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      Binge Drinking of Ethanol during Adolescence Induces Oxidative Damage and Morphological Changes in Salivary Glands of Female Rats

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          Abstract

          This study investigates morphological and biochemistry effects of binge ethanol consumption in parotid (PG) and submandibular (SG) salivary glands of rats from adolescence to adulthood. Female Wistar rats ( n = 26) received ethanol at 3 g/kg/day (20% w/v) for 3 consecutive days/week from the 35th until the 62nd day of life. Animals were treated in two periods: 1 week (G1) and 4 weeks (G2), with a control (treated with distilled water) and an ethanol group to each period. In morphological analysis, morphometric and immunohistochemistry evaluation for smooth muscle actin ( αSMA), cytokeratin-18 (CK-18), and vimentin (VIM) were made. Biochemical changes were analyzed by concentration of nitrites and levels of malondialdehyde (MDA). The difference between groups in each analysis was evaluated by Mann-Whitney U test or Student's t-test ( p ≤ 0.05). PG showed, at one week of ethanol exposure, lower CK-18 and α-SMA expression, as well as MDA levels. After four weeks, lower CK-18 and higher MDA levels were observed in PG exposed to ethanol, in comparison to control group. SG showed lower α-SMA expression after 1 and 4 weeks of ethanol exposure as well as higher MDA levels after 1 week. Ethanol binge consumption during adolescence promotes tissue and biochemical changes with only one-week binge in acinar and myoepithelial PG cells.

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          Most cited references33

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          The adolescent brain and age-related behavioral manifestations.

          L Spear (2000)
          To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence.
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            [42] Determination of aldehydic lipid peroxidation products: Malonaldehyde and 4-hydroxynonenal

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              Oxidative stress, mitochondrial DNA mutation, and impairment of antioxidant enzymes in aging.

              Mitochondria do not only produce less ATP, but they also increase the production of reactive oxygen species (ROS) as by-products of aerobic metabolism in the aging tissues of the human and animals. It is now generally accepted that aging-associated respiratory function decline can result in enhanced production of ROS in mitochondria. Moreover, the activities of free radical-scavenging enzymes are altered in the aging process. The concurrent age-related changes of these two systems result in the elevation of oxidative stress in aging tissues. Within a certain concentration range, ROS may induce stress response of the cells by altering expression of respiratory genes to uphold the energy metabolism to rescue the cell. However, beyond the threshold, ROS may cause a wide spectrum of oxidative damage to various cellular components to result in cell death or elicit apoptosis by induction of mitochondrial membrane permeability transition and release of apoptogenic factors such as cytochrome c. Moreover, oxidative damage and large-scale deletion and duplication of mitochondrial DNA (mtDNA) have been found to increase with age in various tissues of the human. Mitochondria act like a biosensor of oxidative stress and they enable cell to undergo changes in aging and age-related diseases. On the other hand, it has recently been demonstrated that impairment in mitochondrial respiration and oxidative phosphorylation elicits an increase in oxidative stress and causes a host of mtDNA rearrangements and deletions. Here, we review work done in the past few years to support our view that oxidative stress and oxidative damage are a result of concurrent accumulation of mtDNA mutations and defective antioxidant enzymes in human aging.
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                Author and article information

                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi Publishing Corporation
                1942-0900
                1942-0994
                2016
                7 August 2016
                : 2016
                : 7323627
                Affiliations
                1Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Street Augusto Corrêa 1, Guamá, 66075-900 Belém, PA, Brazil
                2Laboratory of Inflammation and Behaviour Pharmacology, Pharmacy Faculty, Institute of Health Science, Federal University of Pará, Street Augusto Corrêa 1, Guamá, 66075-900 Belém, PA, Brazil
                3Laboratory of Molecular Pharmacology, Institute of Biological Sciences, Federal University of Pará, Street Augusto Corrêa 1, Guamá, 66075-900 Belém, PA, Brazil
                4Department of Oral Pathology, School of Dentistry, Federal University of Pará, Street Augusto Corrêa 1, Guamá, 66075-900 Belém, PA, Brazil
                Author notes
                *Rafael Rodrigues Lima: rafalima@ 123456ufpa.br

                Academic Editor: Francisco J. Romero

                Author information
                http://orcid.org/0000-0001-5051-7129
                http://orcid.org/0000-0003-4493-7375
                http://orcid.org/0000-0003-1486-4013
                Article
                10.1155/2016/7323627
                4992539
                898f6cbf-e864-4168-aa5a-bf8203c249bc
                Copyright © 2016 Nathalia Carolina Fernandes Fagundes 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
                : 8 March 2016
                : 1 July 2016
                : 5 July 2016
                Categories
                Research Article

                Molecular medicine
                Molecular medicine

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