Mouse dioxin-inducible NAD(P)H

Vasiliou, Vasilis; Theurer, Mary J.; Puga, Alvaro; Reuter, Steven F.; Nebert, Daniel W.

doi:10.1097/00008571-199412000-00007

Cited by 27 publications

(3 citation statements)

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“…Several clones were characterized, and one, designated EMBL3-mNQO1g-10, was used for further studies and analysis. To determine the nucleotide sequences encompassing the exon-intron junctions of mouse NQO1 gene, oligonucleotides 15-17 bp in length were selected at random from the corresponding mouse NQO1 cDNA (20) and used for sequencing NQO1 gene fragments subcloned into pUC18 by procedures described previously (21). The process of sequencing continued until the coding region from mouse NQO1 gene was completely covered.…”

Section: Methodsmentioning

confidence: 99%

“…In a related experiment, the DNAs from wild-type (NQO1ϩ/ϩ), heterozygous (NQO1ϩ/Ϫ), and NQO1Ϫ/Ϫ mice were digested with BamHI, run on agarose gel, blotted, and hybridized with 1.1 kb of human NQO1 cDNA (complete coding region) and the 2.0-kb neo-cassette probes. The NQO1 cDNAs are highly conserved among humans, rats, and mice and are known to hybridize each other in Southern analysis (25,20). The blots were washed and autoradiographed.…”

Section: Methodsmentioning

confidence: 99%

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Disruption of the DT Diaphorase (NQO1) Gene in Mice Leads to Increased Menadione Toxicity

Venugopal

Joseph

Lee

et al. 1998

Journal of Biological Chemistry

231

151

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NAD(P)H:quinone oxidoreductase 1 (NQO1) is a flavoenzyme that catalyzes two-electron reductive metabolism and detoxification of quinones and their derivatives leading to protection of cells against redox cycling and oxidative stress. To examine the in vivo role of NQO1, a NQO1-null mouse was produced using targeted gene disruption. Mice lacking NQO1 gene expression showed no detectable phenotype and were indistinguishable from wild-type mice. However, NQO1-null mice exhibited increased toxicity when administered menadione compared with wild-type mice. These results establish a role for NQO1 in protection against quinone toxicity. The NQO1-null mice are a model for NQO1 deficiency in humans and can be used to determine the role of this enzyme in sensitivity to toxicity and carcinogenesis.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Disruption of the DT Diaphorase (NQO1) Gene in Mice Leads to Increased Menadione Toxicity

Venugopal

Joseph

Lee

et al. 1998

Journal of Biological Chemistry

231

151

View full text Add to dashboard Cite

show abstract

“…The Nrf2-regulated HO-1 gene plays a crucial role in the development of oxidative and age-related disorders [ 34 ]. NQO1, another Nrf2-regulated gene [ 35 ], is one of the two mammalian forms of the NAD(P)H:quinone acceptor oxidoreductases family belonging to obligate two-electron reductase [ 36 , 37 ]. In this study, the expression levels of SOD, CAT, and GPx, and Nrf2 genes did not change in response to B. formosana callus extract treatment after 6 h and 24 h in Hs68 fibroblast cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Extract of Bletilla formosana callus elevates cellular antioxidative activity via Nrf2/HO-1 signaling pathway and inhibits melanogenesis in zebrafish

Wang¹,

Yen

Liao³

et al. 2023

Journal of Genetic Engineering and Biotechnology

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Background Bletilla species are endangered terrestrial orchids used in natural skin care formulas in Asia for a long history. In order to explore the bioactivity potential of Bletilla species as a cosmetic ingredient in a sustainable resource manner, the callus of Bletilla formosana (Hayata) Schltr. was established and extracted by an eco-friendly supercritical fluid CO2 extraction (SFE-CO2) method. The intracellular reactive oxygen species (ROS) scavenging activity and antioxidation-related gene expression of the callus extract were evaluated in both Hs68 fibroblast cells and HaCaT keratinocytes. The melanogenesis-inhibitory effect was investigated in B16F10 melanoma cells and in an in vivo zebrafish model. Results The calli of B. formosana were propagated for 10–15 generations with a consistent yellow friable appearance and then subjected to SFE-CO2 extraction to obtain a yellow pasty extract. Obvious intracellular ROS scavenging activity of the extract was detected in both Hs68 and HaCaT cells with 64.30 ± 8.27% and 32.50 ± 4.05% reduction at the concentration of 250 μg/mL. Moreover, marked expression levels of heme oxygenase-1 (HO-1) and (NAD(P)H) quinone oxidoreductase-1 (NQO1) genes were detected after 6-h and 24-h treatments. These results indicate the cellular antioxidative activity of B. formosana callus extract was probably activated via the nuclear factor erythroid 2-related factor 2 (Nrf2)/HO-1 signaling pathway. Melanogenesis-inhibitory effect of the extract was observed in α-MSH stimuli-inducing B16F10 cells with 28.46% inhibition of intracellular melanin content at the concentration of 50 μg/ml. The effect was confirmed with in vivo zebrafish embryos that showed a relative pigmentation density of 80.27 ± 7.98% at the concentration of 100 μg/mL without toxicity. Conclusion Our results shed light on a sustainable utilization of Bletilla species as a potential ingredient for skin.

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Induction of drug metabolizing enzymes by 1,7‐phenanthroline and oltipraz in mice is unrelated to Ah‐responsiveness

Carr

Franklin

1999

J Biochem & Molecular Tox

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The protective effect of several classes of compounds against the toxic and neoplastic effects of xenobiotics has been attributed to the induction of noncytochrome P450 (P450) drug metabolizing enzymes. Glutathione S‐transferases (GST), NAD(P)H:quinone oxidoreductase (QOR), and UDP‐glucuronosyltransferases (UGT) play a prominent role in detoxification and can be induced by oltipraz and other N‐heterocyclic compounds in rats. In contrast to the induction of these enzymes by aryl hydrocarbon (Ah)‐receptor agonists, induction by oltipraz and 1,7‐phenanthroline is not accompanied by CYP1A induction. This study investigated the induction of drug metabolizing enzymes following administration of oltipraz and 1,7‐phenanthroline in four mouse strains (C57B6A‐J, Frings × C57B6J, Frings, CF‐1) exhibiting varying degrees of responsiveness to an Ah‐receptor agonist. The relative Ah responsiveness was determined in all strains by the induction of hepatic Cyp1a after three daily doses of 3‐methylcholanthrene (20 mg/kg). After treatment with 1,7‐phenanthroline and oltipraz (150 mg/kg i.g.) daily for 3 days, all strains showed similar induction of GST and QOR activities for each inducer. Both compounds were equally effective in elevating GST activity, but 1,7‐phenanthroline was more effective than oltipraz in elevating QOR activity. In addition to GST and QOR changes, 1,7‐phenanthroline significantly elevated UGT (1‐naphthol) activity in the Frings strain. Neither compound produced significant changes in Cyp1a parameters. The independence of 1,7‐phenanthroline and oltipraz induction of GST and QOR from Cyp1a‐responsiveness is in line with the concept that N‐heterocycle‐containing inducers act by mechanisms other than an Ah‐receptor‐dependent pathway in which the P450 response has been masked or prevented. © 1998 John Wiley & Sons, Inc. J Biochem Toxicol 13: 77‐82, 1999

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Mouse dioxin-inducible NAD(P)H

Cited by 27 publications

References 0 publications

Disruption of the DT Diaphorase (NQO1) Gene in Mice Leads to Increased Menadione Toxicity

Disruption of the DT Diaphorase (NQO1) Gene in Mice Leads to Increased Menadione Toxicity

Extract of Bletilla formosana callus elevates cellular antioxidative activity via Nrf2/HO-1 signaling pathway and inhibits melanogenesis in zebrafish

Induction of drug metabolizing enzymes by 1,7‐phenanthroline and oltipraz in mice is unrelated to Ah‐responsiveness

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