47
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Effect of Arbutin on The Expression of Tumor Suppressor P53, BAX/BCL-2 Ratio and Oxidative Stress Induced by Tert-Butyl Hydroperoxide in Fibroblast and LNcap Cell Lines

      research-article

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          Arbutin (p-hydroxyphenyl-β-D-glucopyranoside) possesses beneficial functions including antioxidant, anti- inflammatory, and anti-tumoral activities. Due to the important role of oxidative stress and apoptosis in the successful treatment of cancer, understanding mechanisms that lead to apoptosis in cancer cells, is essential. The purpose of the current study was to evaluate the effect of arbutin on tert-butyl hydroperoxide (t-BHP)-induced oxidative stress and the related mechanisms in fibroblast and Lymph Node Carcinoma of the Prostate (LNCaP) cells.

          Materials and Methods

          In this experimental study, the LNCaP and fibroblast cell lines were pre-treated with arbutin (50, 250 and 1000 μM). After 24 hours, t-BHP (30 and 35 μM) was added to the cells. Viability was measured (at 24 and 48 hours) using MTT assay. The antioxidant effect of arbutin was measured by FRAP assay. The mRNA expression of P53 and BAX/BCL-2 ratio were measured using quantitative polymerase chain reaction (PCR). The percentage of apoptotic or necrotic cells was determined using a double staining annexin V fluorescein isothiocyanate (FITC) apoptosis detection kit.

          Results

          Arbutin pre-treatment increased the total antioxidative power and cell viability in the MTT assay and reduced BAX/BCL-2 ratio, P53 mRNA expression and necrosis in fibroblasts exposed to the oxidative agent (P<0.001). In addition, our results showed that arbutin can decrease cell viability, induce apoptosis and increase BAX/BCL-2 ratio in LNCaP cells at some specific concentrations (P<0.001).

          Conclusion

          Arbutin as a potential functional β-D-glucopyranoside has strong ability to selectively protect fibroblasts against t-BHP-induced cell damage and induce apoptosis in LNCaP cells.

          Related collections

          Most cited references40

          • Record: found
          • Abstract: found
          • Article: not found

          The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay.

          A simple, automated test measuring the ferric reducing ability of plasma, the FRAP assay, is presented as a novel method for assessing "antioxidant power." Ferric to ferrous ion reduction at low pH causes a colored ferrous-tripyridyltriazine complex to form. FRAP values are obtained by comparing the absorbance change at 593 nm in test reaction mixtures with those containing ferrous ions in known concentration. Absorbance changes are linear over a wide concentration range with antioxidant mixtures, including plasma, and with solutions containing one antioxidant in purified form. There is no apparent interaction between antioxidants. Measured stoichiometric factors of Trolox, alpha-tocopherol, ascorbic acid, and uric acid are all 2.0; that of bilirubin is 4.0. Activity of albumin is very low. Within- and between-run CVs are <1.0 and <3.0%, respectively, at 100-1000 micromol/liter. FRAP values of fresh plasma of healthy Chinese adults: 612-1634 micromol/liter (mean, 1017; SD, 206; n = 141). The FRAP assay is inexpensive, reagents are simple to prepare, results are highly reproducible, and the procedure is straightforward and speedy. The FRAP assay offers a putative index of antioxidant, or reducing, potential of biological fluids within the technological reach of every laboratory and researcher interested in oxidative stress and its effects.
            • Record: found
            • Abstract: found
            • Article: not found

            Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis.

            Oxidative stress basically defines a condition in which prooxidant-antioxidant balance in the cell is disturbed; cellular biomolecules undergo severe oxidative damage, ultimately compromising cells viability. In recent years, a number of studies have shown that oxidative stress could cause cellular apoptosis via both the mitochondria-dependent and mitochondria-independent pathways. Since these pathways are directly related to the survival or death of various cell types in normal as well as pathophysiological situations, a clear picture of these pathways for various active molecules in their biological functions would help designing novel therapeutic strategy. This review highlights the basic mechanisms of ROS production and their sites of formation; detail mechanism of both mitochondria-dependent and mitochondria-independent pathways of apoptosis as well as their regulation by ROS. Emphasis has been given on the redox-sensitive ASK1 signalosome and its downstream JNK pathway. This review also describes the involvement of oxidative stress under various environmental toxin- and drug-induced organ pathophysiology and diabetes-mediated apoptosis. We believe that this review would provide useful information about the most recent progress in understanding the mechanism of oxidative stress-mediated regulation of apoptotic pathways. It will also help to figure out the complex cross-talks between these pathways and their modulations by oxidative stress. The literature will also shed a light on the blind alleys of this field to be explored. Finally, readers would know about the ROS-regulated and apoptosis-mediated organ pathophysiology which might help to find their probable remedies in future.
              • Record: found
              • Abstract: found
              • Article: not found

              Prooxidant Activity of Polyphenols, Flavonoids, Anthocyanins and Carotenoids: Updated Review of Mechanisms and Catalyzing Metals.

              Natural antioxidants, including polyphenols, flavonoids, anthocyanins and carotenoids, play an important role in the treatment and prevention of a large number of diseases. However, studies indicate that natural antioxidants can act as prooxidants, which produce free radicals and cause DNA damage and mutagenesis. The prooxidant activity is typically catalyzed by metals, particularly transition metals such as Fe and Cu, present in biological systems. In this article, we aim to review new in vitro and in vivo evidence of the prooxidant activity of phenolics, flavonoids, anthocyanins and carotenoids. We highlight the role of catalyzing metals, including transition metals, non-transition metals and metalloids, in the prooxidant activity of natural antioxidants. Prooxidant structure-activity relationships of simple phenolics, flavonoids and anthocyanins and the role of cellular antioxidant defense, including endogenous antioxidant compounds and antioxidant enzymes, are also addressed in this review. In addition, we discuss the question, With respect to in vitro evidence of the prooxidant activity of antioxidants, can we translate this activity into biological systems and the human body? Copyright © 2016 John Wiley & Sons, Ltd.

                Author and article information

                Journal
                Cell J
                Cell J
                Royan Institute
                Cell Journal (Yakhteh)
                Royan Institute
                2228-5806
                2228-5814
                Jan-Mar 2021
                22 April 2020
                : 22
                : 4
                : 532-541
                Affiliations
                [1. ]Department of Clinical Biochemistry, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran
                [2. ]Student Research Committee, Babol University of Medical Sciences, Babol, Iran
                [3. ]Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
                [4. ]Cellular and Molecular Biology Research Center, Student Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
                [5. ]Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
                [6. ]Department of Genetics, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran
                Author notes
                [*Corresponding Address: ]P.O.Box: 4136747176Department of Clinical BiochemistryFaculty of MedicineBabol University of Medical Sciences BabolIran Email: pouramir@ 123456yahoo.com
                Article
                Cell-J-22-532
                10.22074/cellj.2021.6902
                7211292
                32347047
                aeb03812-0c07-4743-aadf-62e587e8a9e0
                Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited.

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

                History
                : 16 April 2019
                : 29 July 2019
                Categories
                Original Article
                Biochemistry
                Cellular and Molecular Biology
                Custom metadata
                Ebadollahi Sh, Pouramir M, Zabihi E, Golpour M, Aghajanpour-Mir M. The effect of arbutin on the expression of tumor suppressor P53, BAX/BCL- 2 ratio and oxidative stress induced by tert-butyl hydroperoxide in fibroblast and LNcap cell lines. Cell J. 2021; 22(4): 532-541. doi: 10.22074/cellj.2021.6902. This open-access article has been published under the terms of the Creative Commons Attribution Non-Commercial 3.0 (CC BY-NC 3.0).

                arbutin,fibroblast,lncap,oxidative stress,tert-butyl hydroperoxide

                Comments

                Comment on this article

                Related Documents Log