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Published: 10 septembre 2022 (3 semaines ago)

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In Windows, select the Language Support tab in the Control Panel and change the current language if needed.
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P-glycoprotein (P-gp) inhibits intracellular accumulation and cellular toxicity of 9,10-phenanthrenequinone.
The resistance-conferring ATP-binding cassette transporter P-glycoprotein (P-gp) is the major factor responsible for the poor response of multidrug-resistant (MDR) tumor cells to anticancer drugs. Cells overexpressing P-gp have lower intracellular concentrations of toxins and other anticancer drugs, and often exhibit lower cell killing. We determined whether P-gp alters the membrane permeability and cellular toxicity of the toxic metabolite 9,10-phenathrenequinone (PQ). P-gp-overexpressing cells containing a functional cytochrome P450 1A1 (CYP1A1) enzyme had a 60- to 170-fold increase in the cellular toxicity of PQ. Cells overexpressing P-gp had only a 50% increase in PQ uptake, despite a 40- to 50-fold increase in P-gp expression. P-gp also reduced the cellular toxicity of PQ, independent of P-gp-mediated PQ uptake. The combination of P-gp with CYP1A1 increased the membrane permeability of PQ by >10-fold, more than additive of the effects of the individual proteins. Overexpression of CYP1A1-binding protein in the nucleus increased the cellular toxicity of PQ only in cells that overexpressed P-gp. P-gp down-regulated the mRNA expression of CYP1A1 and reduced the activity of CYP1A1 toward coumarin 7-hydroxylation by 60%. Furthermore, P-gp reduced the rates of metabolism and uptake of the prodrugs entacapone and ibuprofen. These findings suggest that P-gp may serve as an MDR gene product by altering the cellular toxicity of a number of anticancer drugs through cell-mediated transport and metabolism.Laser-induced optical nonlinearity and its application to a supercontinuum generation in an optical fiber.
A third-order nonlinear material was shown to be very useful for the generation of a continuum tunable over 1.5