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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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Impaired mitochondrial complex III and melatonin responsive reactive oxygen species generation in kidney mitochondria of db/db mice.

TL;DR: In this article, the role of mitochondrial dysfunction in the development of diabetic nephropathy was investigated in db/db mice, and it was shown that diminished melatonin-induced reactive oxygen species (ROS) generation at the antimycin-A sensitive site of mitochondrial complex III (MC-3) is associated with diminished MC-3 activity.
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Targeting host defense system and rescuing compromised mitochondria to increase tolerance against pathogens by melatonin may impact outcome of deadly virus infection pertinent to COVID-19

TL;DR: Melatonin is a molecule that can enhance the host’s tolerance against pathogen invasions and maintenance of mitochondrial function by melatonin supplementation can be expected to generate beneficial effects on the outcome of viral infectious diseases, particularly COVID-19.
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Melatonin prevents the suppression of cardiac Ca(2+)-stimulated ATPase activity induced by alloxan.

TL;DR: Melatonin, likely because of its antioxidant capacity, exerts a protective effect on heart sarcolemmal membrane function in alloxan-injected rats, and the results indicate that Ca2+ pump activity is suppressed by acutealloxan treatment, whereas the density of voltage-sensitive calcium channels is increased.
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Inhibitory effect of melatonin on diquat-induced lipid peroxidation in vivo as assessed by the measurement of F2-isoprostanes.

TL;DR: These findings, using a sensitive and specific index of lipid peroxidation, show that the hepatoxicity of diquat, at least partially, is a consequence of reactive oxygen species‐induced lipid damage.
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Red-light-induced suppression of melatonin synthesis is mediated by N-methyl-D-aspartate receptor activation in retinally normal and retinally degenerate rats.

TL;DR: The findings indicate that the activation of central hypothalamic NMDA receptors might mediate the photic inhibition of nocturnal melatonin synthesis in the pineal gland elicited by the exposure to red light at night.