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Fluoranthene induced

B-cell lymphopoiesis in mouse bone marrow has been shown to be inhibited by incubation with fluoranthene In vitro at concentrations of >5 ig/mL (25 pmol). This effect on B- cell precursors may be mediated in part by a stimulation of programmed cell death, as demonstrated by the increase in DNA fragmentation induced by fluoranthene 15-17 hours after addition to the incubation medium. Furthermore, fluoranthene-induced DNA fragmentation always preceded fluoranthene-induced B-cell precursor death. Another mechanism for fluoranthene-induced inhibition of B-cell lymphopoiesis may be alterations in cell growth rates (fluoranthene was shown to slow the rate of B-cell precursor growth at concentrations <5 ig/mL) and/or altered cell survival (Hinoshita et al. 1992). [Pg.117]

Hinoshita F, Hardin JA, Sherr DH. 1992. Fluoranthene induces programmed cell death and alters growth of immature B cell populations in bone marrow cultures. Toxicology 73(2) 203-218. [Pg.476]

Saimders, C. R., Shockley, D. C. Knuckles, M. E. (2003). Fluoranthene-induced neurobehavioral toxicity in F-344 rats. International Journal of Toxicology, 22,263—276. [Pg.421]

An older procedure based upon the thermally induced decarboxylation of sodium chlorodifluoroacetate in the presence of triphenylphosphine was used to introduce the difluoromethylene group into a substituted benzo[h]fluoranthene [48] (equation 46)... [Pg.583]

Human activities have resulted in exposure of Antarctic fishes to petroleum-derived PAHs (McDonald et al. 1992). Fish captured near Palmer station on the Antarctic peninsula had induced EROD activities and elevated concentrations of biliary PAH metabolites of phenanthrene and naphthalene when compared to conspecifics from reference sites (McDonald et al. 1995). Artificial reefs consisting of oil and coal flyash stabilized with cement and lime in Florida waters near Vero Beach contained elevated PAH levels ranging from as high as 1.2 mg fluoranthene/kg and 0.25 mg naphthalene/kg. But there is negligible leaching because seawater is not an effective medium for removing PAHs from reef bricks or the ash (Frease and Windsor 1991). [Pg.1346]

Fig. 12. Procedure for analyzing and determining the TU of the eighth PAH compound in mixture 8-C1 (i.e., TU8 for fluoranthene, Table 9) that would induce 50% growth inhibition for the fresh water alga Selenastrum capricornutum... Fig. 12. Procedure for analyzing and determining the TU of the eighth PAH compound in mixture 8-C1 (i.e., TU8 for fluoranthene, Table 9) that would induce 50% growth inhibition for the fresh water alga Selenastrum capricornutum...
If PAH-degrading microorganisms use broad-specificity enzymes or common pathways to transform multiple PAHs, then inducers for the metabolism of one PAH substrate might co-induce the transformation of a range of PAHs. Preliminary evidence indicated that the transformation of naphthalene, phenanthrene, fluoranthene, and pyrene by Pseudomonas saccharophila P15 was stimulated by salicylate [132], a known inducer of naphthalene metabolism in pseudomonads [43]. However, Chen and Aitken [181] reported in more detail the inducing effects of salicylate on the transformation of various HMW PAHs by Pseudomonas saccharophila P15 isolated from contaminated soil, including... [Pg.382]

In a two-year toxicological study (Culp et al., 2000), the incidences of tumours and DNA adducts in mice fed either coal tar or pure benzo[a] pyrene were examined. Benzo[a]pyrene formed adducts readily with DNA and appeared to be responsible for forestomach tumours, like those induced by ingestion of coal tar, but not for lung tumours. Other mice that were fed coal tar (Koganti et al., 2001) had DNA adducts with benzo[u]pyrene, benzo[c]fluorene and benzo[Z)]fluoranthene in the lungs, but those fed coal tar-contaminated soil had only the adducts with benzo[c]fluorene and benzo[ ]fluoranthene. Although benzo[u]pyrene activation has been studied extensively, little is known about the activation mechanisms of benzofluor-enes and benzofluoranthenes. [Pg.185]

The - C NMR spectrum for C ) (18 h integration) consists of a single line (Fig. 3n), as required, at 142.68 ppm, and unaltered by proton decoupling. This is significantly down-field from the peaks for the corresponding positions in naphthalene (133.7 ppm), acenaphthylene (128.65 ppm), and benzo(g./i,i,]fluoranthene (126.85,128.05 and 137.75 ppm). This is not unexpected since strain produces downfield shifts which may be attributed to strain-induced hybridisation changes, as shown for example by the C peaks for the bridgehead carbons in tetralin (136.8 ppm), indane (143.9 ppm) and benzcyclobutene (146.3 ppm). ... [Pg.36]

Weinstein, I.E., l.T. Oris and D.H. Taylor. An ultrastructural examination of the mode of UV-induced toxic action of fluoranthene in fathead minnows, Pimephales promelas. Aquat. Toxicol. 39 1-22, 1997. [Pg.84]

Complete Carcinogenesis Studies. Studies in laboratory animals have demonstrated the ability of benz[a]anthracene, benzo[b]fluoranthene, benzo[j]fluoranthene, benzo[a]pyrene, chrysene, dibenz[a,h,]anthracene, and indeno[1,2,3-c,d]pyrene to induce skin tumors (i.e., they are complete carcinogens) following intermediate dermal exposure. Anthracene, fluoranthene, fluorene, phenanthrene, and pyrene do not act as complete carcinogens. The data supporting these conclusions are discussed below by chemical. Only those studies considered adequate and reliable with respect to study design and adequacy of reporting are presented in Table 2-3. [Pg.74]

BenzoUJfI uoranthene. Benzo[j]fluoranthene (0.1% or 0.5%) applied to the skin of female Swiss mice thrice weekly for life induced skin papillomas in 70% and 95% of the animals, respectively, and skin carcinomas in 105% and 95% of the animals, respectively, after 9 months of treatment (Wynder and Hoffmann 1959b). [Pg.75]

Chronic dermal application of up to 1 % fluoranthene to the backs of mice did not induce skin tumors following a lifetime of application (Hoffmann et al. 1972 Horton and Christian 1974 Wynder and Hoffmann 1959a). [Pg.78]

Interactions between selected noncarcinogenic PAHs and carcinogenic benzo[a]pyrene have also been documented to reduce the carcinogenic potential of benzo[a]pyrene in animals. Benzo[a]fluoranthene, benzo[k]fluoranthene, chrysene, perylene, and a mixture of anthracene, phenanthracene, and pyrene significantly inhibited benzo[a]pyrene-induced injection-site sarcomas. However, other PAHs including anthracene, benzo[g,h,i]perylene, fluorene, and indeno[1,2,3-c,d]pyrene had no antagonistic effects (Falk et al. 1964). Coexposure of tracheal explants to benzo[e]pyrene and benzo[a]pyrene resulted in an increased incidence of tracheal epithelial sarcomas over that seen with either PAH alone (Topping et al. 1981). Phenanthrene administration with benzo[a]pyrene decreased the DNA adduct formation in mice (Rice et al. 1984). [Pg.187]

Benzo[a]pyrene and dibenz[a,h]anthracene in combination with 10 noncarcinogenic PAHs were less potent tumor-inducers than was dibenz[a,h]anthracene alone or in combination with benzo[a]pyrene. The noncarcinogenic or weakly carcinogenic PAHs include benzo[e]pyrene, phenanthrene, anthracene, pyrene, fluoranthene, chrysene, perylene, benzo[g,h,i]pyrene, and coronene. Dose-response relationships for tumor incidences were observed for benzo[a]pyrene and dibenz[a,h]anthracene either along or in combination with the 10 noncarcinogenic PAHs however, no treatment-related sarcoma incidences were observed for any of the 10 noncarcinogenic PAHs (Pfeiffer 1977). [Pg.188]

Minnows. Only preliminary results were available with pyrene and fluoranthene. Pyrene induced no immediate acute toxicity, but a 24-h liCcQ value of 0.2 ppm was observed after only 30 min of incubation ana 1 h of irradiation with sunlight (Fig 3). In contrast, fluoranthene produced immediate light-dependent toxicity (Fig 4). [Pg.199]


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See also in sourсe #XX -- [ Pg.389 ]




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