Hydroxylation of quinocetone and carbadox is mediated by CYP1As in the chicken (Gallus gallus)

Yang, Jijin; Liu, Zhaoying; Li, Mei; Qiu, Xinghui

doi:10.1016/j.cbpc.2013.05.008

Cited by 1 publication

(3 citation statements)

References 32 publications

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“…AO, acridine orange; cCBR1, chicken carbonyl reductase 1; porcine carbonyl reductase 1; SsAOX1, porcine aldehyde oxidase. Cited from (Chen et al, 2013;Huang et al, 2015bHuang et al, , 2015cLi et al, 2014aLi et al, , 2014bLiu et al, 2008Liu et al, , 2009Liu et al, , 2010aLiu et al, , 2010bLiu et al, , 2010cLiu et al, , 2011aLiu et al, , 2011bLiu & Sun, 2013;Mu et al, 2014;Tang et al, 2012;Wang et al, 2016b;Yang et al, 2013a;Zheng et al, 2011). marked as less genotoxicity than other kinds Wang et al, , 2011b.…”

Section: Resultsmentioning

confidence: 97%

“…It was revealed that CYP1A5 catalyzed QCT to three hydroxylated metabolites, such as one hydroxylated on the phenyl ring, one on the quinoxaline ring and one on the double-bond of side chain, respectively. In addition, chicken CYP1A5 can convert CBX to a hydroxylated CBX (Yang et al, 2013a). Chicken CYP1A4 only catalyzed QCT to the metabolite with one hydroxylated on the phenyl ring and exhibited no detectable activity of CBX hydroxylation.…”

Section: Metabolizing Enzymesmentioning

confidence: 98%

“…Chicken CYP1A4 only catalyzed QCT to the metabolite with one hydroxylated on the phenyl ring and exhibited no detectable activity of CBX hydroxylation. However, chicken CYP1A4 and CYP1A5 had no detectable hydroxylation activity toward MEQ and CYA, indicating that the side chain of QdNOs will greatly affect the metabolism progress and the corresponding enzymes (Yang et al, 2013a).…”

Section: Metabolizing Enzymesmentioning

confidence: 99%

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The critical role of oxidative stress in the toxicity and metabolism of quinoxaline 1,4-di-N-oxides in vitro and in vivo

Wang

Martínez

Cheng

et al. 2016

Drug Metabolism Reviews

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Quinoxaline 1,4-dioxide derivatives (QdNOs) have been widely used as growth promoters and antibacterial agents. Carbadox (CBX), olaquindox (OLA), quinocetone (QCT), cyadox (CYA) and mequindox (MEQ) are the classical members of QdNOs. Some members of QdNOs are known to cause a variety of toxic effects. To date, however, almost no review has addressed the toxicity and metabolism of QdNOs in relation to oxidative stress. This review focused on the research progress associated with oxidative stress as a plausible mechanism for QdNO-induced toxicity and metabolism. The present review documented that the studies were performed over the past 10 years to interpret the generation of reactive oxygen species (ROS) and oxidative stress as the results of QdNO treatment and have correlated them with various types of QdNO toxicity, suggesting that oxidative stress plays critical roles in their toxicities. The major metabolic pathways of QdNOs are N→O group reduction and hydroxylation. Xanthine oxidoreductase (XOR), aldehyde oxidase (SsAOX1), carbonyl reductase (CBR1) and cytochrome P450 (CYP) enzymes were involved in the QdNOs metabolism. Further understanding the role of oxidative stress in QdNOs-induced toxicity will throw new light onto the use of antioxidants and scavengers of ROS as well as onto the blind spots of metabolism and the metabolizing enzymes of QdNOs. The present review might contribute to revealing the QdNOs toxicity, protecting against oxidative damage and helping to improve the rational use of concurrent drugs, while developing novel QdNO compounds with more efficient potentials and less toxic effects.

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