Zobrazeno 1 - 10
of 31
pro vyhledávání: '"Yakov M. Koen"'
Publikováno v:
Toxicological Sciences. 135:390-401
Many low molecular weight compounds undergo biotransformation to chemically reactive metabolites (CRMs) that covalently modify cellular proteins. However, the mechanisms by which this covalent binding leads to cytotoxicity are not understood. Prior a
Autor:
Robert P. Hanzlik, Heather Hajovsky, Yakov M. Koen, Todd D. Williams, Jeff L. Staudinger, Nadezhda A. Galeva, Diganta Sarma
Publikováno v:
Chemical Research in Toxicology. 26:564-574
Thioacetamide (TA) has long been known as a hepatotoxicant whose bioactivation requires S-oxidation to thioacetamide S-oxide (TASO) and then to the very reactive S,S-dioxide (TASO2). The latter can tautomerize to form acylating species capable of cov
Publikováno v:
Chemical research in toxicology. 29(11)
The hepatotoxicity of acetaminophen (APAP) is generally attributed to the formation of a reactive quinoneimine metabolite (NAPQI) that depletes glutathione and covalently binds to hepatocellular proteins. To explore the importance of the N-acyl group
Publikováno v:
Chemical research in toxicology. 29(6)
Isoniazid (INH) has been a first-line drug for the treatment of tuberculosis for more than 40 years. INH is well-tolerated by most patients, but some patients develop hepatitis that can be severe in rare cases or after overdose. The mechanisms underl
Autor:
Diganta Sarma, David S. Moore, Gang Hu, Robert P. Hanzlik, Wenqi Cui, Jeff L. Staudinger, Yakov M. Koen, Heather Hajovsky
Publikováno v:
Chemical Research in Toxicology. 25:1955-1963
The hepatotoxicity of thioacetamide (TA) has been known since 1948. In rats, single doses cause centrolobular necrosis accompanied by increases in plasma transaminases and bilirubin. To elicit these effects, TA requires oxidative bioactivation, leadi
Autor:
Robert P. Hanzlik, Diganta Sarma, Todd D. Williams, Jeff L. Staudinger, Heather Hajovsky, Yakov M. Koen, Nadezhda A. Galeva
Publikováno v:
Chemical Research in Toxicology. 25:1868-1877
Thioacetamide (TA) is a well-known hepatotoxin in rats. Acute doses cause centrilobular necrosis and hyperbilirubinemia while chronic administration leads to biliary hyperplasia and cholangiocarcinoma. Its acute toxicity requires its oxidation to a s
Autor:
Kelin Li, James S. Leeder, Jennifer L. Goldman, Yakov M. Koen, Steven A. Rogers, Robert P. Hanzlik
The formation of drug-protein adducts via metabolic activation and covalent binding may stimulate an immune response or may result in direct cell toxicity. Protein covalent binding is a potentially pivotal step in the development of idiosyncratic adv
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::85f438025b348d444e72e148ce115055
Autor:
Yakov M. Koen, Tao Ji, Steven Wynn Esch, Todd D. Williams, Robert P. Hanzlik, Keisuke Ikehata
Publikováno v:
Chemical Research in Toxicology. 20:701-708
Thiobenzamide (TB) is hepatotoxic in rats causing centrolobular necrosis, steatosis, cholestasis and hyperbilirubinemia. It serves as a model compound for a number of thiocarbonyl compounds that undergo oxidative bioactivation to chemically reactive
Publikováno v:
Chemical Research in Toxicology. 19:1426-1434
The hepatotoxicity of bromobenzene (BB) derives from its reactive metabolites (epoxides and quinones), which arylate cellular proteins. Application of proteomic methods to liver proteins from rats treated with a hepatotoxic dose of [ 14 C]-BB has ide
Publikováno v:
Chemical Research in Toxicology. 18:1748-1754
The cytotoxicity of many small organic compounds often apparently derives from their metabolic activation and covalent binding to cellular proteins. It is therefore of considerable interest to be able to determine, for a given protoxin, which metabol