No role of DT-diaphorase (NQO1) in the protection against oxidized quercetin.

نویسندگان

  • Agnes W Boots
  • Aalt Bast
  • Guido R M M Haenen
چکیده

Quercetin is one of the most studied alimentary antioxidants. During its antioxidant activity, quercetin becomes oxidized into its ortho-quinone/quinone methide, denoted as QQ. QQ is toxic since it is highly reactive towards thiols. DT-diaphorase (NQO1) might protect against QQ toxicity by reducing QQ to quercetin. However, conflicting data have been reported. The aim of the present study is to elucidate the role of DT-diaphorase in the protection against QQ-mediated thiol reactivity. It was found that QQ is indeed a substrate for DT-diaphorase. However, QQ reacted much faster with glutathione or protein thiols than with DT-diaphorase in experiments with isolated compounds as well as with human liver cytosol or blood plasma. This indicates that DT-diaphorase has no role in the protection against QQ.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Establishment of an isogenic human colon tumor model for NQO1 gene expression: application to investigate the role of DT-diaphorase in bioreductive drug activation in vitro and in vivo.

Many tumors overexpress the NQO1 gene, which encodes DT-diaphorase (NADPH:quinone oxidoreductase; EC 1.6.99.2). This obligate two-electron reductase deactivates toxins and activates bioreductive anticancer drugs. We describe the establishment of an isogenic human tumor cell model for DT-diaphorase expression. An expression vector was used in which the human elongation factor 1alpha promoter pro...

متن کامل

An alternatively spliced form of NQO1 (DT-diaphorase) messenger RNA lacking the putative quinone substrate binding site is present in human normal and tumor tissues.

DT-diaphorase is a ubiquitously expressed flavoenzyme responsible for the two-electron reduction of a number of quinone and other anticancer drugs. The majority of DT-diaphorase enzyme activity in human tissues is the product of the NQO1 gene. We have now identified a novel alternatively spliced form of human NQO1 mRNA lacking exon 4 at levels equal to or exceeding those of wild-type NQO1 mRNA....

متن کامل

DT-Diaphorase expression and tumor cell sensitivity to 17-allylamino, 17-demethoxygeldanamycin, an inhibitor of heat shock protein 90.

BACKGROUND To our knowledge, 17-allylamino,17-demethoxygeldanamycin (17AAG) is the first inhibitor of heat shock protein 90 (Hsp90) to enter a phase I clinical trial in cancer. Inhibition of Hsp90, a chaperone protein (a protein that helps other proteins avoid misfolding pathways that produce inactive or aggregated states), leads to depletion of important oncogenic proteins, including Raf-1 and...

متن کامل

DNA Damage and Cytotoxicity in Human Colon Carcinoma Oxidoreductase (DT-Diaphorase): Role in Diaziquone-induced Metabolism of Diaziquone by NAD(P)H:(Quinone Acceptor)

Reduction of 2,5-diaziridinyl-3,6-bis(carboethoxyamino)-l,4-benzoquinone (diaziquone; AZQ) by purified rat hepatic DT-diaphorase »as NADH and enzyme dependent and was inhibited by prior boiling of the enzyme or by dicumarol. Under aerobic conditions some of the hydroquinone (AZQH2) formed by reduction oxidized to regenerate AZQ and an approximate 1:1 stoichiometry was observed between V/(.)l I...

متن کامل

Commentary Benzene, NQO1, and genetic susceptibility to cancer

NAD(P)H:quinone oxidoreductase 1 (NQO1; EC 1.6.99.2), originally called DT-diaphorase (1), is an enzyme that has attracted considerable attention because of its ability to detoxify a number of natural and synthetic compounds and, conversely, to activate certain anticancer agents (2, 3). It is also a highly inducible enzyme. Synthetic antioxidants, such as butylated hydroxyanisole, and extracts ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • FEBS letters

دوره 579 3  شماره 

صفحات  -

تاریخ انتشار 2005