C
Chao-Hen Kuo
Researcher at Michigan State University
Publications - 19
Citations - 502
Chao-Hen Kuo is an academic researcher from Michigan State University. The author has contributed to research in topics: Nephrotoxicity & Kidney. The author has an hindex of 11, co-authored 19 publications receiving 495 citations. Previous affiliations of Chao-Hen Kuo include Beaumont Hospital.
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Journal ArticleDOI
Lipid peroxidation: A possible mechanism of cephaloridine-induced nephrotoxicity
TL;DR: Findings in the present study are consistent with a major role of lipid peroxidation in the etiology of cephaloridine nephrotoxicity, and removal of selenium and/or vitamin E from the diet, which should enhance lipidperoxidation, potentiated cep KhaloridineNephrot toxicity and enhanced cepHaloridine-induced morphological damage in the kidney.
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Depletion of renal glutathione content and nephrotoxicity of cephaloridine in rabbits, rats, and mice.
Chao-Hen Kuo,Jerry B. Hook +1 more
TL;DR: It is demonstrated that cephaloridine is most nephrotoxic to rabbits, intermediate in toxicity to rats, and least toxic to mice, confirming previous histopathological findings and suggesting a relationship between glutathione depletion and cep Khaloridine toxicity.
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Effect of monocrotaline ingestion on liver, kidney, and lung of rats
TL;DR: Lung, liver, and kidney are each affected by this MCT treatment regimen, and functional effects on lung precede effects on other tissues.
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The role of p-aminophenol in acetaminophen-induced nephrotoxicity: Effect of bis(p-nitrophenyl) phosphate on acetaminophen and p-aminophenol nephrotoxicity and metabolism in Fischer 344 rats
J.F. Newton,J.F. Newton,Chao-Hen Kuo,Chao-Hen Kuo,G M DeShone,G M DeShone,D Hoefle,D Hoefle,J. Bernstein,J. Bernstein,Jerry B. Hook,Jerry B. Hook +11 more
TL;DR: It is concluded that PAP formation, in vivo, accounts for APAP-induced renal tubular necrosis and appears to be due to inhibition of APAP deacetylation.
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Induction of drug-metabolizing enzymes and toxicity of trans-stilbene oxide in rat liver and kidney.
TL;DR: It appears that TSO induces hepatic and renal enzyme activities in a similar manner and led to negligible alteration in liver and the higher dose resulted in mild to moderate hepatic cellular.