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Antioxidants
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Oxidative Stress in Vascular Disease...
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Oxidative Stress in Vascular Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2019) | Viewed by 18181

Special Issue Editor

Dr. Salvatore Santo Signorelli

E-Mail Website
Guest Editor
1. Department of Clinic and Experimental Medicine, University of Catania (I), Via Santa Sofia, 78, Catania, Italy
2. Director of Internal Medicine Unit, University Hospital "G.Rodolico", Via Santa Sofia, 78, Catania, Italy
Interests: peripheral arterial disease; carotid diseases; venous disease; vascular-related chronic disease; inflammation; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress theory remains one of the most well-studied and debated topics, particularly with regard to its role in both the promotion and progression of vascular disease. A large number of studies have demonstrated the deleterious effects of activated levels of oxidative stress in chronic inflammation and vascular disease (both arterial and venous). On the other hand, unbalanced or lowered antioxidant capability has also been a subject of focus, with the aim of reducing the detrimental effects of oxidative stress damage. These studies have also led to increased knowledge and the development of innovative approaches in counteracting active oxidative stress. Furthermore, it is crucial to identify both direct and indirect markers of oxidative stress damage. Thus, evaluating the role of oxidative stress on the dysregulation of redox-sensitive biological pathways in vascular diseases is an area of great interest. This Special Issue will publish both review and research articles pertaining to the role of oxidative stress in different types of vascular disease.

Prof. Salvatore Santo Signorelli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • biomarkers
  • vascular diseases

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Published Papers (4 papers)

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Research

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18 pages, 1274 KiB  
Article
Antioxidant and Anti-Inflammatory Effects of Curcumin Nanoparticles on Drug-Induced Acute Myocardial Infarction in Diabetic Rats
by Paul-Mihai Boarescu, Ioana Boarescu, Ioana Corina Bocșan, Dan Gheban, Adriana Elena Bulboacă, Cristina Nicula, Raluca Maria Pop, Ruxandra-Mioara Râjnoveanu and Sorana D. Bolboacă
Antioxidants 2019, 8(10), 504; https://doi.org/10.3390/antiox8100504 - 22 Oct 2019
Cited by 52 | Viewed by 5419
Abstract
We have investigated the cardio-protective effects of pretreatment with curcumin nanoparticles (CUN) compared to conventional curcumin (CUS) on the changes in oxidative stress parameters and inflammatory cytokine levels during induced acute myocardial infarction (AMI) in rats with diabetes mellitus (DM). DM was induced [...] Read more.
We have investigated the cardio-protective effects of pretreatment with curcumin nanoparticles (CUN) compared to conventional curcumin (CUS) on the changes in oxidative stress parameters and inflammatory cytokine levels during induced acute myocardial infarction (AMI) in rats with diabetes mellitus (DM). DM was induced with streptozotocin, and AMI with isoproterenol. Eight groups of seven Wister Bratislava rats were included in the study. The N-C was the normal control group, AMI-C was the group with AMI, DM-C was the group with DM, and DM-AMI-C was the group with DM and AMI. All four groups received saline solution orally during the whole experiment. S-DM-CUS-AMI and S-DM-CUN-AMI groups received saline for seven days prior to DM induction and continued with CUS (200 mg/kg bw, bw = body weight) for S-DM-CUS-AMI and CUN for S-DM-CUN-AMI (200 mg/kg bw) for 15 days before AMI induction. The CUS-DM-CUS-AMI group received CUS (200 mg/kg bw), while the CUN-DM-CUN-AMI received CUN (200 mg/kg bw) for seven days prior to DM induction, and both groups continued with administration in the same doses for 15 days before AMI induction. CUS and CUN prevented elevation of creatine kinase, creatine kinase-MB, lactate dehydrogenase in all groups, with better results in the CUN (S-DM-CUN-AMI and CUN-DM-CUN-AMI groups). CUS and CUN significantly reduced serum levels of oxidative stress markers (malondialdehyde, the indirect assessment of nitric oxide synthesis, and total oxidative status) and enhanced antioxidative markers (total antioxidative capacity and thiols, up to 2.5 times). All groups that received CUS or CUN showed significantly lower serum levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β. The best antioxidative and anti-inflammatory effects were obtained for the group that received CUN before DM induction (CUN-DM-CUN-AMI group). Pretreatment with CUN proved higher cardio-protective effects exerting an important antioxidative and anti-inflammatory impact in the case of AMI in DM. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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12 pages, 2141 KiB  
Communication
Inhibition of Heme Oxygenase Antioxidant Activity Exacerbates Hepatic Steatosis and Fibrosis In Vitro
by Marco Raffaele, Giuseppe Carota, Giuseppe Sferrazzo, Maria Licari, Ignazio Barbagallo, Valeria Sorrenti, Salvatore S. Signorelli and Luca Vanella
Antioxidants 2019, 8(8), 277; https://doi.org/10.3390/antiox8080277 - 05 Aug 2019
Cited by 14 | Viewed by 3872
Abstract
The progression of non-alcoholic fatty liver disease (NAFLD) and the development of hepatic fibrosis is caused by changes in redox balance, leading to an increase of reactive oxygen species (ROS) levels. NAFLD patients are at risk of progressing to non-alcoholic steatohepatitis (NASH), associated [...] Read more.
The progression of non-alcoholic fatty liver disease (NAFLD) and the development of hepatic fibrosis is caused by changes in redox balance, leading to an increase of reactive oxygen species (ROS) levels. NAFLD patients are at risk of progressing to non-alcoholic steatohepatitis (NASH), associated to cardiovascular diseases (CVD), coronary heart disease and stroke. Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. The present work was directed to determine whether use of an inhibitor of HO-1 activity affects lipid metabolism and fibrosis process in hepatic cells. Oil Red assay and mRNA analysis were used to evaluate the triglycerides content and the lipid metabolism pathway in HepG2 cells. ROS measurement, RT-PCR and Soluble collagen assay were used to assess the intracellular oxidant, the fibrosis pathway and the soluble collagen in LX2 cells. The activity of HO-1 was inhibited using Tin Mesoporphyrin IX (SnMP). Our study demonstrates that a non-functional HO system results in an increased lipid storage and collagen release in hepatocytes. Consequently, an increase of HO-1 levels may provide a therapeutic approach to address the metabolic alterations associated with NAFLD and its progression to NASH. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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Review

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14 pages, 590 KiB  
Review
Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?
by Caterina Ledda, Emanuele Cannizzaro, Piero Lovreglio, Ermanno Vitale, Angela Stufano, Angelo Montana, Giovanni Li Volti and Venerando Rapisarda
Antioxidants 2020, 9(1), 30; https://doi.org/10.3390/antiox9010030 - 28 Dec 2019
Cited by 27 | Viewed by 4202
Abstract
Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B12, and transsulfuration to cystathionine, which needs pyridoxal-5’-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, [...] Read more.
Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B12, and transsulfuration to cystathionine, which needs pyridoxal-5’-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, peripheral vascular diseases, and cognitive impairment. Some evidence showed that exposure to these metals increased plasma homocysteine levels. Methods: A systematic review was carried out to clarify the relationship between homocysteine blood levels and exposure to toxic heavy metals (Lead, Cadmium, Mercury, and Chromium). Results: The results of this systematic review indicate that exposure to Pb, Cr, Cd, and Hg is connected with nonphysiological homocysteine levels or vitamin B12 and folate serum concentrations. Conclusions: These findings reinforce the importance of involvement in exposure to heavy metals in homocysteine metabolism. This supports the role of blood metals as potential upstream modifiable risk factors to prevent the development of other established risk factors as hyperhomocysteinemia. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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11 pages, 883 KiB  
Review
Oxidative Stress in Peripheral Arterial Disease (PAD) Mechanism and Biomarkers
by Salvatore Santo Signorelli, Salvatore Scuto, Elisa Marino, Anastasia Xourafa and Agostino Gaudio
Antioxidants 2019, 8(9), 367; https://doi.org/10.3390/antiox8090367 - 02 Sep 2019
Cited by 29 | Viewed by 4227
Abstract
Hemodynamic dysfunction mainly characterizes pathophysiology of peripheral arterial disease (PAD) leading to chronic ischemia. Hemodynamic dysfunction is the origin of intermittent claudication (chronic PAD) or of critical limb ischemia (very severe PAD). Notably, it is well known that oxidative stress (OxS) plays a [...] Read more.
Hemodynamic dysfunction mainly characterizes pathophysiology of peripheral arterial disease (PAD) leading to chronic ischemia. Hemodynamic dysfunction is the origin of intermittent claudication (chronic PAD) or of critical limb ischemia (very severe PAD). Notably, it is well known that oxidative stress (OxS) plays a pathophysiological role in PAD. The higher production of reactive oxygen species (ROS) from OxS and reduced redox capability are two crucial players in initiating and progressing PAD. A number of biomarkers highlight OxS and monitor it in PAD. The present review summarizes data on OxS, on biomarkers available to mark OxS occurrence and to monitor on PAD progression, as well as to evaluate the effects treatments in PAD patients. In conclusion, by detailing OxS and its biomarkers, we hope to encourage more studies to focus on drugs which combat OxS and inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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