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      Oxidative Stress in Aging Human Skin

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          Abstract

          Oxidative stress in skin plays a major role in the aging process. This is true for intrinsic aging and even more for extrinsic aging. Although the results are quite different in dermis and epidermis, extrinsic aging is driven to a large extent by oxidative stress caused by UV irradiation. In this review the overall effects of oxidative stress are discussed as well as the sources of ROS including the mitochondrial ETC, peroxisomal and ER localized proteins, the Fenton reaction, and such enzymes as cyclooxygenases, lipoxygenases, xanthine oxidases, and NADPH oxidases. Furthermore, the defense mechanisms against oxidative stress ranging from enzymes like superoxide dismutases, catalases, peroxiredoxins, and GSH peroxidases to organic compounds such as L-ascorbate, α-tocopherol, beta-carotene, uric acid, CoQ10, and glutathione are described in more detail. In addition the oxidative stress induced modifications caused to proteins, lipids and DNA are discussed. Finally age-related changes of the skin are also a topic of this review. They include a disruption of the epidermal calcium gradient in old skin with an accompanying change in the composition of the cornified envelope. This modified cornified envelope also leads to an altered anti-oxidative capacity and a reduced barrier function of the epidermis.

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          ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis.

          Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.
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            Oxidative stress shortens telomeres.

            Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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              Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

              Oncogenic ras can transform most immortal rodent cells to a tumorigenic state. However, transformation of primary cells by ras requires either a cooperating oncogene or the inactivation of tumor suppressors such as p53 or p16. Here we show that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest. The arrest induced by ras is accompanied by accumulation of p53 and p16, and is phenotypically indistinguishable from cellular senescence. Inactivation of either p53 or p16 prevents ras-induced arrest in rodent cells, and E1A achieves a similar effect in human cells. These observations suggest that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an oncogenic stimulus. Negation of ras-induced senescence may be relevant during multistep tumorigenesis.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Biomolecules
                Biomolecules
                biomolecules
                Biomolecules
                MDPI
                2218-273X
                21 April 2015
                June 2015
                : 5
                : 2
                : 545-589
                Affiliations
                [1 ]Department of Cell Biology, Division of Genetics, University of Salzburg, Salzburg 5020, Austria; E-Mails: mark.rinnerthaler@ 123456sbg.ac.at (M.R.); johannes.bischof@ 123456stud.sbg.ac.at (J.B.); mariakarolin.streubel@ 123456stud.sbg.ac.at (M.K.S.)
                [2 ]Department of Ophthalmology and Optometry, Paracelsus Medical University, Muellner Hauptstrasse 48, 5020 Salzburg, Austria; E-Mail: A.Zurl@ 123456salk.at
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: klaus.richter@ 123456sbg.ac.at ; Tel.: +43-0-662-8044-5763; Fax: +43-0-662-8044-144.
                Article
                biomolecules-05-00545
                10.3390/biom5020545
                4496685
                25906193
                dfb9f15a-36ce-4d8d-b96b-6d37690d8a1a
                © 2015 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/4.0/).

                History
                : 12 January 2015
                : 09 April 2015
                Categories
                Review

                lipofuscin,ages,cornified envelope,calcium gradient,extrinsic and intrinsic aging,dna damage,lipid peroxidation,antioxidants,carbonylation

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