of rats treated with arsenic trioxide (AsIII). Ultrastructural changes in the mitochondria have also been reported. We show that cotreatments with ascorbic acid and AsIII improve mitochondrial structure and function. We attribute these improvements mainly to antioxidative role of ascorbic acid. Apoptosis was restricted due to caspase-3 inhibition. Ascorbic acid could protect DNA from the attack of reactive oxygen species generated by AsIII. Consequently its events led to improved ADP:O ratio, normalized ATPase activity and restored the activity of succinic dehydrogenase. Overall, results support the protective role of ascorbic acid against As III-induced liver injury.

scholarly journals Effects of Glutathione and Ascorbic Acid on Streptomycin Sensitivity of Escherichia coli

2007 ◽  
Vol 51 (3) ◽  
pp. 1119-1122 ◽  
Author(s):  
Manish Goswami ◽  
Suhas H. Mangoli ◽  
Narendra Jawali
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Reactive Oxygen ◽  
Antibacterial Action ◽  
Oxygen Species

ABSTRACT We examined the effects of antioxidants and the role of reactive oxygen species (ROS) on the antibacterial action of aminoglycosides in Escherichia coli. We concluded that reduced streptomycin sensitivity in the presence of glutathione and ascorbic acid is not due to the antioxidant-mediated scavenging of ROS.

Ovariectomy and its Antioxidative Effect on Bone

2010 ◽  
Author(s):  
Durg V. Rai ◽  
Harcharan Singh Ranu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Bone Loss ◽  
Wistar Rats ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Female Wistar Rats ◽  
The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p<0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p<0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

scholarly journals Role of Melatonin in Angiotensin and Aging

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4666
Author(s):  
Ahmet Ozer Sehirli ◽  
Serkan Sayıner ◽  
Ugochukwu Chukwunyere ◽  
Nedime Serakinci
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Angiotensin Ii ◽  
Reactive Oxygen ◽  
Mitochondrial Calcium ◽  
Oxygen Species ◽  
Age Related ◽  
Mitochondrial Calcium Uptake

The cellular utilization of oxygen leads to the generation of free radicals in organisms. The accumulation of these free radicals contributes significantly to aging and several age-related diseases. Angiotensin II can contribute to DNA damage through oxidative stress by activating the NAD(P)H oxidase pathway, which in turn results in the production of reactive oxygen species. This radical oxygen-containing molecule has been linked to aging and several age-related disorders, including renal damage. Considering the role of angiotensin in aging, melatonin might relieve angiotensin-II-induced stress by enhancing the mitochondrial calcium uptake 1 pathway, which is crucial in preventing the mitochondrial calcium overload that may trigger increased production of reactive oxygen species and oxidative stress. This review highlights the role and importance of melatonin together with angiotensin in aging and age-related diseases.

Effects of polyphenols in aging and neurodegeneration associated with oxidative stress

2021 ◽  
Vol 28 ◽  
Author(s):  
Francisca Rivas ◽  
Carlos Poblete-Aro ◽  
María Elsa Pando ◽  
María José Allel ◽  
Valentina Fernandez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Reactive Nitrogen Species ◽  
Reactive Oxygen ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
Nitrogen Species ◽  
Over Time

: Aging is defined as the functional loss of tissues and organs over time. This is a biological, irreversible, progressive, and universal process that results from genetic and environmental factors, such as diet, physical activity, smoking, harmful alcohol consumption, and exposure to toxins, among others. Aging is a consequence of molecular and cellular damage built up over time. This damage begins with a gradual decrease in physical and mental capacity, thus increasing the risk of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Neuronal, functional, and structural damage can be explained by an imbalance among free radicals, reactive oxygen species, reactive nitrogen species, and antioxidants, which finally lead to oxidative stress. Due to the key role of free radicals, reactive oxygen species, and reactive nitrogen species, antioxidant therapy may reduce the oxidative damage associated with neurodegeneration. Exogenous antioxidants are molecules that may help maintain the balance between the formation and elimination of free radicals, thus protecting the cell from their toxicity. Among them, polyphenols are a broad group of secondary plant metabolites with potent antioxidant properties. Here, we review several studies that show the potential role of polyphenol consumption to prevent, or slow down, harmful oxidative processes linked to neurodegenerative disorders.

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