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      Curcumin attenuates harmful effects of arsenic on neural stem/progenitor cells

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          Abstract

          Objective:

          Arsenic, an environmental pollutant, decreases neuronal migration as well as cellular maturation and inhibits the proliferation of neural progenitor cells. Curcumin has been described as an antioxidant and neuroprotective agent with strong therapeutic potential in some neurological disorders. Human adipose-derived stem cells (hADSCs), a source of multipotent stem cells, can self-renew and differentiate into neural cells. The aim of the present study was to investigate the preventive effect of curcumin against arsenic toxic effects on the viability, telomerase activity, and apoptosis of neural stem/progenitor cells (NSPCs) derived from hADSCs.

          Materials and Methods:

          The characteristics of human adipose tissue were identified by immunocytochemistry for surface markers namely, CD105, CD73, and CD90. Using neurosphere assay, hADSCs were differentiated into neuronal cells. To characterize neural cells, expression of nestin, SOX2, MAP2, and GFAP were assessed by immunocytochemistry. Cytotoxicity and viability of NSPCs were evaluated by MTT assay. Reactive oxygen species (ROS) generated by arsenic exposure, were measured and caspase 3/7 activity and caspase-3 processing as well as the telomerase activity were determined.

          Results:

          The isolated hADSCs positively expressed CD105, CD73, and CD90. Nestin, Sox2, GFAP, and MAP2 were expressed in the neurospheres derived from hADSCs. Curcumin/arsenic co-treatment significantly increased telomerase activity of NSPCs compared to arsenic group. Furthermore, curcumin significantly reduced arsenic-induced apoptosis (via inactivation of caspases) as well as arsenic-associated ROS generation.

          Conclusion:

          Our findings revealed that curcumin has the potential to prevent harmful effects of arsenic on neurogenesis.

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          Zinc deficiency, DNA damage and cancer risk.

          Emily Ho (2004)
          A large body of evidence suggests that a significant percentage of deaths resulting from cancer in the United States could be avoided through greater attention to proper and adequate nutrition. Although many dietary compounds have been suggested to contribute to the prevention of cancer, there is strong evidence to support the fact that zinc, a key constituent or cofactor of over 300 mammalian proteins, may be of particular importance in host defense against the initiation and progression of cancer. Remarkably, 10% of the U.S. population consumes less than half the recommended dietary allowance for zinc and are at increased risk for zinc deficiency. Zinc is known to be an essential component of DNA-binding proteins with zinc fingers, as well as copper/zinc superoxide dismutase and several proteins involved in DNA repair. Thus, zinc plays an important role in transcription factor function, antioxidant defense and DNA repair. Dietary deficiencies in zinc can contribute to single- and double-strand DNA breaks and oxidative modifications to DNA that increase risk for cancer development. This review will focus on potential mechanisms by which zinc deficiency impairs host protective mechanisms designed to protect against DNA damage, enhances susceptibility to DNA-damaging agents and ultimately increases risk for cancer.
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            Arsenic Contamination of Groundwater: A Review of Sources, Prevalence, Health Risks, and Strategies for Mitigation

            Sangaru Shiv Shankar, Uma Shanker, Shikha (2014)
            Arsenic contamination of groundwater in different parts of the world is an outcome of natural and/or anthropogenic sources, leading to adverse effects on human health and ecosystem. Millions of people from different countries are heavily dependent on groundwater containing elevated level of As for drinking purposes. As contamination of groundwater, poses a serious risk to human health. Excessive and prolonged exposure of inorganic As with drinking water is causing arsenicosis, a deteriorating and disabling disease characterized by skin lesions and pigmentation of the skin, patches on palm of the hands and soles of the feet. Arsenic poisoning culminates into potentially fatal diseases like skin and internal cancers. This paper reviews sources, speciation, and mobility of As and global overview of groundwater As contamination. The paper also critically reviews the As led human health risks, its uptake, metabolism, and toxicity mechanisms. The paper provides an overview of the state-of-the-art knowledge on the alternative As free drinking water and various technologies (oxidation, coagulation flocculation, adsorption, and microbial) for mitigation of the problem of As contamination of groundwater.
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              MiR-219 Protects Against Seizure in the Kainic Acid Model of Epilepsy.

              Honghua Zheng, Rong Tang, Yi Yao … (2016)
              Emerging evidence indicates that certain microRNAs (miRNAs) play important roles in epileptogenesis. MiR-219 is a brain-specific miRNA and has been shown to negatively regulate the function of N-methyl-D-aspartate (NMDA) receptors by targeting Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)γ. Herein, we found that the level of miR-219 was decreased in both the kainic acid (KA)-induced epilepsy model and in cerebrospinal fluid specimens of epilepsy patients. Importantly, silencing of miR-219 by its antagomir in vivo resulted in seizure behaviors, abnormal cortical electroencephalogram (EEG) recordings in the form of high-amplitude and high-frequency discharges, and increased levels of CaMKIIγ and an NMDA receptor component, NR1, in a pattern similar to that found in KA-treated mice. Moreover, treatments with the miR-219 agomir in vivo alleviated seizures, abnormal EEG recordings, and decreased levels of CaMKIIγ and NR1 in KA-treated mice. Furthermore, treatment with MK-801, an antagonist of NMDA receptors, significantly alleviated abnormal EEG recordings induced by miR-219 antagomir. Together, these results demonstrate that miR-219 plays a crucial role in suppressing seizure formation in experimental models of epilepsy through modulating the CaMKII/NMDA receptor pathway and that miR-219 supplement may be a potential anabolic strategy for ameliorating epilepsy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Avicenna J Phytomed
                Journal ID (iso-abbrev): Avicenna J Phytomed
                Journal ID (publisher-id): IJP
                Title: Avicenna Journal of Phytomedicine
                Publisher: Mashhad University of Medical Sciences (Mashhad, Iran )
                ISSN (Print): 2228-7930
                ISSN (Electronic): 2228-7949
                Publication date (Print): Jul-Aug 2017
                Volume: 7
                Issue: 4
                Pages: 376-388
                Affiliations
                [1 ] Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran
                [2 ] Department of Clinical Biochemistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [3 ] Department of Biology, Kharazmi University of Tehran, Iran
                [4 ] Department of Neuroscience, Mashhad University of Medical Sciences, Mashhad, Iran
                [5 ] Epilepsy Research Center, Department of Neurology, and Department of Neurosurgery, Westfälische Wilhelms-Universität Münster, Münster, Germany
                Author notes
                [* ]Corresponding Author: Tel:+49 251 8355564, Fax:+49 251 8355551, gorjial@uni-muenster.de
                Article
                Publisher ID: AJP-7-376
                DOI: 10.22038/ajp.2016.19241.1742
                PMC ID: 5580875
                PubMed ID: 28884087
                SO-VID: edaac154-9bc8-44c2-acc9-c09a2855ac41
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 September 2016
                Date revision received : 8 December 2016
                Date accepted : 24 December 2016
                Categories
                Subject: Original Article

                Keywords: medicinal plants,toxicity,stem cells,neuronal injury
                Data availability:
                Keywords: medicinal plants, toxicity, stem cells, neuronal injury

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