T
T. B. Smith
Researcher at Harvard University
Publications - 13
Citations - 1142
T. B. Smith is an academic researcher from Harvard University. The author has contributed to research in topics: DNA damage & Oxidative stress. The author has an hindex of 12, co-authored 13 publications receiving 942 citations. Previous affiliations of T. B. Smith include University of Newcastle & Newcastle University.
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Journal ArticleDOI
Oxidative stress and male reproductive health
TL;DR: The high prevalence of oxidative DNA damage in the spermatozoa of male infertility patients may have implications for the health of children conceived in vitro and serves as a driver for current research into the origins of free radical generation in the germ line.
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The presence of a truncated base excision repair pathway in human spermatozoa that is mediated by OGG1
T. B. Smith,Matthew D. Dun,Nathan D. Smith,Ben J. Curry,Haley S. Connaughton,Robert John Aitken +5 more
TL;DR: The limited capacity of mature spermatozoa to mount a DNA repair response to oxidative stress is emphasized, and the importance of such mechanisms in the oocyte in order to protect the embryo from paternally mediated genetic damage is highlighted.
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The source and significance of DNA damage in human spermatozoa; a commentary on diagnostic strategies and straw man fallacies
TL;DR: The origins of DNA damage in human spermatozoa, the methods that are available to monitor this aspect of semen quality and the clinical significance of such measurements are discussed in this paper.
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On methods for the detection of reactive oxygen species generation by human spermatozoa: analysis of the cellular responses to catechol oestrogen, lipid aldehyde, menadione and arachidonic acid.
Robert John Aitken,T. B. Smith,Tessa Lord,L. Kuczera,A. J. Koppers,Nenad Naumovski,Haley S. Connaughton,Mark Baker,G. N. De Iuliis +8 more
TL;DR: Examination of spontaneous ROS generation by defective human spermatozoa revealed that MitoSOX Red was the most effective indicator of oxidative stress, thereby emphasizing the general importance of mitochondrial dysregulation in the aetiology of defective sperm function.
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Functional deletion of Txndc2 and Txndc3 increases the susceptibility of spermatozoa to age-related oxidative stress.
TL;DR: The results suggest that although there is considerable redundancy in the systems employed by spermatozoa to defend themselves against oxidative stress, the sperm-specific thioredoxins are critically important in protecting these cells against the increases in oxidative stress associated with paternal age.