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Chemistry and Pharmacology of Modulators of Oxidative Stress 2018

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A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (28 February 2019) | Viewed by 82998

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Prof. Dr. Luciano Saso

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Faculty of Pharmacy and Medicine, Sapienza University of Rome, 00185 Rome, Italy
Interests: pharmacology; therapeutic modulators of oxidative stress
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Prof. Dr. Neda Mimica-Dukić

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Biochemistry and Environmental Protection, Department of Chemistry, University of Novi Sad, Trg Dositeja Obradovića 3, 21000 Novi Sad, Serbia
Interests: chemotaxonomy; volatile compounds; antioxidant activity; anti-inflammatory; plant phenolics
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Prof. Dr. Ryszard Amarowicz

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Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, 10-748 Olsztyn, Poland
Interests: analytical chemistry; polymer chemistry; food science
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Dear Colleagues,

As we all know, oxidative stress (OS) is involved to many pathologies, ranging from cancer to neurodegenerative diseases, and modulators of OS can be of therapeutic value in some of them, acting by different mechanisms, such as scavenging and metal chelating effects, mimicking the antioxidant enzymes or upregulation of their expression, activating the nuclear factor erythroid 2-related factor 2 (Nrf2), inhibiting pro-oxidant enzymes, etc.

This Special Issue aims to provide a forum for the dissemination of the latest information on new methods for extraction, isolation, synthesis, or derivatization of modulators of OS stress, and on in vitro and in vivo testing of their biological activities in view of possible pharmacological

Prof. Dr. Luciano SASO
Prof. Dr. Neda MIMICA-DUKIĆ
Prof. Dr. Ryszard AMAROWICZ
Guest Editors

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Keywords

oxidative stress modulators
antioxidants
pro-oxidants
enzymes
synthesis
chemistry
pharmacology
polyphenols
Nrf2

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Chemistry, Biology and Pharmacology of Modulators of Oxidative Stress in Molecules (5 articles)

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Research

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14 pages, 1415 KiB

Open AccessArticle

A Low Glycemic Index Decreases Inflammation by Increasing the Concentration of Uric Acid and the Activity of Glutathione Peroxidase (GPx3) in Patients with Polycystic Ovary Syndrome (PCOS)

by Małgorzata Szczuko, Marta Zapalowska-Chwyć and Radosław Drozd

Molecules 2019, 24(8), 1508; https://doi.org/10.3390/molecules24081508 - 17 Apr 2019

Cited by 29 | Viewed by 5605

Abstract

Introduction: According to a review of the literature, there is a lack of data on the mechanisms that participate in the suppression of inflammation that accompanies polycystic ovary syndrome (PCOS). Additionally, the changes in oxidative status resulting from a low-calorie diet have not been studied in a group of women with PCOS, and the oxidation and reduction processes associated with PCOS have not been explained. Material and methods: The study involved 49 women who were diagnosed with PCOS according to Rotterdam’s criteria, and 24 women voluntarily agreed to a three-month dietary intervention. The dietary intervention was carried out for 3 months. Glutathione peroxidase (GPx3) activity, the Ferric reducing ability of plasma, and uric acid concentration were measured spectrophotometrically both before and after the intervention. Statistical analysis was performed with the Statistica 10.0 software package, and a Pearson’s correlation matrix was generated. Results: A lower concentration of GPx3 was observed in women with PCOS (before the dietetic intervention began) compared with the GPx3 levels in healthy women. A relationship was shown between GPx3 levels and the concentration of prolactin, insulin on fasting, and triglycerides. After the dietary intervention, increases in uric acid and GPx3 activity were noted, as well as numerous relationships between anthropometric and biochemical parameters. The ferric reducing/antioxidant power did not change significantly. Conclusions: Inhibiting the effect of prolactin (by the level of reactive oxygen species) on the activity of GPx3 could be a starting point for the increase in antioxidative stress and the development of the inflammatory state associated with PCOS pathophysiology. Following a low-calorie diet with a lower glycemic index is proposed to silence inflammation by increasing the concentration of uric acid. During GPx3 mobilization, women with PCOS have a higher demand for selenium, and its deficiencies may contribute to disordered thyroid hormone synthesis. The three-month dietary intervention did not silence redox processes in the examined group of women. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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20 pages, 2932 KiB

Open AccessFeature PaperArticle

Regulation of the Nrf2 Pathway by Glycogen Synthase Kinase-3β in MPP⁺-Induced Cell Damage

by Güliz Armagan, Elvin Sevgili, Fulya Tuzcu Gürkan, Fadime Aydın Köse, Tuğçe Bilgiç, Taner Dagcı and Luciano Saso

Molecules 2019, 24(7), 1377; https://doi.org/10.3390/molecules24071377 - 8 Apr 2019

Cited by 37 | Viewed by 3940

Abstract

Recently, nuclear translocation and stability of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) have gained increasing attention in the prevention of oxidative stress. The present study was aimed to evaluate the regulatory role of glycogen synthase kinase-3β (GSK-3β) inhibition by tideglusib through the Nrf2 pathway in a cellular damage model. Gene silencing (siRNA-mediated) was performed to examine the responses of Nrf2-target genes (i.e., heme oxygenase-1, NAD(P)H:quinone oxidoreductase1) to siRNA depletion of Nrf2 in MPP⁺-induced dopaminergic cell death. Nrf2 and its downstream regulated genes/proteins were analyzed using Real-time PCR and Western Blotting techniques, respectively. Moreover, free radical production, the changes in mitochondrial membrane potential, total glutathione, and glutathione-S-transferase were examined. The possible contribution of peroxisome proliferator-activated receptor gamma (PPARγ) to tideglusib-mediated neuroprotection was evaluated. The number of viable cells and mitochondrial membrane potential were increased following GSK-3β enzyme inhibition against MPP⁺. HO-1, NQO1 mRNA/protein expressions and Nrf2 nuclear translocation significantly triggered by tideglusib. Moreover, the neuroprotection by tideglusib was not observed in the presence of siRNA Nrf2. Our study supports the idea that GSK-3β enzyme inhibition may modulate the Nrf2/ARE pathway in cellular damage and the inhibitory role of tideglusib on GSK-3β along with PPARγ activation may be responsible for neuroprotection. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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18 pages, 2983 KiB

Open AccessArticle

Resveratrol and Quercetin Administration Improves Antioxidant DEFENSES and reduces Fatty Liver in Metabolic Syndrome Rats

by Maria Esther Rubio-Ruiz, Verónica Guarner-Lans, Agustina Cano-Martínez, Eulises Díaz-Díaz, Linaloe Manzano-Pech, Anel Gamas-Magaña, Vicente Castrejón-Tellez, Concepción Tapia-Cortina and Israel Pérez-Torres

Molecules 2019, 24(7), 1297; https://doi.org/10.3390/molecules24071297 - 3 Apr 2019

Cited by 51 | Viewed by 4970

Abstract

Mixtures of resveratrol (RSV) + quercetin (QRC) have antioxidant properties that probably impact on fatty liver in metabolic syndrome (MS) individuals. Here, we study the effects of a mixture of RSV + QRC on oxidative stress (OS) and fatty liver in a rat model of MS. Weanling male Wistar rats were separated into four groups (n = 8): MS rats with 30% sucrose in drinking water plus RSV + QRC (50 and 0.95 mg/kg/day, respectively), MS rats without treatment, control rats (C), and C rats plus RSV + QRC. MS rats had increased systolic blood pressure, triglycerides, insulin levels, insulin resistance index homeostasis model (HOMA), adiponectin, and leptin. The RSV + QRC mixture compensated these variables to C values (p < 0.01) in MS rats. Lipid peroxidation and carbonylation were increased in MS. Total antioxidant capacity and glutathione (GSH) were decreased in MS and compensated in MS plus RVS + QRC rats. Catalase, superoxide dismutase isoforms, peroxidases, glutathione-S-transferase, glutathione reductase, and the expression of Nrf2 were decreased in MS and reversed in MS plus RVS + QRC rats (p < 0.01). In conclusion, the mixture of RSV + QRC has benefic effects on OS in fatty liver in the MS rats through the improvement of the antioxidant capacity and by the over-expression of the master factor Nrf2, which increases the antioxidant enzymes and GSH recycling. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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14 pages, 2912 KiB

Open AccessArticle

Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload

by Peng Guan, Zhi-Min Sun, Li-Fei Luo, Ya-Shuo Zhao, Sheng-Chang Yang, Fu-Yang Yu, Na Wang and En-Sheng Ji

Molecules 2019, 24(6), 1184; https://doi.org/10.3390/molecules24061184 - 26 Mar 2019

Cited by 25 | Viewed by 4653

Abstract

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H₂ can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H₂ against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H₂ treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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13 pages, 3984 KiB

Open AccessArticle

Autophagy in Crotonaldehyde-Induced Endothelial Toxicity

by Seung Eun Lee, Hye Rim Park, Cheung-Seog Park, Hyun-Jong Ahn, Jeong-Je Cho, Jongsung Lee and Yong Seek Park

Molecules 2019, 24(6), 1137; https://doi.org/10.3390/molecules24061137 - 21 Mar 2019

Cited by 8 | Viewed by 2920

Abstract

Crotonaldehyde is an extremely toxic α,β-unsaturated aldehyde found in cigarette smoke, and it causes inflammation and vascular dysfunction. Autophagy has been reported to play a key role in the pathogenesis of vascular diseases. However, the precise mechanism underlying the role of acute exposure crotonaldehyde in vascular disease development remains unclear. In the present study, we aimed to investigate the effect of crotonaldehyde-induced autophagy in endothelial cells. Acute exposure to crotonaldehyde decreased cell viability and induced autophagy followed by cell death. In addition, inhibiting the autophagic flux markedly promoted the viability of endothelial cells exposed to high concentrations of crotonaldehyde. Crotonaldehyde activated the AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK) pathways, and pretreatment with inhibitors specific to these kinases showed autophagy inhibition and partial improvement in cell viability. These data show that acute exposure to high concentrations of crotonaldehyde induces autophagy-mediated cell death. These results might be helpful to elucidate the mechanisms underlying crotonaldehyde toxicity in the vascular system and contribute to environmental risk assessment. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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13 pages, 3738 KiB

Open AccessArticle

Proanthocyanidins Protect against β-Hydroxybutyrate-Induced Oxidative Damage in Bovine Endometrial Cells

by Xi Cheng, Shuhua Yang, Chuang Xu, Lanzhi Li, Yi Zhang, Yang Guo, Cai Zhang, Peng Li, Miao Long and Jianbin He

Molecules 2019, 24(3), 400; https://doi.org/10.3390/molecules24030400 - 22 Jan 2019

Cited by 21 | Viewed by 4459

Abstract

Metabolic diseases, such as ketosis, are closely associated with decreased reproductive performance (such as delayed estrus and decreased pregnancy rate) in dairy cows. The change of β-hydroxybutyrate (BHBA) concentration in dairy cattle is an important mechanism leading to ketosis, and its blood concentration in ketotic cows is always significantly higher than in nonketotic cows. Many studies indicated that BHBA can induce oxidative damage in liver and other organs. Proanthocyanidins (PCs) have gained substantial attention in the last decade as strong antioxidative substances. This study aimed to demonstrate a protective effect of PCs against BHBA-induced oxidative stress damage in bovine endometrial (BEND) cells by activating the nuclear erythroid2-related factor2 (Nrf2) signaling pathway. Our research show that PCs could significantly increase activities of catalase (CAT) and glutathione peroxidase (GSH-PX), glutathione (GSH) content, and antioxidant capacity (T-AOC), while significantly decreasing malondialdehyde (MDA) content in BEND cells. Both mRNA and protein expression levels of Nrf2 were significantly increased in BEND cells, and glutamate–cysteine ligase catalytic subunit (GCLC), heme oxygenase 1 (HO-1), manganese superoxide dismutase (Mn-SOD), and NAD(P)H quinone dehydrogenase 1 (NQO-1) were also significantly increased. These results indicate that PCs can antagonize BHBA-induced oxidative damage by activating the Nrf2 signaling pathway to exert an antioxidant effect. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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15 pages, 1429 KiB

Open AccessArticle

Synthesis, In Vitro Biological Evaluation, and Oxidative Transformation of New Flavonol Derivatives: The Possible Role of the Phenyl-N,N-Dimethylamino Group

by Peter Szabados-Furjesi, David Pajtas, Aliz Barta, Evelin Csepanyi, Attila Kiss-Szikszai, Arpad Tosaki and Istvan Bak

Molecules 2018, 23(12), 3161; https://doi.org/10.3390/molecules23123161 - 30 Nov 2018

Cited by 11 | Viewed by 3653

Abstract

Six new flavonols (6a–f) were synthesized with Claisen–Schmidt and Suzuki reactions and they were fully characterized by spectroscopic methods. In order to evaluate their antioxidant activities, their oxygen radical absorption capacity and ferric reducing antioxidant power were measured, along with their free radical scavenging activity against 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) and 2,2-diphenyl-1-picrylhydrazylradicals. In addition, their cytotoxicity on H9c2 cardiomyoblast cells was also assessed by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Compounds bearing the phenyl-N,N-dimethylamino group (6a, 6c, and 6e) exhibited promising antioxidant potency and did not have any cytotoxic effect. After a consideration of these data, the oxidative transformation of the 6c compound was investigated in vitro with a chemical Fenton reaction and the identification of the formed oxidation products was performed by mass spectrometry. Two potential metabolites were detected. Based on these results, compound 6c can be a model compound for future developments. Overall, this work has proved the involvement of the phenyl-N,N-dimethylamino group in the antioxidant activity of flavonols. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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15 pages, 797 KiB

Open AccessArticle

Correlation of Paraoxonase-1 with the Severity of Crohn’s Disease

by Katarzyna Szczeklik, Tomasz Mach, Dorota Cibor, Danuta Owczarek, Jacek Sapa, Monika Papież, Jolanta Pytko-Polończyk and Wirginia Krzyściak

Molecules 2018, 23(10), 2603; https://doi.org/10.3390/molecules23102603 - 11 Oct 2018

Cited by 10 | Viewed by 3276

Abstract

Diagnostics of Crohn’s disease (CD) requires noninvasive biomarkers facilitating early detection and differentiation of the disease. Therefore, in this study, we aimed to determine the relationship between paraoxonase-1 (PON-1), the severity of CD, oxidative stress, and inflammation in CD. The CD activity index was based on the current classification. Plasma PON-1 was measured in 47 patients with CD, and in 23 control volunteers. Using quantitative variables such as receiver operating characteristics (ROC) (area under the curve (AUC)), the diagnostic utility of PON-1 in differentiating the severity of CD was assessed. Circulating PON-1 was found to be decreased in the CD group compared to the control group (269.89 vs. 402.56 U/L, respectively), and it correlated well with the disease activity. PON-1 correlated positively with hemoglobin (Hb) (r = 0.539, p < 0.001), hematocrit (Ht) (r = 0.48, p < 0.001), total cholesterol (TC) (r = 0.343, p < 0.001), high density lipoprotein (HDL) (r = 0.536, p < 0.001), low density lipoprotein (LDL) (r = 0.54, p < 0.001), and triglyceride (TG) (r = 0.561, p < 0.001) and correlated negatively with white blood cell count (WBC) (r = −0.262, p = 0.029), platelet count (PLT) (r = −0.326, p = 0.006), C-reactive protein (CRP) (r = −0.61, p < 0.001), and malondialdehyde (MDA) (r = −0.924, p < 0.001). PON-1 as a marker for CD differentiation possessed a sensitivity and specificity of 93.62% and 91.30%, respectively. CD was found to be associated with the decrease in the levels of PON-1, which correlates well with activity of the disease and reflects the intensification of inflammation, as well as intensified lipid peroxidation. High sensitivity and specificity of PON-1 determines its selection as a good screening test for CD severity. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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12 pages, 2029 KiB

Open AccessArticle

Kaempferol Attenuates ROS-Induced Hemolysis and the Molecular Mechanism of Its Induction of Apoptosis on Bladder Cancer

by Ping Wu, Xiaofeng Meng, Huade Zheng, Qin Zeng, Tianfeng Chen, Wen Wang, Xia Zhang and Jianyu Su

Molecules 2018, 23(10), 2592; https://doi.org/10.3390/molecules23102592 - 10 Oct 2018

Cited by 79 | Viewed by 5080

Abstract

Bladder cancer has become the most common malignant urinary carcinoma. Studies have shown that significant antioxidant and bladder cancer-fighting properties of several plant-based diets like Psidium guajava, ginger and amomum, are associated with their high kaempferol content. In this paper, we evaluated the antioxidant and anticancer activities of kaempferol and its mechanism of induction to apoptosis on bladder cancer cells. Our findings demonstrated that kaempferol showed an obvious radical scavenging activity in erythrocytes damaged by oxygen. Kaempferol promoted antioxidant enzymes, inhibited ROS generation and lipid peroxidation and finally prevented the occurrence of hemolysis. Additionally, kaempferol exhibited a strong inhibitory effect on bladder cancer cells and high safety on normal bladder cells. At the molecular level, kaempferol suppressed EJ bladder cancer cell proliferation by inhibiting the function of phosphorylated AKT (p-AKT), CyclinD1, CDK4, Bid, Mcl-1 and Bcl-xL, and promoting p-BRCA1, p-ATM, p53, p21, p38, Bax and Bid expression, and finally triggering apoptosis and S phase arrest. We found that Kaempferol exhibited strong anti-oxidant activity on erythrocyte and inhibitory effects on the growth of cancerous bladder cells through inducing apoptosis and S phase arrest. These findings suggested that kaempferol might be regarded as a bioactive food ingredient to prevent oxidative damage and treat bladder cancer. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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Oxidative Stress: A Key Modulator in Neurodegenerative Diseases

by Anju Singh, Ritushree Kukreti, Luciano Saso and Shrikant Kukreti

Molecules 2019, 24(8), 1583; https://doi.org/10.3390/molecules24081583 - 22 Apr 2019

Cited by 1389 | Viewed by 43471

Abstract

Oxidative stress is proposed as a regulatory element in ageing and various neurological disorders. The excess of oxidants causes a reduction of antioxidants, which in turn produce an oxidation–reduction imbalance in organisms. Paucity of the antioxidant system generates oxidative-stress, characterized by elevated levels of reactive species (oxygen, hydroxyl free radical, and so on). Mitochondria play a key role in ATP supply to cells via oxidative phosphorylation, as well as synthesis of essential biological molecules. Various redox reactions catalyzed by enzymes take place in the oxidative phosphorylation process. An inefficient oxidative phosphorylation may generate reactive oxygen species (ROS), leading to mitochondrial dysfunction. Mitochondrial redox metabolism, phospholipid metabolism, and proteolytic pathways are found to be the major and potential source of free radicals. A lower concentration of ROS is essential for normal cellular signaling, whereas the higher concentration and long-time exposure of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, ultimately resulting in necrosis and apoptotic cell death. Normal and proper functioning of the central nervous system (CNS) is entirely dependent on the chemical integrity of brain. It is well established that the brain consumes a large amount of oxygen and is highly rich in lipid content, becoming prone to oxidative stress. A high consumption of oxygen leads to excessive production of ROS. Apart from this, the neuronal membranes are found to be rich in polyunsaturated fatty acids, which are highly susceptible to ROS. Various neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), among others, can be the result of biochemical alteration (due to oxidative stress) in bimolecular components. There is a need to understand the processes and role of oxidative stress in neurodegenerative diseases. This review is an effort towards improving our understanding of the pivotal role played by OS in neurodegenerative disorders. Full article

(This article belongs to the Special Issue Chemistry and Pharmacology of Modulators of Oxidative Stress 2018)

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