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Dun Xian Tan

Researcher at University of Texas Health Science Center at San Antonio

Publications -  315
Citations -  47893

Dun Xian Tan is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Melatonin & Oxidative stress. The author has an hindex of 117, co-authored 308 publications receiving 42258 citations. Previous affiliations of Dun Xian Tan include University of Texas System & University of Texas at Austin.

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A Genome-Wide Expression Profile of Salt-Responsive Genes in the Apple Rootstock Malus zumi

TL;DR: A genome-wide expression analysis resulted in the isolation of 50 novel Malus genes and the elucidation of a new apple-specific mechanism of salt tolerance, including the stabilization of photosynthesis under stress, involvement of phenolic compounds, and sorbitol in ROS scavenging and osmoprotection.
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Hyperglycemia-related pathophysiologic mechanisms and potential beneficial actions of melatonin.

TL;DR: Melatonin is a multifunctional indolamine which counteracts several pathophysiologic steps and displays significant beneficial effects against hyperglycemia-induced cellular toxicity, related to melatonin's antioxidants, anti-inflammatory and possibly epigenetic regulatory properties.
Journal Article

Melatonin suppresses autoxidation and hydrogen peroxide-induced lipid peroxidation in monkey brain homogenate.

TL;DR: Melatonin functions as an antioxidant and neuroprotector in primate brain tissue as was observed previously in rodent brain and provides information supporting the use of melatonin in the treatment of neurodegenerative disorders that involve oxidative damage to brain lipids.
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Autoxidation and toxicant-induced oxidation of lipid and DNA in monkey liver: reduction of molecular damage by melatonin.

TL;DR: The ability of melatonin to protect against oxidative damage to both lipid and DNA in primate tissue, as observed previously in rodent tissue, provides support for the use ofmelatonin as suitable agent to reduce damage inflicted by free radical species in primates.