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Autism Research and Treatment
Volume 2014 (2014), Article ID 164938, 15 pages
Review Article

Potential Role of Selenoenzymes and Antioxidant Metabolism in relation to Autism Etiology and Pathology

1Energy & Environmental Research Center, University of North Dakota, 15 North 23rd Street, Stop 9018, Grand Forks, ND 58202, USA
2Department of Pharmaceutical Sciences, Northeastern University, Boston, MA 02115, USA

Received 11 September 2013; Revised 7 January 2014; Accepted 27 January 2014; Published 5 March 2014

Academic Editor: Klaus-Peter Ossenkopp

Copyright © 2014 Laura J. Raymond 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.


Autism and autism spectrum disorders (ASDs) are behaviorally defined, but the biochemical pathogenesis of the underlying disease process remains uncharacterized. Studies indicate that antioxidant status is diminished in autistic subjects, suggesting its pathology is associated with augmented production of oxidative species and/or compromised antioxidant metabolism. This suggests ASD may result from defects in the metabolism of cellular antioxidants which maintain intracellular redox status by quenching reactive oxygen species (ROS). Selenium-dependent enzymes (selenoenzymes) are important in maintaining intercellular reducing conditions, particularly in the brain. Selenoenzymes are a family of ~25 genetically unique proteins, several of which have roles in preventing and reversing oxidative damage in brain and endocrine tissues. Since the brain’s high rate of oxygen consumption is accompanied by high ROS production, selenoenzyme activities are particularly important in this tissue. Because selenoenzymes can be irreversibly inhibited by many electrophiles, exposure to these organic and inorganic agents can diminish selenoenzyme-dependent antioxidant functions. This can impair brain development, particularly via the adverse influence of oxidative stress on epigenetic regulation. Here we review the physiological roles of selenoproteins in relation to potential biochemical mechanisms of ASD etiology and pathology.