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Wen-Hsing Cheng

Researcher at Cornell University

Publications -  13
Citations -  1069

Wen-Hsing Cheng is an academic researcher from Cornell University. The author has contributed to research in topics: GPX1 & Glutathione peroxidase. The author has an hindex of 12, co-authored 13 publications receiving 1036 citations. Previous affiliations of Wen-Hsing Cheng include National Institutes of Health.

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Cellular Glutathione Peroxidase Is the Mediator of Body Selenium To Protect against Paraquat Lethality in Transgenic Mice

TL;DR: It is indicated that GPX1 is the major, if not the only, metabolic form of body Se that protects mice against the lethal oxidative stress caused by high levels of paraquat; it seems less important, however, in protecting dogs against the moderate oxidative stress by the low level of paraaquat.
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Cellular Glutathione Peroxidase Knockout Mice Express Normal Levels of Selenium-Dependent Plasma and Phospholipid Hydroperoxide Glutathione Peroxidases in Various Tissues

TL;DR: Results indicate that GPX1 is expressed independently of GPX3 or GPX4 and represents approximately 60% of the total hepatic Se in Se-adequate mice.
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Selenium-dependent cellular glutathione peroxidase protects mice against a pro-oxidant-induced oxidation of NADPH, NADH, lipids, and protein

TL;DR: Selenium‐dependent cellular glutathione peroxidase protects mice against a pro‐oxidant‐induced oxidation of NADPH, NADH, lipids, and protein, and seems to be inducible and coordinated with those of other antioxidant enzymes.
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Knockout of cellular glutathione peroxidase gene renders mice susceptible to diquat-induced oxidative stress.

TL;DR: GPX1 is the major selenoprotein to protect mice against the lethal oxidative stress induced by diquat, and Responses of hepatic superoxide dismutase activities to the diqu at treatment were affected by the GPX1 level.
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Overexpression of cellular glutathione peroxidase does not affect expression of plasma glutathione peroxidase or phospholipid hydroperoxide glutathione peroxidase in mice offered diets adequate or deficient in selenium

TL;DR: The overexpression of the GPX1 gene in these mice was tissue specific and did not affect the expression of GPX3, GPX4 or GST and plasma Se levels; dietary Se appeared to affect the GPx1 overexpressing at its mRNA level.