Research paperInhibition of all-trans-retinoic acid metabolism by fluconazole in vitro and in patients with acute promyelocytic leukemia☆
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An adverse outcome pathway on the disruption of retinoic acid metabolism leading to developmental craniofacial defects
2021, ToxicologyCitation Excerpt :Most of these models represent the sensitive developmental stage. In addition, treatment with fluconazole, a pharmaceutical triazole, of adult humans with acute promyelocytic leukemia results in increased RA levels in their blood supporting inhibition of RA catabolism (Schwartz et al., 1995; Vanier et al., 2003). The CYP26-inhibiting effect is thus consistent across numerous cell types and similar with different exposure conditions.
Therapeutic drug monitoring for antifungal triazoles: pharmacologic background and current status
2020, Handbook of Analytical SeparationsThe Ascidian Embryo Teratogenicity assay in Ciona intestinalis as a new teratological screening to test the mixture effect of the co-exposure to ethanol and fluconazole
2018, Environmental Toxicology and PharmacologyCitation Excerpt :The mixture effect of the co-exposure to azole fungicides and Eth has never been investigated until now. This evidence, together with the notions that RA is implicated in the correct differentiation of the anterior structures, suggests that the alterations of the pigmented organs could be the result of a perturbation in RA content during early development (Schwartz et al., 1995; Menegola et al., 2004, 2006a,b), giving rise to the hypothesis that Eth and FLUCO could somehow act affecting the RA pathway. Eth involvement in this process represents an intriguing but still highly speculative hypothesis also for vertebrates and further experiments to confirm azoles and ethanol interferences in RA pathways in mammals are needed.
Molecular recognition of CYP26A1 binding pockets and structure-activity relationship studies for design of potent and selective retinoic acid metabolism blocking agents
2015, Journal of Molecular Graphics and ModellingCitation Excerpt :To date, several chemical families of RAMBAs targeting CYP26A1 have been described [18–23]. The antimycotic substance such as ketoconazole, itraconazole, miconazole and fluconazole were the first generation compounds [18–20], which were evaluated as the potent blocking agents to inhibit CYP26A1 activity. Unfortunately, there are adverse side effects for those compounds that have been attributed to the lack of CYP26 isoform specificity.
Role of Retinoic Acid-Metabolizing Cytochrome P450s, CYP26, in Inflammation and Cancer
2015, Advances in PharmacologyCitation Excerpt :The authors proposed that autoinduction of a CYP enzyme responsible for atRA metabolism occurred with prolonged treatment with atRA (Muindi et al., 1992). This proposal was further confirmed by the observation that pretreatment with fluconazole, an inhibitor of CYP enzymes, caused over fourfold increase in atRA AUC in APL patients (Schwartz, Hallam, Gallagher, & Wiernik, 1995). After identification of CYP26 as the atRA hydroxylase, atRA treatment was shown to induce CYP26 mRNA in APL patient derived model cell lines (NB4 and HL-60) (Idres et al., 2005; Ozpolat, Mehta, & Lopez-Berestein, 2005; Ozpolat, Mehta, Tari, & Lopez-Berestein, 2002).
Biomarkers of teratogenesis: Suggestions from animal studies
2012, Reproductive Toxicology
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