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Oxidative Damage on Biomolecules and Antioxidants

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A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (16 November 2019) | Viewed by 26581

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Prof. Dr. Hafize Uzun

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Guest Editor

Department of Medical Biochemistry, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey

Dr. Karolin Yanar

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Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Department of Medical Biochemistry, Istanbul, Turkey

Prof. Dr. Pınar Atukeren

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Guest Editor

Department of Medical Biochemistry, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey

Special Issue Information

Dear Colleagues,

There is a growing experimental interest to understand oxidative stress-related diseases’ mechanisms and novel therapeutic approaches. Oxidative stress is induced by an impaired redox balance, due to the excessive production of free radical-induced reactive oxygen species (ROS) or the dysfunction of the antioxidant status. ROS are strong oxidants capable of damaging lipids, proteins, and DNA. The oxidative products issuing from each biomolecule are complex and variable. The general mechanisms of oxidative damage to biomolecules, which results in the dysfunction of the biomolecules and interference with the signaling pathways, leading to oxidative stress-induced diseases. Due to the deleterious effects of oxidative stress, cells developed different mechanisms called antioxidants to cope with the challenge. Antioxidant molecules, both enzymatic and non-enzymatic, are preventative or repair-systems against ROS, they may be endogenous and exogenous or primary and secondary, natural or synthetic. Although efficient, the antioxidant enzymes and compounds do not prevent the oxidative damage completely.

Oxidative stress is well known to be involved in the pathogenesis of various diseases, including neurodegenerative diseases, inflammation, aging, atherosclerosis, hypertension, diabetes mellitus, ischemic diseases, and cancer. The biomarkers that can be used to assess oxidative stress have been attracting interest because the accurate assessment of such stress is necessary for investigation of various pathological conditions, as well as to evaluate the efﬁcacy of drugs. With this Special Issue, the most recent experimental and therapeutic information will be discussed and gathered in order to understand the pathophysiological mechanisms related to oxidative stress-mediated diseases, which will serve as a basis for future studies.

Prof. Dr. Hafize Uzun
Dr. Karolin Yanar
Prof. Dr. Pınar Atukeren
Guest Editors

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Keywords

Oxidative stress
Reactive oxygen species
Free radicals
Redox balance
Antioxidant

Published Papers (6 papers)

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Research

15 pages, 3181 KiB

Open AccessArticle

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

by Rade Vukovic, Igor Kumburovic, Jovana Joksimovic Jovic, Nemanja Jovicic, Jelena S. Katanic Stankovic, Vladimir Mihailovic, Milos Djuric, Stefan Velickovic, Aleksandra Arnaut, Dragica Selakovic and Gvozden Rosic

Biomolecules 2019, 9(12), 892; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9120892 - 17 Dec 2019

Cited by 20 | Viewed by 3423

Abstract

Since cisplatin therapy is usually accompanied with numerous toxicities, including neurotoxicity, that involve tissue oxidative damage, the aim of this study was to evaluate the possible protective effect of N-acetylcysteine (NAC) on the anxiogenic response to cisplatin (CIS). Thirty-two male Wistar albino rats divided into four groups (control, cisplatin, NAC, and CIS + NAC). All treatments were delivered intraperitoneally. On day one, the control and cisplatin groups received saline while the NAC and CIS + NAC groups were administered with NAC (500 mg/kg). On the fifth day, the control group received saline while the CIS group was treated with cisplatin (7.5 mg/kg), the NAC group again received NAC (500 mg/kg), and the CIS + NAC group was simultaneously treated with cisplatin and NAC (7.5 and 500 mg/kg, respectively). Behavioral testing, performed on the tenth day in the open field (OF) and elevated plus maze (EPM) tests, revealed the anxiogenic effect of cisplatin that was significantly attenuated by NAC. The hippocampal sections evaluation showed increased oxidative stress (increased lipid peroxidation and decline in antioxidant enzymes activity) and proapoptotic action (predominantly by diminished antiapoptotic gene expression) following a single dose of cisplatin. NAC supplementation along with cisplatin administration reversed the prooxidative and proapoptotic effects of cisplatin. In conclusion, the results obtained in this study confirmed that antioxidant supplementation with NAC may attenuate the cisplatin-induced anxiety. The mechanism of anxiolytic effect achieved by NAC may include the decline in oxidative damage that down regulates increased apoptosis and reverses the anxiogenic action of cisplatin. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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12 pages, 2695 KiB

Open AccessArticle

Characterization and Antioxidant Activity of a Low-Molecular-Weight Xanthan Gum

by Xiaolong Hu, Kangli Wang, Miao Yu, Peixin He, Hanzhen Qiao, Huiru Zhang and Zichao Wang

Biomolecules 2019, 9(11), 730; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9110730 - 12 Nov 2019

Cited by 48 | Viewed by 4057

Abstract

In the present work, a low-molecular-weight xanthan gum (LW-XG) was successfully obtained via biodegradation of commercial xanthan by the endophytic fungus Chaetomium globosum CGMCC 6882. The monosaccharide composition of LW-XG was glucose, mannose, and glucuronic acid in a molar ratio of 1.63:1.5:1.0. The molecular weight of LW-XG was 4.07 × 10⁴ Da and much smaller than that of commercial xanthan (2.95 × 10⁶ Da). Antioxidant assays showed that LW-XG had a good scavenging ability on DPPH radicals, superoxide anions, and hydroxyl radicals and good ferric reducing power. Moreover, LW-XG exhibited excellent protective effect on H₂O₂-injured Caco-2 cells. Results of this work suggested that LW-XG could be used in foods or pharmaceuticals to alleviate and resist the oxidative damage induced by the overproduction of reactive oxygen species. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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17 pages, 1736 KiB

Open AccessArticle

Antioxidant Barrier, Redox Status, and Oxidative Damage to Biomolecules in Patients with Colorectal Cancer. Can Malondialdehyde and Catalase Be Markers of Colorectal Cancer Advancement?

by Justyna Zińczuk, Mateusz Maciejczyk, Konrad Zaręba, Wioletta Romaniuk, Adam Markowski, Bogusław Kędra, Anna Zalewska, Anna Pryczynicz, Joanna Matowicka-Karna and Katarzyna Guzińska-Ustymowicz

Biomolecules 2019, 9(10), 637; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9100637 - 22 Oct 2019

Cited by 74 | Viewed by 4409

Abstract

This study is the first to assess the diagnostic utility of redox biomarkers in patients with colorectal cancer (CRC). Antioxidant barrier (Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), uric acid (UA), reduced glutathione (GSH)), redox status (total antioxidant (TAC)/oxidant status (TOS), ferric reducing ability (FRAP)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA)) were measured in serum/plasma samples of 50 CRC patients. The activity of SOD was significantly higher whereas the activity of CAT, GPx and GR was considerably lower in CRC patients compared to the control group (p < 0.0001). Levels of UA, TOS, and OSI and concentrations of AGE, AOPP, and MDA were significantly higher, and the levels of GSH, TAC, and FRAP were considerably lower in CRC patients compared to the healthy controls (p < 0.0001). AUC for CAT with respect to presence of lymph node metastasis was 0.7450 (p = 0.0036), whereas AUC for MDA according to the depth of tumour invasion was 0.7457 (p = 0.0118). CRC is associated with enzymatic/non-enzymatic redox imbalance as well as increased oxidative damage to proteins and lipids. Redox biomarkers can be potential diagnostic indicators of CRC advancement. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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23 pages, 15042 KiB

Open AccessArticle

Protective Effects of Sesamin against UVB-Induced Skin Inflammation and Photodamage In Vitro and In Vivo

by Tzu-Yu Lin, Po-Yuan Wu, Chien-Wei Hou, Ting-Yi Chien, Qiao-Xin Chang, Kuo-Ching Wen, Chien-Yih Lin and Hsiu-Mei Chiang

Biomolecules 2019, 9(9), 479; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9090479 - 12 Sep 2019

Cited by 48 | Viewed by 5652

Abstract

Ultraviolet (UV) exposure has been demonstrated as the most critical factor causing extrinsic skin aging and inflammation. This study explored the protective effects and mechanisms of sesamin against skin photodamage. Sesamin reduced intracellular reactive oxygen species production after UVB irradiation in human dermal fibroblasts. The sesamin treatment attenuated mitogen-activated protein (MAP) kinase phosphorylation and matrix metalloproteinase (MMPs) overexpression induced by UVB exposure, and it significantly enhanced the tissue inhibitor of metalloproteinase-1 protein expression. Sesamin also elevated the total collagen content in human fibroblasts by inhibiting UVB-induced mothers against decapentaplegic homolog 7 (Smad7) protein expression. Sesamin reduced UVB-induced inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2) overexpression and inhibited nuclear factor-kappa B (NF-κB) translocation. Moreover, sesamin may regulate the c-Jun N-terminal kinases (JNK) and p38 MAP kinase pathways, which inhibit COX-2 expression. Sesamin could reduce UVB-induced inflammation, epidermal hyperplasia, collagen degradation, and wrinkle formation in hairless mice. It also reduced MMP-1, interleukin (IL-1), i-NOS, and NF-κB in the mouse skin. These results demonstrate that sesamin had antiphotodamage and anti-inflammatory activities. Sesamin has potential for use as a skin protection agent in antiphotodamage and skin care products. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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26 pages, 5288 KiB

Open AccessArticle

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

by Kabeer Abubakar, Maryam Muhammad Mailafiya, Abubakar Danmaigoro, Samaila Musa Chiroma, Ezamin Bin Abdul Rahim and Md Zuki Abu Bakar @ Zakaria

Biomolecules 2019, 9(9), 453; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9090453 - 06 Sep 2019

Cited by 40 | Viewed by 5100

Abstract

Lead (Pb) is a toxic, environmental heavy metal that induces serious clinical defects in all organs, with the nervous system being its primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty-six male Sprague Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and 6 rats in each of groups, i.e., the lead-treated group (LTG) (50 mg/kg lead acetate for four weeks), recovery group (RC) (50 mg/kg lead acetate for four weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for four weeks, followed by 100 mg/kg curcumin for four weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for four weeks, followed by 200 mg/kg curcumin for four weeks). All experimental groups received oral treatment via orogastric tube on alternate days. Motor function was assessed using a horizontal bar method. The cerebellar concentration of Pb was evaluated using ICP-MS technique. Pb-administered rats showed a significant decrease in motor scores and Superoxide Dismutase (SOD) activity with increased Malondialdehyde (MDA) levels. In addition, a marked increase in cerebellar Pb concentration and alterations in the histological architecture of the cerebellar cortex layers were recorded. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum, and ameliorated the markers of oxidative stress, as well as restored the histological architecture of the cerebellum. The results of this study suggest that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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13 pages, 4723 KiB

Open AccessArticle

Wu Shan Shen Cha (Malus asiatica Nakai. Leaves)-Derived Flavonoids Alleviate Alcohol-Induced Gastric Injury in Mice via an Anti-Oxidative Mechanism

by Bihui Liu, Chengfeng Zhang, Jing Zhang and Xin Zhao

Biomolecules 2019, 9(5), 169; https://0-doi-org.brum.beds.ac.uk/10.3390/biom9050169 - 03 May 2019

Cited by 14 | Viewed by 3007

Abstract

Wu Shan Shen Cha is the leaf of Malus asiatica Nakai., a special type of tea that is consumed in the same way as green tea. To study the effect of Wu Shan Shen Cha-derived flavonoids (WSSCF) on lesions in the stomach, a 15% hydrochloric acid–95% ethanol (volume ratio 4:6) solution was used to induce gastric injury in mice. The degree of gastric injury was assessed using tissue specimens, and the effects of WSSCF on the serum levels of antioxidant enzymes were investigated. The results showed that WSSCF could alleviate the damage of the gastric mucosa and gastric wall caused by the hydrochloric acid–ethanol solution, decrease the tissue and serum levels of malondialdehyde (MDA) in mice with gastric injury, and increase the serum levels of superoxide dismutase (SOD) and glutathione (GSH). The results of quantitative polymerase chain reaction (qPCR) showed that WSSCF could increase the mRNA expression of Mn-SOD, Cu/Zn-SOD, catalase (CAT), endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) in tissue specimens from mice with gastric injury and decrease the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). At the same time, the results of the high concentration of WSSCF (WSSCFH) group were closer to those of the drug (ranitidine) treatment group. Wu Shan Shen Cha-derived flavonoids had a good antioxidant effect, so as to play a preventive role in alcoholic gastric injury. Full article

(This article belongs to the Special Issue Oxidative Damage on Biomolecules and Antioxidants)

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