Editorial

4 pages, 200 KiB

Open AccessEditorial

Effect of Antioxidant Therapy on Oxidative Stress in Vivo

by Anna Maria Fratta Pasini and Luciano Cominacini

Antioxidants 2021, 10(3), 344; https://doi.org/10.3390/antiox10030344 - 25 Feb 2021

Cited by 1 | Viewed by 1425

Over the last few decades, many efforts have been put into fields that explore the potential benefits of antioxidants, especially with regards to aging, cancer, cardiovascular diseases, and neurodegenerative diseases [...] Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

Research

Jump to: Editorial, Review

15 pages, 2432 KiB

Open AccessArticle

Changes in Lipid Profile of Keratinocytes from Rat Skin Exposed to Chronic UVA or UVB Radiation and Topical Application of Cannabidiol

by Wojciech Łuczaj, Maria do Rosário Domingues, Pedro Domingues and Elżbieta Skrzydlewska

Antioxidants 2020, 9(12), 1178; https://doi.org/10.3390/antiox9121178 - 25 Nov 2020

Cited by 15 | Viewed by 3593

Abstract

UV radiation is a well-established environmental risk factor known to cause oxidative stress and disrupt the metabolism of keratinocyte phospholipids. Cannabidiol (CBD) is a phytocannabinoid with anti-inflammatory and antioxidant effects. In this study, we examined changes in the keratinocyte phospholipid profile from nude [...] Read more.

UV radiation is a well-established environmental risk factor known to cause oxidative stress and disrupt the metabolism of keratinocyte phospholipids. Cannabidiol (CBD) is a phytocannabinoid with anti-inflammatory and antioxidant effects. In this study, we examined changes in the keratinocyte phospholipid profile from nude rat skin exposed to UVA and UVB radiation that was also treated topically with CBD. UVA and UVB radiation promoted up-regulation of phosphatidylcholines (PC), lysophosphatidylcholines (LPC), phosphatidylethanolamines (PE) and down-regulation of sphingomyelin (SM) levels and enhanced the activity of phospholipase A2 (PLA2) and sphingomyelinase (SMase). Application of CBD to the skin of control rats led to down-regulation of SM and up-regulation of SMase activity. After CBD treatment of rats irradiated with UVA or UVB, SM was up-regulated and down-regulated, respectively, while ceramide (CER) levels and SMase activity were down-regulated and up-regulated, respectively. CBD applied to the skin of UV-irradiated rats down-regulated LPC, up-regulated PE and phosphatidylserines (PS) and reduced PLA2 activity. In conclusion, up-regulation of PS may suggest that CBD inhibits their oxidative modification, while changes in the content of PE and SM may indicate a role of CBD in promoting autophagy and improving the status of the transepidermal barrier. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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18 pages, 5281 KiB

Open AccessArticle

SIRT1 Activation Using CRISPR/dCas9 Promotes Regeneration of Human Corneal Endothelial Cells through Inhibiting Senescence

by Hye Jun Joo, Dae Joong Ma, Jin Sun Hwang and Young Joo Shin

Antioxidants 2020, 9(11), 1085; https://doi.org/10.3390/antiox9111085 - 04 Nov 2020

Cited by 6 | Viewed by 2574

Abstract

Human corneal endothelial cells (hCECs) are restricted in proliferative capacity in vivo. Reduction in the number of hCEC leads to persistent corneal edema requiring corneal transplantation. This study demonstrates the functions of SIRT1 in hCECs and its potential for corneal endothelial regeneration. Cell [...] Read more.

Human corneal endothelial cells (hCECs) are restricted in proliferative capacity in vivo. Reduction in the number of hCEC leads to persistent corneal edema requiring corneal transplantation. This study demonstrates the functions of SIRT1 in hCECs and its potential for corneal endothelial regeneration. Cell morphology, cell growth rates and proliferation-associated proteins were compared in normal and senescent hCECs. SIRT1 was activated using the CRISPR/dCas9 activation system (SIRT1a). The plasmids were transfected into CECs of six-week-old Sprague–Dawley rats using electroporation and cryoinjury was performed. Senescent cells were larger, elongated and showed lower proliferation rates and lower SIRT1 levels. SIRT1 activation promoted the wound healing of CECs. In vivo transfection of SIRT1a promoted the regeneration of CECs. The proportion of the S-phase cells was lower in senescent cells and elevated upon SIRT1a activation. SIRT1 regulated cell proliferation, proliferation-associated proteins, mitochondrial membrane potential, and oxidative stress levels. In conclusion, corneal endothelial senescence is related with a decreased SIRT1 level. SIRT1a promotes the regeneration of CECs by inhibiting cytokine-induced cell death and senescence. Gene function activation therapy using SIRT1a may serve as a novel treatment strategy for hCEC diseases. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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16 pages, 625 KiB

Open AccessArticle

Changes in the Activity and Concentration of Superoxide Dismutase Isoenzymes (Cu/Zn SOD, MnSOD) in the Blood of Healthy Subjects and Patients with Acute Pancreatitis

by Milena Ściskalska, Monika Ołdakowska, Grzegorz Marek and Halina Milnerowicz

Antioxidants 2020, 9(10), 948; https://doi.org/10.3390/antiox9100948 - 01 Oct 2020

Cited by 24 | Viewed by 3744

Abstract

This study was aimed at evaluating the changes in the concentration and activity of all superoxide dismutase isoenzymes (SOD1, SOD2, SOD3) in the blood of patients with acute pancreatitis (AP) and healthy subjects, taking into account the extracellular (plasma) and intracellular (erythrocyte lysate) [...] Read more.

This study was aimed at evaluating the changes in the concentration and activity of all superoxide dismutase isoenzymes (SOD1, SOD2, SOD3) in the blood of patients with acute pancreatitis (AP) and healthy subjects, taking into account the extracellular (plasma) and intracellular (erythrocyte lysate) compartment. The relationships between the activity/concentration of SODs, metal concentration and the markers of inflammation were evaluated. To assess the pro/antioxidative imbalance, the malonyldialdehyde (MDA) concentration and the value of total antioxidant capacity (TAC) were measured. The impact of single-nucleotide polymorphism (SNP) in the SOD1 gene (rs2070424) on the activity/concentration of SOD1 as the main isoenzyme of the SOD family was also analyzed in this study. The SOD2 activity in erythrocytes was increased compared to plasma: 10-fold in the AP patient group and 5-fold in healthy subjects. The plasma of AP patients showed an increased SOD1 concentration and decreased SOD2 and SOD3 concentrations compared to healthy subjects. The Cu/Zn SOD (SOD1 + SOD3) concentration in plasma of AP patients was elevated compared to healthy subjects, but changes in plasma Cu/Zn SOD (SOD1 + SOD3) activity in the examined groups were not observed. An influence of SNP rs2070424 in the SOD1 gene on the total activity of SOD in AP patients (with AG genotype), accompanied by an increased IL-6 concentration, was observed. In oxidative stress conditions induced by inflammation, the participation of individual forms of plasma SOD isoenzymes in total antioxidative activity of SOD changed. A significant increase in the intracellular SOD1 concentration in plasma of AP patients proves the important role of this isoenzyme in the neutralization of oxidative stress induced by impaired Cu and Zn homeostasis. The presence of increased concentration of SOD2 in erythrocytes of healthy subjects and AP patients confirms the important function of this isoenzyme in the antioxidative defense. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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17 pages, 1783 KiB

Open AccessArticle

Modulating Laying Hens Productivity and Immune Performance in Response to Oxidative Stress Induced by E. coli Challenge Using Dietary Propolis Supplementation

by Ahmed O. Abbas, Abdulaziz A. Alaqil, Hossam S. El-Beltagi, Hanaa K. Abd El-Atty and Nancy N. Kamel

Antioxidants 2020, 9(9), 893; https://doi.org/10.3390/antiox9090893 - 21 Sep 2020

Cited by 25 | Viewed by 5381

Abstract

Propolis (PR) is a resin product of bee colonies that has rich bioactive antioxidant and bactericidal compounds. Endotoxin, a byproduct of bacterial growth, is reported to cause progressive induction of endogenous oxidative stress and has negative impacts on individual health and wellbeing. Hereby, [...] Read more.

Propolis (PR) is a resin product of bee colonies that has rich bioactive antioxidant and bactericidal compounds. Endotoxin, a byproduct of bacterial growth, is reported to cause progressive induction of endogenous oxidative stress and has negative impacts on individual health and wellbeing. Hereby, we investigated the ability of PR to alleviate the oxidative stress and immunosuppression imposed by avian pathogenic Escherichia coli using laying hen as a based model. In this study, PR was dietary supplemented to hens for 4 weeks at a concentration of 0.1%. At the beginning of the 4th week of the experiment, hens from control and PR treatment were injected with E. coli (O157:H7; 10⁷ colonies/hen) or saline. The results showed significant (p < 0.05) negative impact of E. coli challenge on antioxidant status, immune response and productive performance. PR supplementation reduced (p < 0.05) inflammation markers levels (tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β)) and plasma corticosterone concentration. The antioxidant status was ameliorated with dietary PR supplementation to challenged hens, showing significant (p < 0.05) reduction in malondialdehyde (MDA) levels and increasing total antioxidant capacity (TAC) concentrations. Cell mediated, as well as, humeral immune response improved significantly (p < 0.05) with dietary PR verified by the enhancement of T- and B-lymphocyte proliferation and the positive respond to phytohemagglutinin (PHA). Leucocyte cells viability increased significantly and the apoptotic factor forkhead box O3 (Foxo3) was reduced with PR supplementation. The current study revealed that dietary PR supplementation can effectively be used as an organic feed additive to overcome the endogenous oxidative stress induced by endotoxins challenge. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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12 pages, 2311 KiB

Open AccessArticle

Cardamonin Inhibits Oxazolone-Induced Atopic Dermatitis by the Induction of NRF2 and the Inhibition of Th2 Cytokine Production

by Ok-Kyung Yoo, Won Jun Choi and Young-Sam Keum

Antioxidants 2020, 9(9), 834; https://doi.org/10.3390/antiox9090834 - 07 Sep 2020

Cited by 11 | Viewed by 3411

Abstract

The skin is constantly exposed to various types of chemical stresses that challenge the immune cells, leading to the activation of T cell-mediated hypersensitivity reactions including atopic dermatitis. Previous studies have demonstrated that a variety of natural compounds are effective against development of [...] Read more.

The skin is constantly exposed to various types of chemical stresses that challenge the immune cells, leading to the activation of T cell-mediated hypersensitivity reactions including atopic dermatitis. Previous studies have demonstrated that a variety of natural compounds are effective against development of atopic dermatitis by modulating immune responses. Cardamonin is a natural compound abundantly found in cardamom spices and many other medicinal plant species. In the present study, we attempted to examine whether cardamonin could inhibit oxazolone-induced atopic dermatitis in vivo. Our results show that topical application of cardamonin onto the ear of mice suppressed oxazolone-induced inflammation in the ear and hyperplasia in the spleen. Cardamonin also inhibited oxazolone-induced destruction of connective tissues and subsequent infiltration of mast cells into the skin. In addition, we found that the production of Th2 cytokines is negatively regulated by NRF2, and the induction of NRF2 by cardamonin contributed to suppressing oxazolone-induced Th2 cytokine production and oxidative damages in vivo. Together, our results demonstrate that cardamonin is a promising natural compound, which might be effective for treatment of atopic dermatitis. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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18 pages, 3341 KiB

Open AccessArticle

Oral Administration of Sodium Nitrate to Metabolic Syndrome Patients Attenuates Mild Inflammatory and Oxidative Responses to Acute Exercise

by Xavier Capó, Miguel D. Ferrer, Robert A. Olek, Eduardo Salaberry, Rafael Suau, Bartolomé Marí, Isabel Llompart, Josep A. Tur, Antoni Sureda and Antoni Pons

Antioxidants 2020, 9(7), 596; https://doi.org/10.3390/antiox9070596 - 07 Jul 2020

Cited by 8 | Viewed by 2610

Abstract

The beneficial effects of exercise for the treatment and prevention of metabolic syndrome pathologies have been related to its anti-inflammatory and antioxidant effects. Dietary nitrate supplementation is an emerging treatment strategy to alleviate the symptoms of metabolic syndrome affections and to improve vascular [...] Read more.

The beneficial effects of exercise for the treatment and prevention of metabolic syndrome pathologies have been related to its anti-inflammatory and antioxidant effects. Dietary nitrate supplementation is an emerging treatment strategy to alleviate the symptoms of metabolic syndrome affections and to improve vascular function. In this double-blind crossover trial, metabolic syndrome patients performed two exercise tests for 30 min at 60–70% maximal heart rate after the intake of a placebo or a nitrate-enriched beverage. Acute exercise increased the plasma concentration of TNFα, intercellular adhesion molecule ICAM1, PGE1, PGE2 and the newly detected 16-hydroxypalmitic acid (16-HPAL) in metabolic syndrome patients. The cytokine and oxylipin production by peripheral blood mononuclear cells (PBMCs) and neutrophils could be responsible for the plasma concentrations of TNFα and IL6, but not for the plasma concentration of oxylipins nor its post-exercise increase. The intake of sodium nitrate 30 min before exercise increased the concentration of nitrate and nitrite in the oral cavity and plasma and reduced the oxygen cost of exercise. Additionally, nitrate intake prevented the enhancing effects of acute exercise on the plasma concentration of TNFα, ICAM1, PGE1, PGE2 and 16-HPAL, while reducing the capabilities of PBMCs and neutrophils to produce oxylipins. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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15 pages, 955 KiB

Open AccessArticle

Serum Malondialdehyde is Associated with Non-Alcoholic Fatty Liver and Related Liver Damage Differentially in Men and Women

by Shira Zelber-Sagi, Dana Ivancovsky-Wajcman, Naomi Fliss-Isakov, Michal Hahn, Muriel Webb, Oren Shibolet, Revital Kariv and Oren Tirosh

Antioxidants 2020, 9(7), 578; https://doi.org/10.3390/antiox9070578 - 02 Jul 2020

Cited by 33 | Viewed by 3487

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are associated with increased oxidative stress and lipid peroxidation, but large studies are lacking. The aim was to test the association of malondialdehyde (MDA), as a marker of oxidative damage of lipids, with NAFLD [...] Read more.

Background: Non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are associated with increased oxidative stress and lipid peroxidation, but large studies are lacking. The aim was to test the association of malondialdehyde (MDA), as a marker of oxidative damage of lipids, with NAFLD and liver damage markers, and to test the association between dietary vitamins E and C intake and MDA levels. Methods: A cross-sectional study was carried out among subjects who underwent blood tests including FibroMax for non-invasive assessment of NASH and fibrosis. MDA was evaluated by reaction with Thiobarbituric acid and HPLC-fluorescence detection method. NAFLD was diagnosed by abdominal ultrasound. Findings: MDA measurements were available for 394 subjects. In multivariate analysis, the odds for NAFLD were higher with the rise of MDA levels in a dose–response manner, adjusting for age, gender, BMI, and lifestyle factors. Only among men, higher serum MDA was associated of higher odds for NAFLD and NASH and/or fibrosis (OR = 2.59, 95% CI 1.33–5.07, P = 0.005; OR = 2.04, 1.02–4.06, P = 0.043, respectively). Higher vitamin E intake was associated with lower odds of high serum MDA level (OR = 0.28 95% CI 0.13–0.62, P = 0.002). In conclusion, serum MDA is associated with NAFLD and markers of NASH or fibrosis among men. Dietary vitamin E may be protective among women. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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15 pages, 2100 KiB

Open AccessEditor’s ChoiceArticle

Polyphenols Attenuate Highly-Glycosylated Haemoglobin-Induced Damage in Human Peritoneal Mesothelial Cells

by Carolina Sánchez-Rodríguez, Concepción Peiró, Leocadio Rodríguez-Mañas and Julián Nevado

Antioxidants 2020, 9(7), 572; https://doi.org/10.3390/antiox9070572 - 01 Jul 2020

Cited by 3 | Viewed by 3541

Abstract

We investigated the cytoprotective role of the dietary polyphenols on putative damage induced by Amadori adducts in Human Peritoneal Mesothelial Cells (HPMCs). Increased accumulation of early products of non-enzymatic protein glycation—Amadori adducts—in the peritoneal dialysis fluid due to their high glucose, induces severe [...] Read more.

We investigated the cytoprotective role of the dietary polyphenols on putative damage induced by Amadori adducts in Human Peritoneal Mesothelial Cells (HPMCs). Increased accumulation of early products of non-enzymatic protein glycation—Amadori adducts—in the peritoneal dialysis fluid due to their high glucose, induces severe damage in mesothelial cells during peritoneal dialysis. Dietary polyphenols reportedly have numerous health benefits in various diseases and have been used as an efficient antioxidant in the context of several oxidative stress-related pathologies. HPMCs isolated from different patients were exposed to Amadori adducts (highly glycated haemoglobin, at physiological concentrations), and subsequently treated with several polyphenols, mostly presented in our Mediterranean diet. We studied several Amadori-induced effects in pro-apoptotic and oxidative stress markers, as well as the expression of several pro-inflammatory genes (nuclear factor-kappaB, NF-kB; inducible Nitric Oxide synthetase, iNOS), different caspase-activities, level of P53 protein or production of different reactive oxygen species in the presence of different polyphenols. In fact, cytoprotective agents such as dietary polyphenols may represent an alternate approach to protect mesothelial cells from the cytotoxicity of Amadori adducts. The interference with the Amadori adducts-triggered mechanisms could represent a therapeutic tool to reduce complications associated with peritoneal dialysis in the peritoneum, helping to maintain peritoneal membrane function longer in patients undergoing peritoneal dialysis. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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25 pages, 6609 KiB

Open AccessArticle

Antioxidant Effects of Walnut (Juglans regia L.) Kernel and Walnut Septum Extract in a D-Galactose-Induced Aging Model and in Naturally Aged Rats

by Marius Emil Rusu, Carmen Georgiu, Anca Pop, Andrei Mocan, Bela Kiss, Oliviu Vostinaru, Ionel Fizesan, Maria-Georgia Stefan, Ana-Maria Gheldiu, Letitia Mates, Rebeca Moldovan, Dana Maria Muntean, Felicia Loghin, Laurian Vlase and Daniela-Saveta Popa

Antioxidants 2020, 9(5), 424; https://doi.org/10.3390/antiox9050424 - 14 May 2020

Cited by 49 | Viewed by 5111

Abstract

Antioxidant dietary intervention is considered a potential strategy in delaying age-related dysfunctions. In this study of 56 days, we assessed the antioxidant effects of walnut kernel (WK) and walnut septum extract (WSE) in a D-galactose (D-gal)-induced aging model and in a naturally aged [...] Read more.

Antioxidant dietary intervention is considered a potential strategy in delaying age-related dysfunctions. In this study of 56 days, we assessed the antioxidant effects of walnut kernel (WK) and walnut septum extract (WSE) in a D-galactose (D-gal)-induced aging model and in a naturally aged rat model. Young Wistar rats, treated with D-gal (1200 mg/week), and old rats received daily WK or WSE added to the feed. After 8 weeks, blood, liver, and brain samples were collected and hematological, biochemical, oxidative stress biomarkers, histological, and immunohistochemical analyses were performed. Moreover, acetylcholinesterase activity was investigated in brain homogenates. The outcomes demonstrated significant improvement in cellular antioxidant activity and/or decrease of reactive oxygen species, advanced glycation end products, nitric oxide, malondialdehyde, or increase of glutathione after WK or WSE intake in both models. Additionally, WSE showed hypoglycemic effect, and both WK and WSE lowered acetylcholinesterase activity. Both diets could protect neurons against the induced senescence and could reverse the pathological conditions in the physiological aged brain. Thus, dietary supplementation with WK or WSE can maintain the liver and brain health and reduce the risk of age-related diseases, as well as delaying the onset of aging processes. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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Review

Jump to: Editorial, Research

22 pages, 1397 KiB

Open AccessReview

Potential Role of Antioxidant and Anti-Inflammatory Therapies to Prevent Severe SARS-Cov-2 Complications

by Anna M. Fratta Pasini, Chiara Stranieri, Luciano Cominacini and Chiara Mozzini

Antioxidants 2021, 10(2), 272; https://doi.org/10.3390/antiox10020272 - 10 Feb 2021

Cited by 44 | Viewed by 6235

Abstract

The coronavirus disease 2019 (COVID-19) pandemic is caused by a novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2). Here, we review the molecular pathogenesis of SARS-CoV-2 and its relationship with oxidative stress (OS) and inflammation. Furthermore, we analyze the potential role of antioxidant [...] Read more.

The coronavirus disease 2019 (COVID-19) pandemic is caused by a novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2). Here, we review the molecular pathogenesis of SARS-CoV-2 and its relationship with oxidative stress (OS) and inflammation. Furthermore, we analyze the potential role of antioxidant and anti-inflammatory therapies to prevent severe complications. OS has a potential key role in the COVID-19 pathogenesis by triggering the NOD-like receptor family pyrin domain containing 3 inflammasome and nuclear factor-kB (NF-kB). While exposure to many pro-oxidants usually induces nuclear factor erythroid 2 p45-related factor2 (NRF2) activation and upregulation of antioxidant related elements expression, respiratory viral infections often inhibit NRF2 and/or activate NF-kB pathways, resulting in inflammation and oxidative injury. Hence, the use of radical scavengers like N-acetylcysteine and vitamin C, as well as of steroids and inflammasome inhibitors, has been proposed. The NRF2 pathway has been shown to be suppressed in severe SARS-CoV-2 patients. Pharmacological NRF2 inducers have been reported to inhibit SARS-CoV-2 replication, the inflammatory response, and transmembrane protease serine 2 activation, which for the entry of SARS-CoV-2 into the host cells through the angiotensin converting enzyme 2 receptor. Thus, NRF2 activation may represent a potential path out of the woods in COVID-19 pandemic. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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27 pages, 1343 KiB

Open AccessReview

Multiple Effects of Ascorbic Acid against Chronic Diseases: Updated Evidence from Preclinical and Clinical Studies

by Massimiliano Berretta, Vincenzo Quagliariello, Nicola Maurea, Raffaele Di Francia, Saman Sharifi, Gaetano Facchini, Luca Rinaldi, Michela Piezzo, Ceccarelli Manuela, Giuseppe Nunnari and Monica Montopoli

Antioxidants 2020, 9(12), 1182; https://doi.org/10.3390/antiox9121182 - 26 Nov 2020

Cited by 57 | Viewed by 5482

Abstract

Severe disease commonly manifests as a systemic inflammatory process. Inflammation is associated withthe enhanced production of reactive oxygen and nitrogen species and with a marked reduction in the plasma concentrations of protective antioxidant molecules. This imbalance gives rise to oxidative stress, which is [...] Read more.

Severe disease commonly manifests as a systemic inflammatory process. Inflammation is associated withthe enhanced production of reactive oxygen and nitrogen species and with a marked reduction in the plasma concentrations of protective antioxidant molecules. This imbalance gives rise to oxidative stress, which is greater in patients with more severe conditions such as sepsis, cancer, cardiovascular disease, acute respiratory distress syndrome, and burns. In these patients, oxidative stress can trigger cell, tissue, and organ damage, thus increasing morbidity and mortality. Ascorbic acid (ASC) is a key nutrient thatserves as an antioxidant and a cofactor for numerous enzymatic reactions. However, humans, unlike most mammals, are unable to synthesize it. Consequently, ASC must be obtained through dietary sources, especially fresh fruit and vegetables. The value of administering exogenous micronutrients, to reestablish antioxidant concentrations in patients with severe disease, has been recognized for decades. Despite the suggestion that ASC supplementation may reduce oxidative stress and prevent several chronic conditions, few large, randomized clinical trials have tested it in patients with severe illness. This article reviews the recent literature on the pharmacological profile of ASC and the role of its supplementation in critically ill patients. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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21 pages, 1141 KiB

Open AccessReview

Antioxidant Therapy against Oxidative Damage of the Inner Ear: Protection and Preconditioning

by Jhang Ho Pak, Yehree Kim, Junyeong Yi and Jong Woo Chung

Antioxidants 2020, 9(11), 1076; https://doi.org/10.3390/antiox9111076 - 02 Nov 2020

Cited by 27 | Viewed by 6270

Abstract

Oxidative stress is an important mechanism underlying cellular damage of the inner ear, resulting in hearing loss. In order to prevent hearing loss, several types of antioxidants have been investigated; several experiments have shown their ability to effectively prevent noise-induced hearing loss, age-related [...] Read more.

Oxidative stress is an important mechanism underlying cellular damage of the inner ear, resulting in hearing loss. In order to prevent hearing loss, several types of antioxidants have been investigated; several experiments have shown their ability to effectively prevent noise-induced hearing loss, age-related hearing loss, and ototoxicity in animal models. Exogenous antioxidants has been used as single therapeutic agents or in combination. Antioxidant therapy is generally administered before the production of reactive oxygen species. However, post-exposure treatment could also be effective. Preconditioning refers to the phenomenon of pre-inducing a preventative pathway by subtle stimuli that do not cause permanent damage in the inner ear. This renders the inner ear more resistant to actual stimuli that cause permanent hearing damage. The preconditioning mechanism is also related to the induction of antioxidant enzymes. In this review, we discuss the mechanisms underlying antioxidant-associated therapeutic effects and preconditioning in the inner ear. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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28 pages, 3164 KiB

Open AccessReview

Pursuing the Elixir of Life: In Vivo Antioxidative Effects of Manganosalen Complexes

by Lara Rouco, Ana M. González-Noya, Rosa Pedrido and Marcelino Maneiro

Antioxidants 2020, 9(8), 727; https://doi.org/10.3390/antiox9080727 - 10 Aug 2020

Cited by 14 | Viewed by 3976

Abstract

Manganosalen complexes are coordination compounds that possess a chelating salen-type ligand, a class of bis-Schiff bases obtained by condensation of salicylaldehyde and a diamine. They may act as catalytic antioxidants mimicking both the structure and the reactivity of the native antioxidant enzymes active [...] Read more.

Manganosalen complexes are coordination compounds that possess a chelating salen-type ligand, a class of bis-Schiff bases obtained by condensation of salicylaldehyde and a diamine. They may act as catalytic antioxidants mimicking both the structure and the reactivity of the native antioxidant enzymes active site. Thus, manganosalen complexes have been shown to exhibit superoxide dismutase, catalase, and glutathione peroxidase activities, and they could potentially facilitate the scavenging of excess reactive oxygen species (ROS), thereby restoring the redox balance in damaged cells and organs. Initial catalytic studies compared the potency of these compounds as antioxidants in terms of rate constants of the chemical reactivity against ROS, giving catalytic values approaching and even exceeding that of the native antioxidative enzymes. Although most of these catalytic studies lack of biological relevance, subsequent in vitro studies have confirmed the efficiency of many manganosalen complexes in oxidative stress models. These synthetic catalytic scavengers, cheaper than natural antioxidants, have accordingly attracted intensive attention for the therapy of ROS-mediated injuries. The aim of this review is to focus on in vivo studies performed on manganosalen complexes and their activity on the treatment of several pathological disorders associated with oxidative damage. These disorders, ranging from the prevention of fetal malformations to the extension of lifespan, include neurodegenerative, inflammatory, and cardiovascular diseases; tissue injury; and other damages related to the liver, kidney, or lungs. Full article

(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress In Vivo)

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