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      Aqueous Extracts of the Edible Gracilaria tenuistipitata are Protective Against H 2O 2-Induced DNA Damage, Growth Inhibition, and Cell Cycle Arrest

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          Abstract

          Potential antioxidant properties of an aqueous extract of the edible red seaweed Gracilaria tenuistipitata (AEGT) against oxidative DNA damage were evaluated. The AEGT revealed several antioxidant molecules, including phenolics, flavonoids and ascorbic acid. In a cell-free assay, the extract exhibited 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity that significantly reduced H 2O 2-induced plasmid DNA breaks in a dose-response manner ( P < 0.001). The AEGT also suppressed H 2O 2-induced oxidative DNA damage in H1299 cells by reducing the percentage of damaged DNA in a dose-response manner ( P < 0.001) as measured by a modified alkaline comet-nuclear extract (comet-NE) assay. The MTT assay results showed that AEGT confers significant protection against H 2O 2-induced cytotoxicity and that AEGT itself is not cytotoxic ( P < 0.001). Moreover, H 2O 2-induced cell cycle G2/M arrest was significantly released when cells were co-treated with different concentrations of AEGT ( P < 0.001). Taken together, these findings suggest that edible red algae Gracilaria water extract can prevent H 2O 2-induced oxidative DNA damage and its related cellular responses.

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          This review covers the marine natural products literature for the year 2000 and is organized phylogenetically, with sections on marine microorganisms and phytoplankton, green algae, brown algae, red algae, sponges, coelenterates, bryozoans, molluscs, tunicates. echinoderms and miscellaneous marine organisms. There is an emphasis on new structures, stressing their biological activities, source organisms and countries of origin, and also syntheses that confirm the structures of known compounds. The review contains 869 structures and 592 references, of which 434 appeared between January and December 2000.
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            Mitochondrial ROS generation and its regulation: mechanisms involved in H(2)O(2) signaling.

            Mitochondria are the main source of reactive oxygen species in the cell. These reactive oxygen species have long been known as being involved in oxidative stress. This is a review of the mechanisms involved in reactive oxygen species generation by the respiratory chain and some of the dehydrogenases and the control by thermodynamic and kinetic constraints. Mitochondrial ROS produced at the level of the bc1 complex as well at the level of complex I are discussed. It was recognized more than a decade ago that they can also function as signaling molecules. This signaling role will be developed both in terms of mechanism and in terms of mitochondrial ROS signaling. The notion that hydrogen peroxide acts not only as a damaging oxidant but also as a signaling molecule was proposed more than a decade ago. Hydrogen peroxide signaling can be either direct (oxidation of its target) or indirect (involving peroxiredoxins, for example). The consequences of ROS signaling on crucial biologic processes such as cell proliferation and differentiation are discussed.
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              Neuroprotective strategies involving ROS in Alzheimer disease.

              Alzheimer disease (AD) is a neurodegenerative disorder in which oxidative stress is a key hallmark. It occurs early in disease pathogenesis and can exacerbate its progression. Several causes of oxidative stress have been determined over the years. First, mitochondria play an important role in the generation and accumulation of free radicals. In addition to mitochondria, inflammation can also induce oxidative damage, especially via microglia, and microglia are also important for Aβ clearance. In AD, both mitochondrial function and inflammatory response are affected, leading to increased ROS formation and oxidative damage to lipid, proteins, and nucleic acids. Some other sources have also been identified. From these findings, various neuroprotective strategies against ROS-mediated damages have been elaborated in AD research. This review recapitulates some of the major strategies used to prevent oxidative stress and disease progression. Outcomes from in vitro and in vivo studies using models of AD are encouraging. However, only a few clinical trials have provided positive results in terms of slowing down cognitive decline. Nonetheless, there is still hope for improved compounds that would better target pathways implicated in ROS production. In fact, facilitating the endogenous antioxidant system by modulating transcription has great promise for AD therapy. Published by Elsevier Inc.
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                Author and article information

                Journal
                Molecules
                Molecules
                molecules
                Molecules
                MDPI
                1420-3049
                13 June 2012
                June 2012
                : 17
                : 6
                : 7241-7254
                Affiliations
                [1 ]Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung 811, Taiwan
                [2 ]Department of Biotechnology, Kaohsiung Medical University, Kaohsiung 807, Taiwan
                [3 ]Institute of Biomedical Science, National Sun Yat-Sen University, Kaohsiung 804, Taiwan
                [4 ]Department of Biomedical Science and Environmental Biology, Graduate Institute of Natural Products, Center of Excellence for Environmental Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
                [5 ]Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan
                Author notes
                [* ] Authors to whom correspondence should be addressed; Email: cntseng@ 123456kmu.edu.tw (C.-N.T.) changhw@ 123456kmu.edu.tw (H.-W.C.); Tel.: +886-7-312-1101 (ext. 2691) (H.-W.C.); Fax: +886-7-312-5339 (H.-W.C.).
                Article
                molecules-17-07241
                10.3390/molecules17067241
                6268842
                22695230
                a8817cc3-726f-47d3-a7db-c4bf2babe7a7
                © 2012 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 16 April 2012
                : 05 June 2012
                : 07 June 2012
                Categories
                Article

                dna damage,antioxidant,comet assay,red algae,cell cycle arrest

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