Relevant bibliographies by topics / A16V-SOD2 polymorphism

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  2. Dissertations / Theses

Academic literature on the topic 'A16V-SOD2 polymorphism'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "A16V-SOD2 polymorphism"

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Tuna, A., G. Ozturk, TB Gerceker, et al. "Superoxide dismutase 1 and 2 gene polymorphism in Turkish vitiligo patients." Balkan Journal of Medical Genetics 20, no. 2 (2017): 67–73. http://dx.doi.org/10.1515/bjmg-2017-0033.

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Abstract Vitiligo is an acquired disease of unknown etiology. Several theories have been proposed to understand the pathogenesis. The role of oxidative stress has been getting more important in recent years. One of the primary antioxidant enzymes in vitiligo is the superoxide dismutase (SOD). The aim of this study is to investigate the polymorphisms of the SOD1 and SOD2 in Turkish vitiligo patients. One hundred one vitiligo patients and 99 healthy controls without family history of vitiligo were included into the study. The SOD1 35 A/C and SOD2 A16V (C/T) polymorphisms were analyzed by polymer
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2

Fortunato, Giuliana, Elio Marciano, Federica Zarrilli, et al. "Paraoxonase and Superoxide Dismutase Gene Polymorphisms and Noise-Induced Hearing Loss." Clinical Chemistry 50, no. 11 (2004): 2012–18. http://dx.doi.org/10.1373/clinchem.2004.037788.

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Abstract Background: Noise-induced cochlear epithelium damage can cause hearing loss in industrial workers. In experimental systems, noise induces the release of free radicals and may damage the cochlear sensorial epithelium. Therefore, genes involved in regulating the reactive oxygen species manganese-superoxide dismutase (SOD2) and the antioxidant paraoxonase (PON) could influence cochlea vulnerability to noise. We evaluated whether susceptibility to noise-induced hearing loss (NIHL) is associated with SOD2, PON1, and PON2 polymorphisms in workers exposed to prolonged loud noise. Methods: We
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3

Liu, Q., H. Liu, H. Bai, et al. "Association of SOD2 A16V and PON2 S311C polymorphisms with polycystic ovary syndrome in Chinese women." Journal of Endocrinological Investigation 42, no. 8 (2019): 909–21. http://dx.doi.org/10.1007/s40618-018-0999-5.

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4

Vecchio, Mercurio, Monica Currò, Fabio Trimarchi, et al. "The Oxidative Stress Response in Elite Water Polo Players: Effects of Genetic Background." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7019694.

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Acute exercise is known to induce oxidative stress. Here we assessed the effects of gene polymorphisms SOD2 A16V, CAT −844 G>A, and GPx-1 rs1800668 C>T on oxidative stress markers in 28 elite water polo male players prior to and after a routinely programmed friendly match. The mean plasma concentrations of derivatives of reactive oxygen metabolites (dROMs), as well as lactic dehydrogenase (LDH) activity, creatine kinase (CK) activity, CK-MB, and myoglobin, were significantly increased after exercise, while blood antioxidant potential (BAP) and total free thiols were significantly decreas
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"Manganese superoxide dismutase (SOD2) A16V Polymorphism Is Not Associated with Increased Mortality in Heart Failure: A Retrospective Study from the Bucindolol Evaluation and Survival (BEST) Trial's DNA-Substudy." Journal of Cardiac Failure 11, no. 6 (2005): S128. http://dx.doi.org/10.1016/j.cardfail.2005.06.142.

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Dissertations / Theses on the topic "A16V-SOD2 polymorphism"

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Montagner, Greice Franciele Feyh dos Santos. "Efeito in vitro do polimorfismo ala16val do gene da superóxido dismutase dependente de manganês no metabolismo oxidativo de linfócitos." Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/11126.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico<br>Epidemiological studies suggest that the imbalance in antioxidant enzymes activity genetically caused, increases the risk of metabolic disorders and chronic noncommunicable diseases. This is the case of polymorphism that occurs in an substitution of Alanine (A) by a Valine (V) at codon 16 of the gene for superoxide dismutase manganese-dependent (Ala16Val-SOD2). The A allele has a higher efficiency of catalysis than allele V. However, this efficiency increases the levels of H2O2 leading to a consequent oxidative imbalance that, in
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