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• W2125405502 abstract "We show here that arsenite (As³⁺) elicits multiple effects on gene control, such as the interruption of cell cycle control by initiating G₂/M arrest as well as inhibiting the aryl hydrocarbon (Ah) receptor-mediated 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin (TCDD)-inducible expression of CYP1A1. This raises the question as to whether As³⁺ is selectively inhibiting TCDD induction of CYP1A1 independent of cell cycle control. As³⁺ stimulated a concentration-dependent increase in G₂/M phase arrest that was detected at 12.5 μM As³. However, cotreatment of HepG2 cells with TCDD and concentrations of As³⁺ as low as 0.5 μM stimulated a pronounced decrease in the induction of CYP1A1-dependent ethoxyresorufin-<i>O</i>-deethylase activity and protein, indicating that the inhibition of CYP1A1 induction by As³⁺ was considerably more sensitive than As³⁺-initiated cell cycle arrest. Low concentrations of As³⁺ also initiate a dose-dependent reduction in TCDD-induced mouse Cyp1a1 as well as human CYP1A1 in primary hepatocytes cultured from transgenic <i>CYP1A1N</i>^+/- mice. Because primary hepatocytes in culture are quiescent, these results indicate that the actions of As³⁺ on TCDD-initiated induction of CYP1A1 are independent of cell cycle control. As³⁺ does not impact on Ah receptor function as evaluated by nuclear transport and binding to xenobiotic responsive element sequences, but it does reduce TCDD-induced CYP1A1 mRNA, a property that is concordant with RNA polymerase II association to the gene and the reduction in transcriptional heteronuclear RNA. We conclude from these studies that interruption of <i>CYP1A1</i>-induced transcription by As³⁺ is not dependent upon cell cycle arrest." @default.
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• W2125405502 date "2005-01-03" @default.
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• W2125405502 title "Arsenite Inhibition of CYP1A1 Induction by 2,3,7,8-Tetrachlorodibenzo-<i>p</i>-dioxin Is Independent of Cell Cycle Arrest" @default.
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• W2125405502 doi "https://doi.org/10.1124/mol.104.006130" @default.
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