Chemoprevention of lung tumorigenesis induced by a mixture of benzo( a )pyrene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone by the organoselenium compound 1,4-phenylenebis(methylene)selenocyanate

Prokopczyk, Bogdan; Rosa, José; Desai, Dhimant; Amin, Shantu; Sohn, Ock Soon; Fiala, Emerich S.; El‐Bayoumy, Karam

doi:10.1016/s0304-3835(00)00590-5

Cited by 52 publications

(27 citation statements)

References 30 publications

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“…In vivo, in rat, hepatic NQO activity was increased by 1,4-phenylenebis(methylene)selenocyanate (Tanaka et al, 1997), and hepatic UGT activity was increased by 1,2-, 1,3-, and 1,4-phenylenebis(methylene) selenocyanate (Sohn et al, 1999). UGT activity was not elevated by 1,4-phenylenebis (methylene)selenocyanate in mouse, however (Prokopczyk et al, 2000). Our present studies in hepatoma cells demonstrate that mouse Nqo l is responsive to some selenocompounds (three 2-alkyl selenazolidines) but not others (SCA, L-selenocystine, L-selenomethionine, Semethyl-L-selenocysteine).…”

Section: Discussionmentioning

confidence: 99%

“…Effects on inactivation and chemoprotective enzymes have received the greatest attention. Reported investigations include studies with phenylenebis(methylene)selenocyanate isomers (Reddy et al, 1992, Tanaka et al, 1997, Sohn et al, 1999, Prokopczyk et al, 2000, benzylselenocyanate, and its glutathione conjugate (Kawamori et al, 1998), and diphenylmethylselenocyanate (Ghosh et al, 2005, Das and. Effects on bioactivation enzyme activities (cytochrome P450s) were investigated for phenylenebis (methylene)selenocyanate isomers (Sohn et al, 1999, Prokopczyk et al, 2000 following demonstration of their inhibitory activity in vitro (Shimada et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Murine hepatoma (Hepa1c1c7) cells: A responsive in vitro system for chemoprotective enzyme induction by organoselenium compounds

El‐Sayed

Aboul‐Fadl

Roberts

et al. 2007

Toxicology in Vitro

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Murine (Hepa1c1c7) hepatoma cells are a suitable in vitro system for investigating the regulation of chemoprotective enzymes by selenazolidines, novel L-selenocysteine prodrugs developed as potential chemopreventive agents. They are less sensitive to the cytotoxic effects of both selenite and the less toxic selenazolidines than rat hepatoma (H4IIE) cells. All four selenazolidine 4-carboxylic acid (SCA) derivatives examined elevated thioredoxin reductase (Txnrd1), alpha-class glutathione transferases (Gsta), and UDP-glucuronosyltransferase (Ugt)1a6 mRNAs. NAD(P)Hquinone oxidoreductase (Nqo1) was induced by the three 2-alkyl derivatives (2-cyclohexylSCA, 2-butylSCA, and 2-methylSCA) but not SCA itself. Transcripts of mu-and pi-class glutathione transferases were induced only by 2-cyclohexylSCA and 2-butylSCA. Only Gsta and Txnrd1 transcripts were elevated by L-selenomethionine, L-selenocystine, or Se-methyl-L-selenocysteine. Txnrd1, Gsta, Nqo1, and Gstp responses to selenazolidines were all abolished by actinomycin D while Ugt1a6 responses were not. Induction responses to the selenazolidines were also eliminated (most) or reduced (Txnrd1 by 2-methylSCA) by cycloheximide, with the exception of Ugt1a6. The Ugt1a6 mRNA levels in the presence of SCAs and cycloheximide were similar to those with cycloheximide alone, and were almost double those of vehicle-treated cells. Thus, Hepa1c1c7 cells appear to provide a viable platform for the study of protective enzyme regulation by selenocompounds, and with the exception of Ugt1a6, the mRNA elevations from selenazolidines are transcriptionally dependent.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Murine hepatoma (Hepa1c1c7) cells: A responsive in vitro system for chemoprotective enzyme induction by organoselenium compounds

El‐Sayed

Aboul‐Fadl

Roberts

et al. 2007

Toxicology in Vitro

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“…[11][12][13][14][15] The resulting enhanced detoxification many contribute to the powerful chemopreventive effects exhibited by supranutritional selenium, which have been observed in approximately 100 small animal studies. 8,16,17 Since supranutritional selenium levels are close to the toxic selenium levels in general, 8,16,17 the safety margin and potential toxic effects of different selenium compounds are critical considerations when evaluating their potential for supplementation.…”

Section: Introductionmentioning

confidence: 99%

Impact of heat treatment on size, structure, and bioactivity of elemental selenium nanoparticles

Zhang¹,

Taylor²,

Wan³

et al. 2012

IJN

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Background: Elemental selenium nanoparticles have emerged as a novel selenium source with the advantage of reduced risk of selenium toxicity. The present work investigated whether heat treatment affects the size, structure, and bioactivity of selenium nanoparticles. Methods and results: After a one-hour incubation of solution containing 80 nm selenium particles in a 90°C water bath, the nanoparticles aggregated into larger 110 nm particles and nanorods (290 nm × 70 nm), leading to significantly reduced bioavailability and phase II enzyme induction in selenium-deficient mice. When a solution containing 40 nm selenium nanoparticles was treated under the same conditions, the nanoparticles aggregated into larger 72 nm particles but did not transform into nanorods, demonstrating that the thermostability of selenium nanoparticles is size-dependent, smaller selenium nanoparticles being more resistant than larger selenium nanoparticles to transformation into nanorods during heat treatment. Conclusion:The present results suggest that temperature and duration of the heat process, as well as the original nanoparticle size, should be carefully selected when a solution containing selenium nanoparticles is added to functional foods.

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“…Synthetic organoselenium compounds such as BSC, and o-, m-and p-XSC, which are recently reported by us to inhibit human CYP1 and 2A enzymes (25,81), have chemopreventive activities in mice administered 7,12-DMBA, B[a]P, and NNK (Table 3) (82)(83)(84)(85)(86)(87)(88)(89). El-Bayoumy et al (87) reported that p-XSC is active in preventing tumor formation caused by NNK when it is injected before the administration of NNK, indicating that the mechanism of action of p-XSC is due to inhibition of P450s that activate NNK to active metabolites (47)(48)(49)(50)(51).…”

Section: T Shimadamentioning

confidence: 99%

Inhibition of Carcinogen-Activating Cytochrome P450 Enzymes by Xenobiotic Chemicals in Relation to Antimutagenicity and Anticarcinogenicity

Shimada

2017

ToxicolRes

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A variety of xenobiotic chemicals, such as polycyclic aromatic hydrocarbons (PAHs), aryl-and heterocyclic amines and tobacco related nitrosamines, are ubiquitous environmental carcinogens and are required to be activated to chemically reactive metabolites by xenobiotic-metabolizing enzymes, including cytochrome P450 (P450 or CYP), in order to initiate cell transformation. Of various human P450 enzymes determined to date, CYP1A1, 1A2, 1B1, 2A13, 2A6, 2E1, and 3A4 are reported to play critical roles in the bioactivation of these carcinogenic chemicals. In vivo studies have shown that disruption of Cyp1b1 and Cyp2a5 genes in mice resulted in suppression of tumor formation caused by 7,12-dimethylbenz[a]anthracene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, respectively. In addition, specific inhibitors for CYP1 and 2A enzymes are able to suppress tumor formation caused by several carcinogens in experimental animals in vivo, when these inhibitors are applied before or just after the administration of carcinogens. In this review, we describe recent progress, including our own studies done during past decade, on the nature of inhibitors of human CYP1 and CYP2A enzymes that have been shown to activate carcinogenic PAHs and tobacco-related nitrosamines, respectively, in humans. The inhibitors considered here include a variety of carcinogenic and/or non-carcinogenic PAHs and acethylenic PAHs, many flavonoid derivatives, derivatives of naphthalene, phenanthrene, biphenyl, and pyrene and chemopreventive organoselenium compounds, such as benzyl selenocyanate and benzyl selenocyanate; o-XSC, 1,2-, 1,3-, and 1,4-phenylenebis(methylene)selenocyanate.

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Chemoprevention of lung tumorigenesis induced by a mixture of benzo( a )pyrene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone by the organoselenium compound 1,4-phenylenebis(methylene)selenocyanate

Cited by 52 publications

References 30 publications

Murine hepatoma (Hepa1c1c7) cells: A responsive in vitro system for chemoprotective enzyme induction by organoselenium compounds

Murine hepatoma (Hepa1c1c7) cells: A responsive in vitro system for chemoprotective enzyme induction by organoselenium compounds

Impact of heat treatment on size, structure, and bioactivity of elemental selenium nanoparticles

Inhibition of Carcinogen-Activating Cytochrome P450 Enzymes by Xenobiotic Chemicals in Relation to Antimutagenicity and Anticarcinogenicity

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