Drug–virus interaction: effect of administration of recombinant adenoviruses on the pharmacokinetics of docetaxel in a rat model

Wonganan, Piyanuch; Zamboni, William C.; Strychor, Sandra; Dekker, Joseph D.; Croyle, Maria A.

doi:10.1038/cgt.2008.99

Cited by 13 publications

(6 citation statements)

References 52 publications

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“…Mice treated with poly rI:rC also had significantly lower mortality with doses of APAP up to 900 mg/kg, with a decrease in necrosis but without any effect on glutathione levels (110). Acute infection with a recombinant adenovirus has been shown to inhibit Cyp3a2, resulting in a depression of docetaxel metabolism (111), and a recent study using mice infected with a replication-deficient adenovirus showed decreased expression of Cyp1a2 and Cyp2e1 mRNA, accompanied by protection against subsequent APAP hepatotoxicity (112). However, activities of the major human cytochrome P450s were found to be similar in both noninfected and chimeric mice with humanized liver (PXB mice) infected with HCV (113) and mice overexpressing the HCV core protein in liver mitochondria showed no change in Cyp2e1 protein levels (A. Ramachandran and H. Jaeschke, unpublished data).…”

Section: Bacterial and Viral Infections And Acetaminophen Toxicitymentioning

confidence: 99%

Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity

Jaeschke

Williams

Ramachandran

et al. 2011

Liver International

417

368

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Acetaminophen (APAP) hepatotoxicity because of overdose is the most frequent cause of acute liver failure in the western world. Metabolic activation of APAP and protein adduct formation, mitochondrial dysfunction, oxidant stress, peroxynitrite formation and nuclear DNA fragmentation are critical intracellular events in hepatocytes. However, the early cell necrosis causes the release of a number of mediators such as high-mobility group box 1 protein, DNA fragments, heat shock proteins (HSPs) and others (collectively named damage-associated molecular patterns), which can be recognized by toll-like receptors on macrophages, and leads to their activation with cytokine and chemokine formation. Although pro-inflammatory mediators recruit inflammatory cells (neutrophils, monocytes) into the liver, neither the infiltrating cells nor the activated resident macrophages cause any direct cytotoxicity. In contrast, pro- and anti-inflammatory cytokines and chemokines can directly promote intracellular injury mechanisms by inducing nitric oxide synthase or inhibit cell death mechanisms by the expression of acute-phase proteins (HSPs, heme oxygenase-1) and promote hepatocyte proliferation. In addition, the newly recruited macrophages (M2) and potentially neutrophils are involved in the removal of necrotic cell debris in preparation for tissue repair and resolution of the inflammatory response. Thus, as discussed in detail in this review, the preponderance of experimental evidence suggests that the extensive sterile inflammatory response during APAP hepatotoxicity is predominantly beneficial by limiting the formation and the impact of pro-inflammatory mediators and by promoting tissue repair.

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Section: Bacterial and Viral Infections And Acetaminophen Toxicitymentioning

confidence: 99%

Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity

Jaeschke

Williams

Ramachandran

et al. 2011

Liver International

417

368

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“…In addition, an increase in AUC and C max of several anti-retrovirals are reported in HCV-infected patients with moderate liver impairment [64, 65]. Other studies also showed significantly higher AUC of docetaxel and reduced glomerular filtration rate, suggesting changes in renal CYP in rats injected with the recombinant adenovirus expressing β-galactosidase [56, 66]. …”

Section: Infection and Inflammationmentioning

confidence: 99%

Drug Disposition in Pathophysiological Conditions

Gandhi¹,

Moorthy²,

Ghose³

2012

CDM

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Expression and activity of several key drug metabolizing enzymes (DMEs) and transporters are altered in various pathophysiological conditions, leading to altered drug metabolism and disposition. This can have profound impact on the pharmacotherapy of widely used clinically relevant medications in terms of safety and efficacy by causing inter-individual variabilities in drug responses. This review article highlights altered drug disposition in inflammation and infectious diseases, and commonly encountered disorders such as cancer, obesity/diabetes, fatty liver diseases, cardiovascular diseases and rheumatoid arthritis. Many of the clinically relevant drugs have a narrow therapeutic index. Thus any changes in the disposition of these drugs may lead to reduced efficacy and increased toxicity. The implications of changes in DMEs and transporters on the pharmacokinetics/pharmacodynamics of clinically-relevant medications are also discussed. Inflammation-mediated release of pro-inflammatory cytokines and activation of toll-like receptors (TLRs) are known to play a major role in down-regulation of DMEs and transporters. Although the mechanism by which this occurs is unclear, several studies have shown that inflammation-associated cell-signaling pathway and its interaction with basal transcription factors and nuclear receptors in regulation of DMEs and transporters play a significant role in altered drug metabolism. Altered regulation of DMEs and transporters in a multitude of disease states will contribute towards future development of powerful in vitro and in vivo tools in predicting the drug response and opt for better drug design and development. The goal is to facilitate a better understanding of the mechanistic details underlying the regulation of DMEs and transporters in pathophysiological conditions.

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“…There are some researches on derivative compounds from taxanes, such as DTX, TM-2 and Larotaxel [27] , [28] , [29] . Compared with DTX, 6258-70 has a longer t 1/2 and a higher CL z [20] .…”

Section: Resultsmentioning

confidence: 99%

Determination of 6258-70, a new semi-synthetic taxane, in rat plasma and tissues: Application to the pharmacokinetics and tissue distribution study

Zhao

Zhang

et al. 2016

Journal of Pharmaceutical Analysis

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Cancer is the leading cause of death all over the world. Among the chemotherapy drugs, taxanes play an important role in cancer treatment. 6258-70 is a new semi-synthetic taxane which has a broad spectrum of antitumor activity. A fast and reliable high performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS) method was developed for quantification of 6258-70 in rat plasma and tissues in this paper. After extraction by liquid-liquid extraction method with methyl tert-butyl ether, the samples were separated on a Kinetex C18 column (50 mm×2.1 mm, 2.6 µm, Phenomenex, USA) within 3 min. The method was fully validated with the matrix effect between 87.7% and 99.5% and the recovery ranging from 80.3% to 90.1%. The intra- and inter-day precisions were less than 9.5% and the accuracy ranged from −3.8% to 6.5%. The reliable method was successfully applied to the pharmacokinetics and tissue distribution studies of 6258-70 after intravenous administration in rats. The pharmacokinetic results indicated that the pharmacokinetic behavior of 6258-70 in rats was in accordance with linear features within tested dosage of 1 to 4 mg/kg, and there was no significant difference between the two genders. The tissue distribution study showed that 6258-70 had an effective penetration, spread widely and rapidly and could cross blood-brain barrier. The results of pharmacokinetics and tissue distribution may provide a guide for future study.

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Drug–virus interaction: effect of administration of recombinant adenoviruses on the pharmacokinetics of docetaxel in a rat model

Cited by 13 publications

References 52 publications

Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity

Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity

Drug Disposition in Pathophysiological Conditions

Determination of 6258-70, a new semi-synthetic taxane, in rat plasma and tissues: Application to the pharmacokinetics and tissue distribution study

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