Induction of the P-450 I family of proteins by polycyclic aromatic hydrocarbons: possible relationship to their carcinogenicity

Epigenetic Toxicity of a Mixture of Polycyclic Aromatic Hydrocarbons on Gap Junctional Intercellular Communication Before and After Biodegradation

“…Also, 5 min is probably not enough time for the metabolic activation of a PAH. These results contrast with the genotoxic properties of PAHs in which the parent compound must be metabolically converted to a strong electrophile (55,56). Also, rat liver epithelial cell lines such as WB-F344 have very low cytochrome p450 activity and are probably incapable of metabolizing PAHs (57)(58)(59).…”

Epigenetic Toxicity of a Mixture of Polycyclic Aromatic Hydrocarbons on Gap Junctional Intercellular Communication Before and After Biodegradation

“…Also, 5 min is probably not enough time for the metabolic activation of a PAH. These results contrast with the genotoxic properties of PAHs in which the parent compound must be metabolically converted to a strong electrophile (55,56). Also, rat liver epithelial cell lines such as WB-F344 have very low cytochrome p450 activity and are probably incapable of metabolizing PAHs (57)(58)(59).…”

Inorganic arsenic trioxide induces gap junction loss in association with the downregulation of connexin43 and E‐cadherin in rat hepatic “stem‐like” cells

“…DDT inhibits GJIC in WB‐F344 rat liver epithelial cells and is regarded to have liver tumorigenic activity [20]. The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31].…”

“…The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31]. Several oncogenes have also been reported as inhibiting GJIC [32].…”

Aryl hydrocarbon hydroxylase activity in F-344 rats subchronically exposed to benzo(a)pyrene and fluoranthene through diet

“…Using the induction equivalency factors, Till et al [29] found that B(a)p was a more effective inducer of EROD activity than FLA in rat hepatocyte cultures. When microsomal preparations incubated with various PAHs were tested by Ayrton et al [30], B(a)p showed more potency than the rest.…”

Epigenetic Toxicity of a Mixture of Polycyclic Aromatic Hydrocarbons on Gap Junctional Intercellular Communication Before and After Biodegradation

“…Also, 5 min is probably not enough time for the metabolic activation of a PAH. These results contrast with the genotoxic properties of PAHs in which the parent compound must be metabolically converted to a strong electrophile (55,56). Also, rat liver epithelial cell lines such as WB-F344 have very low cytochrome p450 activity and are probably incapable of metabolizing PAHs (57)(58)(59).…”

Inorganic arsenic trioxide induces gap junction loss in association with the downregulation of connexin43 and E‐cadherin in rat hepatic “stem‐like” cells

“…DDT inhibits GJIC in WB‐F344 rat liver epithelial cells and is regarded to have liver tumorigenic activity [20]. The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31].…”

“…The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31]. Several oncogenes have also been reported as inhibiting GJIC [32].…”

Aryl hydrocarbon hydroxylase activity in F-344 rats subchronically exposed to benzo(a)pyrene and fluoranthene through diet

“…Using the induction equivalency factors, Till et al [29] found that B(a)p was a more effective inducer of EROD activity than FLA in rat hepatocyte cultures. When microsomal preparations incubated with various PAHs were tested by Ayrton et al [30], B(a)p showed more potency than the rest.…”

Epigenetic Toxicity of a Mixture of Polycyclic Aromatic Hydrocarbons on Gap Junctional Intercellular Communication Before and After Biodegradation

“…Also, 5 min is probably not enough time for the metabolic activation of a PAH. These results contrast with the genotoxic properties of PAHs in which the parent compound must be metabolically converted to a strong electrophile (55,56). Also, rat liver epithelial cell lines such as WB-F344 have very low cytochrome p450 activity and are probably incapable of metabolizing PAHs (57)(58)(59).…”

Inorganic arsenic trioxide induces gap junction loss in association with the downregulation of connexin43 and E‐cadherin in rat hepatic “stem‐like” cells

“…DDT inhibits GJIC in WB‐F344 rat liver epithelial cells and is regarded to have liver tumorigenic activity [20]. The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31].…”

“…The ozonation products of benzo( a )pyrene inhibit cell communication [28] and are believed to be carcinogenic [29]. It has been reported that chemicals such as dioxins, polychlorinated aromatic hydrocarbons, and cadmium, which can promote tumorigenesis, have been linked to decreased gap junctional intercellular communication in cultured hepatocytes [29–31]. Several oncogenes have also been reported as inhibiting GJIC [32].…”

Aryl hydrocarbon hydroxylase activity in F-344 rats subchronically exposed to benzo(a)pyrene and fluoranthene through diet

“…Using the induction equivalency factors, Till et al [29] found that B(a)p was a more effective inducer of EROD activity than FLA in rat hepatocyte cultures. When microsomal preparations incubated with various PAHs were tested by Ayrton et al [30], B(a)p showed more potency than the rest.…”