毒素T3DB ID

T3D0128

目标BioDB ID

BE0001089

目标名称

Glucose-6-phosphate 1-dehydrogenase

目标UniProt ID

P11413

作用机理

Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. (L277, T49, A174, L280)

参考文献

A174 - Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. (17697726) L277 - Wikipedia. Copper. Last Updated 29 May 2009. (http://en.wikipedia.org/wiki/Copper) L280 - US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. (http://www.epa.gov/OGWDW/ccl/pdfs/reg_determine2/healthadvisory_ccl2-reg2_dinitrotoluenes.pdf) T49 - Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.

创建于

2009-05-29 17:55:30 UTC

更新于

2014-09-04 16:18:54 UTC

目标详情