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      Antioxidant Effects of Eugenol on Oxidative Stress Induced by Hydrogen Peroxide in Islets of Langerhans Isolated from Male Mouse

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      1 , , 2 , 3
      International Journal of Hepatology
      Hindawi

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          Abstract

          Background

          The antioxidant system in islets of Langerhans is weak, which can lead to diabetes. Meanwhile, the main component of cloves that produce antioxidant effects is eugenol. Accordingly, the present study was conducted to investigate the antioxidant effect of eugenol on oxidative stress induced by hydrogen peroxide (H 2O 2) in islets of Langerhans isolated from the male mice.

          Materials and Methods

          In this experimental study, adult Naval Medical Research Institute (NMRI) mice (20-25 g) were prepared. The collagenase digestion method was used for dissecting the islets of Langerhans. H 2O 2 50  μM was administered for 30 min to induce oxidative stress, with 50, 100, and 200  μM of eugenol employed for 2 hours before the administration of H 2O 2. The experimental groups were divided into five groups: (control, H 2O 2, and H 2O 2+eugenol 50, 100, and 200  μM). Finally, the islet's lipid peroxidation and antioxidants levels were measured by the ELISA assay method.

          Results

          Malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), and catalase (CAT) increased in all groups when compared to the control ( P < 0.05). MDA diminished in H 2O 2+eugenol 50, 100, and 200  μM ( P < 0.01) groups versus the H 2O 2. TAC was elevated when eugenol 50, 100, and 200  μM was administered in oxidative stress-induced islets ( P < 0.001). Also, CAT increased in the H 2O 2+eugenol 50 ( P < 0.05) group in comparison with the H 2O 2 group.

          Conclusions

          In conclusion, H 2O 2 induced oxidative stress and lipid peroxidation in the islets, and administration of eugenol recovered these alterations by raising the level of TAC and CAT, while reducing MDA as a lipid peroxidation biomarker.

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          Most cited references24

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          Free radicals, metals and antioxidants in oxidative stress-induced cancer.

          Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-kappaB (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-kappaB, AP-1 are also reviewed.
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            Mechanisms of oxidative stress in plants: From classical chemistry to cell biology

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              Diabetes, oxidative stress and therapeutic strategies.

              Diabetes has emerged as a major threat to health worldwide. The exact mechanisms underlying the disease are unknown; however, there is growing evidence that excess generation of reactive oxygen species (ROS), largely due to hyperglycemia, causes oxidative stress in a variety of tissues. Oxidative stress results from either an increase in free radical production, or a decrease in endogenous antioxidant defenses, or both. ROS and reactive nitrogen species (RNS) are products of cellular metabolism and are well recognized for their dual role as both deleterious and beneficial species. In type 2 diabetic patients, oxidative stress is closely associated with chronic inflammation. Multiple signaling pathways contribute to the adverse effects of glucotoxicity on cellular functions. There are many endogenous factors (antioxidants, vitamins, antioxidant enzymes, metal ion chelators) that can serve as endogenous modulators of the production and action of ROS. Clinical trials that investigated the effect of antioxidant vitamins on the progression of diabetic complications gave negative or inconclusive results. This lack of efficacy might also result from the fact that they were administered at a time when irreversible alterations in the redox status are already under way. Another strategy to modulate oxidative stress is to exploit the pleiotropic properties of drugs directed primarily at other targets and thus acting as indirect antioxidants. It appears important to develop new compounds that target key vascular ROS producing enzymes and mimic endogenous antioxidants. This strategy might prove clinically relevant in preventing the development and/or retarding the progression of diabetes associated with vascular diseases. Copyright © 2014 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Int J Hepatol
                Int J Hepatol
                IJH
                International Journal of Hepatology
                Hindawi
                2090-3448
                2090-3456
                2020
                30 December 2020
                : 2020
                : 5890378
                Affiliations
                1Department of Physiology, Faculty of Medicine, Student Research Committee, Dezful University of Medical Sciences, Dezful, Iran
                2Student Research Committee, Faculty School of Paramedical Sciences, Dezful University of Medical Sciences, Dezful, Iran
                3Faculty of Medicine, Dezful University of Medical Sciences, Dezful, Iran
                Author notes

                Academic Editor: Dirk Uhlmann

                Author information
                https://orcid.org/0000-0001-5249-3239
                https://orcid.org/0000-0002-7449-5953
                https://orcid.org/0000-0003-0572-5986
                Article
                10.1155/2020/5890378
                7787786
                33457017
                cc69a712-971d-44a4-a908-5eb7a1f1b643
                Copyright © 2020 Ali Akbar Oroojan et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 July 2020
                : 14 December 2020
                : 17 December 2020
                Funding
                Funded by: Vice-Chancellor of Research, Dezful University of Medical Sciences, Dezful, Iran
                Categories
                Research Article

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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