Selenium‐mediated reduction in the mutagenicity of cigarette smoke

Chortyk, O. T.; Baker, J. L.; Chamberlain, William J.

doi:10.1002/em.2850110308

Cited by 8 publications

(2 citation statements)

References 25 publications

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“…Natriumselenit: Natriumselenit war in An-und Abwesenheit eines metabolischen Aktivierungssystems bis zu einer Konzentration von 0,1 mg/Platte nicht mutagen in S. typhimurium TA98, TA100, TA1537 oder TA1538 (Arlauskas et al 1985;Chortyk et al 1988;Löfroth und Ames 1978;Noda et al 1979;Prasanna et al 1987;Reddy et al 1983). Bei höheren Konzentrationen war es ohne metabolische Aktivierung mutagen in TA100 (2,4 mg/Platte, Noda et al 1979) und bei 4,0 mg/Platte auch in TA104, einem auf oxidierende Substanzen reagierenden Stamm (Kramer und Ames 1988).…”

Section: In Vitrounclassified

Selen und seine anorganischen Verbindungen [MAK Value Documentation in German language, 1999]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 29. Lieferung, Ausgabe 1999 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Wirkungsmechanismus Toxikokinetik und Metabolismus Erfahrungen beim Menschen Einmalige Exposition Wiederholte Exposition Wirkung auf Haut und Schleimhäute Allergene Wirkung Reproduktionstoxizität Genotoxizität Kanzerogene Wirkung Tierexperimentelle Befunde und In‐vitro‐Untersuchungen Akute Toxizität Subakute, subchronische und chronische Toxizität Wirkung auf Haut und Schleimhäute Allergene Wirkung Reproduktionstoxizität Genotoxizität Kanzerogenität Sonstige Wirkungen Bewertung

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Section: In Vitrounclassified

Selen und seine anorganischen Verbindungen [MAK Value Documentation in German language, 1999]

2012

The MAK‐Collection for Occupational Health and Safety

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“…Since that time, the antimutagenic effect of selenium, largely in the form of inorganic selenite, has been observed with numerous chemicals including 3,6-bis(dimethylamino)acridine (acridine orange) and 7,12-dimethylbenz [a]anthracene [3], benzo [a]pyrene (B[a]P) [4,5], 3-methylcholanthrene and 3-methylcholanthrylene [5], mainstream and sidestream cigarette smoke condensate [6], and Nmethyl-N-nitrosourea and N-methyl-N'-nitro-N-nitrosoguanidine [7,8]. The selenite inhibition of B[a]P mutagenicity was attributed to its inhibitory effect on arylhydrocarbon hydroxylase (CYP1A) activity [5,9] an action which decreases the bioactivating metabolism to mutagenic metabolites [4,10].…”

Section: Introductionmentioning

confidence: 99%

The antimutagenicity of 2-substituted selenazolidine-4-(R)-carboxylic acids

El‐Sayed¹,

Hussin²,

Franklin³

2007

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Selenium can have cancer chemopreventive activity, although the mechanism of action has not been well defined. Selenazolidine-4-(R)-carboxylic acids (SCAs) were devised as prodrugs of Lselenocysteine, to provide selenium in a form and at a concentration commensurate with cancer chemopreventive activity. In the present study, a series of selenazolidines has been evaluated in the Salmonella typhimurium TA98 tester strain and all were found to possess antimutagenic activity. There was little difference between the seven selenazolidines in their effectiveness against either benzo[a]pyrene (B[a]P) or 3,6-bis(dimethylamino)acridine (acridine orange), agents which differ in their requirement for mammalian enzyme bioactivation for mutagenicity. Antimutagenic activity against acridine orange was dependent on selenazolidine concentration, and EC50 values were in the 5 -10 μM range. At 25 μM, the concentration tested in common for the two mutagens, the selenazolidines were more effective antimutagens against acridine orange than against B[a]P, with reductions in mutant frequency ranging from 54-71% for B[a]P and 79-93% for acridine orange. Efficacy against B[a]P was not enhanced when the concentration was increased to 50 μM. The similarity in efficacy among the selenazolidines against B[a]P mutagenicity, contrasted with intercompound differences in their ability to inhibit S9 CYP1A activity. The CYP1A Ki values ranged from a low of 63 μM (2-[2'-hydroxyphenyl]SCA) to a high of 1.1 mM (2-cyclohexylSCA), but all were above the concentration required to inhibit mutagenicity by 50%. Thus, all the SCAs possess antimutagenic activity against both B[a]P and acridine orange, the efficacy varies little between the individual selenazolidines, and for B[a]P, the efficacy is not proportional to the inhibitory effect on the mutagen bioactivating enzyme.

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Comparative carcinogenicity of cigarette mainstream and sidestream smoke condensates on the mouse skin

Mohtashamipur

Germann

et al. 1990

J Cancer Res Clin Oncol

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The direct carcinogenic effects of sidestream (SS) and mainstream (MS) smoke condensates of a filtered commercial brand of blond cigarettes were compared using a lifetime mouse skin tumorigenicity assay on female NMRI mice. Each cigarette was smoked by a smoking machine under the standard conditions, and the separately collected SS and MS smoke condensates were extracted with acetone/methanol as described elsewhere. These were tested for carcinogenicity on an area of 1-1.5 cm shaved skin of mice on the lower back. The mice were treated with half of each dose (5, 10 or 15 mg) twice a week, for only 3 months. No substance was used as promoter or as an additional initiator of carcinogenicity. No statistically significant difference was found when the life spans of MS-treated and untreated animals were compared. In contrast, the life spans of SS-treated mice were significantly (P less than 0.01) shorter than those of MS-treated animals or those of all three negative control groups together. The observed carcinogenic effects were based on tumours and lesions found only on the site of application of the test material. Of 210 mice (effective number, 129) serving as the negative controls, 3 developed skin lesions but no tumours. Of 210 MS-treated mice (effective number, 177), 7 developed tumours (4 malignant and 3 benign) and 35 had a uniform type of precancerous skin lesions. The numbers of tumours or lesions were not increased dose-dependently. Of 210 SS-treated animals (effective number, 182), 30 developed tumours (16 malignant and 14 benign) and 56 had a uniform type of precancerous skin lesion. The initiation of these latter lesions was found to be dose-dependent (P less than 0.001). The SS-treated animals developed two to six times more skin tumours than the MS-treated mice. Comparing the negative controls with the MS- or SS-treated animals, the overall carcinogenic effect observed was statistically significant. Comparing the MS- with SS-treated animals, the overall carcinogenic effect of SS was much higher than that of MS (P less than 0.001).

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Selenium‐mediated reduction in the mutagenicity of cigarette smoke

Cited by 8 publications

References 25 publications

Selen und seine anorganischen Verbindungen [MAK Value Documentation in German language, 1999]

Selen und seine anorganischen Verbindungen [MAK Value Documentation in German language, 1999]

The antimutagenicity of 2-substituted selenazolidine-4-(R)-carboxylic acids

Comparative carcinogenicity of cigarette mainstream and sidestream smoke condensates on the mouse skin

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