Next Issue
Previous Issue

Table of Contents

Antioxidants, Volume 7, Issue 8 (August 2018)

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
Cover Story (view full-size image) The cytokine IL-1β, depending on the context, can contribute to neural injury as well as [...] Read more.
View options order results:
result details:
Displaying articles 1-14
Export citation of selected articles as:
Open AccessArticle Inhibitory Effects of Auraptene and Naringin on Astroglial Activation, Tau Hyperphosphorylation, and Suppression of Neurogenesis in the Hippocampus of Streptozotocin-Induced Hyperglycemic Mice
Antioxidants 2018, 7(8), 109; https://doi.org/10.3390/antiox7080109
Received: 24 July 2018 / Revised: 10 August 2018 / Accepted: 17 August 2018 / Published: 19 August 2018
PDF Full-text (5500 KB) | HTML Full-text | XML Full-text
Abstract
Auraptene, a citrus-related compound, exerts anti-inflammatory effects in peripheral tissues, and we demonstrated these effects in the brains of a lipopolysaccharide-injected systemic inflammation animal model and a brain ischemic mouse model. Naringin, another citrus-related compound, has been shown to exert antioxidant effects in
[...] Read more.
Auraptene, a citrus-related compound, exerts anti-inflammatory effects in peripheral tissues, and we demonstrated these effects in the brains of a lipopolysaccharide-injected systemic inflammation animal model and a brain ischemic mouse model. Naringin, another citrus-related compound, has been shown to exert antioxidant effects in several animal models. Hyperglycemia induces oxidative stress and inflammation and causes extensive damage in the brain; therefore, we herein evaluated the anti-inflammatory and other effects of auraptene and naringin in streptozotocin-induced hyperglycemic mice. Both compounds inhibited astroglial activation and the hyperphosphorylation of tau at 231 of threonine in neurons, and also recovered the suppression of neurogenesis in the dentate gyrus of the hippocampus in hyperglycemic mice. These results suggested that auraptene and naringin have potential effects as neuroprotective agents in the brain. Full article
(This article belongs to the Special Issue Phytochemical Antioxidants and Health)
Figures

Figure 1

Open AccessReview Evening Primrose (Oenothera biennis) Biological Activity Dependent on Chemical Composition
Antioxidants 2018, 7(8), 108; https://doi.org/10.3390/antiox7080108
Received: 11 July 2018 / Revised: 31 July 2018 / Accepted: 8 August 2018 / Published: 14 August 2018
PDF Full-text (471 KB) | HTML Full-text | XML Full-text
Abstract
Evening primrose (Oenothera L.) is a plant belonging to the family Onagraceae, in which the most numerous species is Oenothera biennis. Some plants belonging to the genus Oenothera L. are characterized by biological activity. Therefore, studies were conducted to determine the
[...] Read more.
Evening primrose (Oenothera L.) is a plant belonging to the family Onagraceae, in which the most numerous species is Oenothera biennis. Some plants belonging to the genus Oenothera L. are characterized by biological activity. Therefore, studies were conducted to determine the dependence of biological activity on the chemical composition of various parts of the evening primrose, mainly leaves, stems, and seeds. Common components of all parts of the Oenothera biennis plants are fatty acids, phenolic acids, and flavonoids. In contrast, primrose seeds also contain proteins, carbohydrates, minerals, and vitamins. Therefore, it is believed that the most interesting sources of biologically active compounds are the seeds and, above all, evening primrose seed oil. This oil contains mainly aliphatic alcohols, fatty acids, sterols, and polyphenols. Evening primrose oil (EPO) is extremely high in linoleic acid (LA) (70–74%) and γ-linolenic acid (GLA) (8–10%), which may contribute to the proper functioning of human tissues because they are precursors of anti-inflammatory eicosanoids. EPO supplementation results in an increase in plasma levels of γ-linolenic acid and its metabolite dihomo-γ-linolenic acid (DGLA). This compound is oxidized by lipoxygenase (15-LOX) to 15-hydroxyeicosatrienoic acid (15-HETrE) or, under the influence of cyclooxygenase (COX), DGLA is metabolized to series 1 prostaglandins. These compounds have anti-inflammatory and anti-proliferative properties. Furthermore, 15-HETrE blocks the conversion of arachidonic acid (AA) to leukotriene A4 (LTA4) by direct inhibition of 5-LOX. In addition, γ-linolenic acid suppresses inflammation mediators such as interleukin 1β (IL-1β), interleukin 6 (IL-6), and cytokine - tumor necrosis factor α (TNF-α). The beneficial effects of EPO have been demonstrated in the case of atopic dermatitis, psoriasis, Sjögren’s syndrome, asthma, and anti-cancer therapy. Full article
(This article belongs to the Special Issue Antioxidants and Second Messengers of Free Radicals)
Figures

Figure 1

Open AccessReview Mitochondria-Targeted Antioxidants and Skeletal Muscle Function
Antioxidants 2018, 7(8), 107; https://doi.org/10.3390/antiox7080107
Received: 4 July 2018 / Revised: 6 August 2018 / Accepted: 7 August 2018 / Published: 8 August 2018
PDF Full-text (1202 KB) | HTML Full-text | XML Full-text
Abstract
One of the main sources of reactive oxygen species (ROS) in skeletal muscle is the mitochondria. Prolonged or very high ROS exposure causes oxidative damage, which can be deleterious to muscle function, and as such, there is growing interest in targeting antioxidants to
[...] Read more.
One of the main sources of reactive oxygen species (ROS) in skeletal muscle is the mitochondria. Prolonged or very high ROS exposure causes oxidative damage, which can be deleterious to muscle function, and as such, there is growing interest in targeting antioxidants to the mitochondria in an effort to prevent or treat muscle dysfunction and damage associated with disease and injury. Paradoxically, however, ROS also act as important signalling molecules in controlling cellular homeostasis, and therefore caution must be taken when supplementing with antioxidants. It is possible that mitochondria-targeted antioxidants may limit oxidative stress without suppressing ROS from non-mitochondrial sources that might be important for cell signalling. Therefore, in this review, we summarise literature relating to the effect of mitochondria-targeted antioxidants on skeletal muscle function. Overall, mitochondria-targeted antioxidants appear to exert beneficial effects on mitochondrial capacity and function, insulin sensitivity and age-related declines in muscle function. However, it seems that this is dependent on the type of mitochondrial-trageted antioxidant employed, and its specific mechanism of action, rather than simply targeting to the mitochondria. Full article
(This article belongs to the Special Issue Feature Papers in Antioxidants in 2018)
Figures

Figure 1

Open AccessReview Redox Biology of Right-Sided Heart Failure
Antioxidants 2018, 7(8), 106; https://doi.org/10.3390/antiox7080106
Received: 25 June 2018 / Revised: 21 July 2018 / Accepted: 7 August 2018 / Published: 8 August 2018
PDF Full-text (999 KB) | HTML Full-text | XML Full-text
Abstract
Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures.
[...] Read more.
Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures. However, differences between the RV and LV formed after birth have not been well defined. Work from our laboratory and others has accumulated evidence that redox signaling, oxidative stress and antioxidant regulation are important components that define the RV/LV differences. The present article summarizes the progress in understanding the roles of redox biology in the RV chamber-specificity. Understanding the mechanisms of RV/LV differences should help develop selective therapeutic strategies to help patients who are susceptible to and suffering from right-sided heart failure. Modulations of redox biology may provide effective therapeutic avenues for these conditions. Full article
(This article belongs to the Special Issue Novel Aspects of Redox and Antioxidant Signaling)
Figures

Figure 1

Open AccessArticle Mechanisms of LPS-Induced Acute Kidney Injury in Neonatal and Adult Rats
Antioxidants 2018, 7(8), 105; https://doi.org/10.3390/antiox7080105
Received: 27 June 2018 / Revised: 28 July 2018 / Accepted: 6 August 2018 / Published: 8 August 2018
PDF Full-text (5442 KB) | HTML Full-text | XML Full-text
Abstract
Neonatal sepsis is one of the major causes of mortality and morbidity in newborns, greatly associated with severe acute kidney injury (AKI) and failure. Handling of newborns with kidney damage can be significantly different compared to adults, and it is necessary to consider
[...] Read more.
Neonatal sepsis is one of the major causes of mortality and morbidity in newborns, greatly associated with severe acute kidney injury (AKI) and failure. Handling of newborns with kidney damage can be significantly different compared to adults, and it is necessary to consider the individuality of an organism’s response to systemic inflammation. In this study, we used lipopolysaccharide (LPS)-mediated acute kidney injury model to study mechanisms of kidney cells damage in neonatal and adult rats. We found LPS-associated oxidative stress was more severe in adults compared to neonates, as judged by levels of carbonylated proteins and products of lipids peroxidation. In both models, LPS-mediated septic simulation caused apoptosis of kidney cells, albeit to a different degree. Elevated levels of proliferating cell nuclear antigen (PCNA) in the kidney dropped after LPS administration in neonates but increased in adults. Renal fibrosis, as estimated by smooth muscle actin levels, was significantly higher in adult kidneys, whereas these changes were less profound in LPS-treated neonatal kidneys. We concluded that in LPS-mediated AKI model, renal cells of neonatal rats were more tolerant to oxidative stress and suffered less from long-term pathological consequences, such as fibrosis. In addition, we assume that by some features LPS administration simulates the conditions of accelerated aging. Full article
(This article belongs to the Special Issue Antioxidant Defense and Oxidant Load in Pediatric Health and Disease)
Figures

Graphical abstract

Open AccessArticle Human Lymphocyte-Protective Effects of an Ethanol Extract from Detarium microcarpum Guill. and Perr. (Caesalpiniaceae) Fruit Pulp
Antioxidants 2018, 7(8), 104; https://doi.org/10.3390/antiox7080104
Received: 15 July 2018 / Revised: 1 August 2018 / Accepted: 2 August 2018 / Published: 4 August 2018
PDF Full-text (1529 KB) | HTML Full-text | XML Full-text
Abstract
The current study aimed to evaluate, in vitro, the antioxidant capacity and the human lymphocyte-protective effect of the ethanolic extract from Detarium microcarpum fruit pulp against oxidative stress damage. Human lymphocytes were incubated with different concentrations of extract, followed by the addition of
[...] Read more.
The current study aimed to evaluate, in vitro, the antioxidant capacity and the human lymphocyte-protective effect of the ethanolic extract from Detarium microcarpum fruit pulp against oxidative stress damage. Human lymphocytes were incubated with different concentrations of extract, followed by the addition of hydrogen peroxide or tert-butyl hydroperoxide. Cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Furthermore, the antioxidant property of the extract was evaluated in vitro using hydrogen peroxide and nitric oxide radical-scavenging assays. Compared to the vehicle, the fruit pulp ethanol extract did not exhibit a cytotoxic effect on human lymphocytes. Furthermore, the cytotoxicity of hydrogen peroxide and tert-butyl hydroperoxide to human lymphocytes was significantly reduced by fruit extract pretreatment. The extract and ascorbic acid exhibited similar cytoprotective activity (p > 0.05). The fruit pulp extract showed more antioxidant activity than gallic acid in the hydrogen peroxide-scavenging model, while in the nitric oxide-quenching model, the fruit extract and gallic acid showed similar activity. The fruit pulp of D. microcarpum contains potent antioxidant and cell-protective compounds. The use of the fruit pulp of D. microcarpum as a food supplement could rescue cellular oxidative damage responsible for numerous pathologies. Full article
Figures

Figure 1

Open AccessArticle Solvent Extraction of Polyphenolics from the Indigenous African Fruit Ximenia caffra and Characterization by LC-HRMS
Antioxidants 2018, 7(8), 103; https://doi.org/10.3390/antiox7080103
Received: 11 July 2018 / Revised: 24 July 2018 / Accepted: 31 July 2018 / Published: 1 August 2018
PDF Full-text (885 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Indigenous and non-commercial fruits can be an important source of antioxidant polyphenols; however, the identity and content of polyphenols from non-commercial fruits are often poorly described. The study aimed to extract, identify, and quantify polyphenols from the skin of the indigenous Africa fruit
[...] Read more.
Indigenous and non-commercial fruits can be an important source of antioxidant polyphenols; however, the identity and content of polyphenols from non-commercial fruits are often poorly described. The study aimed to extract, identify, and quantify polyphenols from the skin of the indigenous Africa fruit Ximenia caffra, using solvent extraction. Three solvents (hexane, acetone, and 70% v/v ethanol) over three extraction times (30, 60 and 120 min) were used in a 32 full factorial experimental design to determine effects on polyphenol recovery, and individual polyphenolics were characterised using liquid chromatography high-resolution mass spectrometry (LC-HRMS). Ethanol was the most effective extraction solvent, and extracts had high levels of total phenolics and flavonoids (65 mg gallic and 40 mg catechin equivalents per gram dry sample respectively), and high antioxidant activity (18.2 mg mL−1 ascorbic acid equivalents). LC-HRMS positively identified 16 compounds, of which 14 were flavonoids including flavonoid glycosides, and indicated that concentrations of some flavonoids decreased for extraction times beyond 60 min. It was concluded that the fruit of Ximenia caffra is rich in natural polyphenolic antioxidants; the present work identified and quantified a number of these, while also establishing suitable solvent extraction conditions for the recovery of these potentially high-value compounds. Full article
Figures

Graphical abstract

Open AccessReview Lipid Peroxidation-Derived Aldehydes, 4-Hydroxynonenal and Malondialdehyde in Aging-Related Disorders
Antioxidants 2018, 7(8), 102; https://doi.org/10.3390/antiox7080102
Received: 29 June 2018 / Revised: 26 July 2018 / Accepted: 27 July 2018 / Published: 30 July 2018
Cited by 1 | PDF Full-text (1258 KB) | HTML Full-text | XML Full-text
Abstract
Among the various mechanisms involved in aging, it was proposed long ago that a prominent role is played by oxidative stress. A major way by which the latter can provoke structural damage to biological macromolecules, such as DNA, lipids, and proteins, is by
[...] Read more.
Among the various mechanisms involved in aging, it was proposed long ago that a prominent role is played by oxidative stress. A major way by which the latter can provoke structural damage to biological macromolecules, such as DNA, lipids, and proteins, is by fueling the peroxidation of membrane lipids, leading to the production of several reactive aldehydes. Lipid peroxidation-derived aldehydes can not only modify biological macromolecules, by forming covalent electrophilic addition products with them, but also act as second messengers of oxidative stress, having relatively extended lifespans. Their effects might be further enhanced with aging, as their concentrations in cells and biological fluids increase with age. Since the involvement and the role of lipid peroxidation-derived aldehydes, particularly of 4-hydroxynonenal (HNE), in neurodegenerations, inflammation, and cancer, has been discussed in several excellent recent reviews, in the present one we focus on the involvement of reactive aldehydes in other age-related disorders: osteopenia, sarcopenia, immunosenescence and myelodysplastic syndromes. In these aging-related disorders, characterized by increases of oxidative stress, both HNE and malondialdehyde (MDA) play important pathogenic roles. These aldehydes, and HNE in particular, can form adducts with circulating or cellular proteins of critical functional importance, such as the proteins involved in apoptosis in muscle cells, thus leading to their functional decay and acceleration of their molecular turnover and functionality. We suggest that a major fraction of the toxic effects observed in age-related disorders could depend on the formation of aldehyde-protein adducts. New redox proteomic approaches, pinpointing the modifications of distinct cell proteins by the aldehydes generated in the course of oxidative stress, should be extended to these age-associated disorders, to pave the way to targeted therapeutic strategies, aiming to alleviate the burden of morbidity and mortality associated with these disturbances. Full article
(This article belongs to the Special Issue Antioxidants and Second Messengers of Free Radicals)
Figures

Graphical abstract

Open AccessEditorial Inspired by Nature: Antioxidants and Nanotechnology
Antioxidants 2018, 7(8), 101; https://doi.org/10.3390/antiox7080101
Received: 24 July 2018 / Accepted: 25 July 2018 / Published: 29 July 2018
PDF Full-text (148 KB) | HTML Full-text | XML Full-text
Abstract
Since the advent of modern nanotechnology a couple of decades ago, the field of “nano-bio-med” has attracted particular interest, culminating in an almost meteoric rise of common, feasible, more speculative, and, on occasion, outrightly exotic applications of nanomaterials. [...] Full article
(This article belongs to the Special Issue Inspired by Nature: Antioxidants and Nanotechnology)
Open AccessArticle Coenzyme Q10 Modulates Remodeling Possibly by Decreasing Angiotensin-Converting Enzyme in Patients with Acute Coronary Syndrome
Antioxidants 2018, 7(8), 99; https://doi.org/10.3390/antiox7080099
Received: 2 June 2018 / Revised: 18 July 2018 / Accepted: 20 July 2018 / Published: 25 July 2018
PDF Full-text (246 KB) | HTML Full-text | XML Full-text
Abstract
The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. In a double blind, randomized, placebo-controlled, parallel
[...] Read more.
The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. In a double blind, randomized, placebo-controlled, parallel group study (a retrospective analysis of an earlier trial) in 55 patients with left ventricular ejection fraction <50% after AMI, the effects of coenzyme Q10 (120 mg/day) or placebo were studied for 24 weeks. Two-dimensional echocardiography was performed at discharge, (approximately 5–10 days after admission) and at 6 months after AMI. The results revealed that wall thickness opposite the site of infarction decreased from (mean ± standard deviation (SD)) 12.2 ± 2.0 mm to 10.0 ± 1.8 mm with coenzyme Q10 compared with 12.8 ± 2.2 mm to 13.3 ± 2.3 mm with placebo (p < 0.01). Left ventricular mass changed from 236 ± 72 g to 213 ± 61 g with coenzyme Q10 compared with 230 ± 77 g to 255 ± 86 g with placebo (p < 0.01). Treatment with coenzyme Q10 also prevented alteration of sphericity index which is a ratio of the long and short axis of the left ventricle (which changed from 1.61 ± 0.28 to 1.63 ± 0.30 with coenzyme Q10 compared with 1.61 ± 0.32 to 1.41 ± 0.31 with placebo (p < 0.05)). Coenzyme Q10 also prevented alteration of the wall thickening abnormality at the infarct site, which changed from 9.4 ± 3.0 cm2 to 9.1 ± 2.8 cm2 compared with 10.1 ± 3.1 to 13.7 ± 4.2 cm2 with placebo (p < 0.05). End diastolic and systolic volumes also showed significant reduction with coenzyme Q10 compared to placebo. The serum level of ACE showed significant decline in the coenzyme Q10 group compared to the control group. Treatment with coenzyme Q10 early after AMI causes attenuation of left ventricular remodeling and decreases the serum ACE level in patients with left ventricular dysfunction. Full article
(This article belongs to the Special Issue CoQ10 in Longevity)
Open AccessArticle Interleukin-1β Protects Neurons against Oxidant-Induced Injury via the Promotion of Astrocyte Glutathione Production
Antioxidants 2018, 7(8), 100; https://doi.org/10.3390/antiox7080100
Received: 8 June 2018 / Revised: 4 July 2018 / Accepted: 21 July 2018 / Published: 25 July 2018
Cited by 1 | PDF Full-text (2737 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervous System (CNS), is enhanced in many neurological diseases/disorders. Although IL-1β contributes to and/or sustains pathophysiological processes in the CNS, we recently demonstrated that IL-1β can protect cortical astrocytes from oxidant injury
[...] Read more.
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervous System (CNS), is enhanced in many neurological diseases/disorders. Although IL-1β contributes to and/or sustains pathophysiological processes in the CNS, we recently demonstrated that IL-1β can protect cortical astrocytes from oxidant injury in a glutathione (GSH)-dependent manner. To test whether IL-1β could similarly protect neurons against oxidant stress, near pure neuronal cultures or mixed cortical cell cultures containing neurons and astrocytes were exposed to the organic peroxide, tert-butyl hydroperoxide (t-BOOH), following treatment with IL-1β or its vehicle. Neurons and astrocytes in mixed cultures, but not pure neurons, were significantly protected from the toxicity of t-BOOH following treatment with IL-1β in association with enhanced GSH production/release. IL-1β failed to increase the GSH levels or to provide protection against t-BOOH toxicity in chimeric mixed cultures consisting of IL-1R1+/+ neurons plated on top of IL-1R1−/− astrocytes. The attenuation of GSH release via block of multidrug resistance-associated protein 1 (MRP1) transport also abrogated the protective effect of IL-1β. These protective effects were not strictly an in vitro phenomenon as we found an increased striatal vulnerability to 3-nitropropionic acid-mediated oxidative stress in IL-1R1 null mice. Overall, our data indicate that IL-1β protects neurons against oxidant injury and that this likely occurs in a non-cell-autonomous manner that relies on an increase in astrocyte GSH production and release. Full article
(This article belongs to the Special Issue Astrocyte Antioxidant Systems)
Figures

Figure 1

Open AccessReview Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review
Antioxidants 2018, 7(8), 98; https://doi.org/10.3390/antiox7080098
Received: 17 June 2018 / Revised: 10 July 2018 / Accepted: 20 July 2018 / Published: 24 July 2018
PDF Full-text (1587 KB) | HTML Full-text | XML Full-text
Abstract
Wound healing is a well-tuned biological process, which is achieved via consecutive and overlapping phases including hemostasis, inflammatory-related events, cell proliferation and tissue remodeling. Several factors can impair wound healing such as oxygenation defects, aging, and stress as well as deleterious health conditions
[...] Read more.
Wound healing is a well-tuned biological process, which is achieved via consecutive and overlapping phases including hemostasis, inflammatory-related events, cell proliferation and tissue remodeling. Several factors can impair wound healing such as oxygenation defects, aging, and stress as well as deleterious health conditions such as infection, diabetes, alcohol overuse, smoking and impaired nutritional status. Growing evidence suggests that reactive oxygen species (ROS) are crucial regulators of several phases of healing processes. ROS are centrally involved in all wound healing processes as low concentrations of ROS generation are required for the fight against invading microorganisms and cell survival signaling. Excessive production of ROS or impaired ROS detoxification causes oxidative damage, which is the main cause of non-healing chronic wounds. In this context, experimental and clinical studies have revealed that antioxidant and anti-inflammatory strategies have proven beneficial in the non-healing state. Among available antioxidant strategies, treatments using mitochondrial-targeted antioxidants are of particular interest. Specifically, mitochondrial-targeted peptides such as elamipretide have the potential to mitigate mitochondrial dysfunction and aberrant inflammatory response through activation of nucleotide-binding oligomerization domain (NOD)-like family receptors, such as the pyrin domain containing 3 (NLRP3) inflammasome, nuclear factor-kappa B (NF-κB) signaling pathway inhibition, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Full article
Figures

Figure 1

Open AccessReview Cerium Oxide Nanoparticles: A Brief Review of Their Synthesis Methods and Biomedical Applications
Antioxidants 2018, 7(8), 97; https://doi.org/10.3390/antiox7080097
Received: 29 May 2018 / Revised: 12 July 2018 / Accepted: 19 July 2018 / Published: 24 July 2018
PDF Full-text (227 KB) | HTML Full-text | XML Full-text
Abstract
Cerium oxide nanoparticles (CeNPs) exhibit antioxidant properties both in vitro and in vivo. This is due to the self-regeneration of their surface, which is based on redox-cycling between 3+ and 4+ states for cerium, in response to their immediate environment. Additionally, oxygen vacancies
[...] Read more.
Cerium oxide nanoparticles (CeNPs) exhibit antioxidant properties both in vitro and in vivo. This is due to the self-regeneration of their surface, which is based on redox-cycling between 3+ and 4+ states for cerium, in response to their immediate environment. Additionally, oxygen vacancies in the lattice structure allow for alternating between CeO2 and CeO2−x during redox reactions. Research to identify and characterize the biomedical applications of CeNPs has been heavily focused on investigating their use in treating diseases that are characterized by higher levels of reactive oxygen species (ROS). Although the bio-mimetic activities of CeNPs have been extensively studied in vitro, in vivo interactions and associated protein corona formation are not well understood. This review describes: (1) the methods of synthesis for CeNPs, including the recent green synthesis methods that offer enhanced biocompatibility and a need for establishing a reference CeNP material for consistency across studies; (2) their enzyme-mimetic activities, with a focus on their antioxidant activities; and, (3) recent experimental evidence that demonstrates their ROS scavenging abilities and their potential use in personalized medicine. Full article
(This article belongs to the Special Issue Feature Papers in Antioxidants in 2018)
Open AccessArticle Profiling of Omega-Polyunsaturated Fatty Acids and Their Oxidized Products in Salmon after Different Cooking Methods
Antioxidants 2018, 7(8), 96; https://doi.org/10.3390/antiox7080096
Received: 5 June 2018 / Revised: 13 July 2018 / Accepted: 14 July 2018 / Published: 24 July 2018
PDF Full-text (2386 KB) | HTML Full-text | XML Full-text
Abstract
Consumption of food containing n-3 PUFAs, namely EPA and DHA, are known to benefit health and protect against chronic diseases. Both are richly found in marine-based food such as fatty fish and seafood that are commonly cooked prior to consumption. However, the elevated
[...] Read more.
Consumption of food containing n-3 PUFAs, namely EPA and DHA, are known to benefit health and protect against chronic diseases. Both are richly found in marine-based food such as fatty fish and seafood that are commonly cooked prior to consumption. However, the elevated temperature during cooking potentially degrades the EPA and DHA through oxidation. To understand the changes during different cooking methods, lipid profiles of raw, boiled, pan-fried and baked salmon were determined by LC-MS/MS. Our results showed that pan-frying and baking elevated the concentration of peroxides in salmon, whereas only pan-frying increased the MDA concentration, indicating it to be the most severe procedure to cause oxidation among the cooking methods. Pan-frying augmented oxidized products of n-3 and n-6 PUFAs, while only those of n-3 PUFA were elevated in baked salmon. Notably, pan-frying and baking increased bioactive oxidized n-3 PUFA products, in particular F-4t-neuroprostanes derived from DHA. The results of this study provided a new insight into the application of heat and its effect on PUFAs and the release of its oxidized products in salmon. Full article
(This article belongs to the Special Issue Lipid Peroxidation: Analysis and Applications in Biological Systems)
Figures

Figure 1

Back to Top