Relevant bibliographies by topics / Beta-naphthoflavone

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Beta-naphthoflavone'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Beta-naphthoflavone"

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Bars, R. G., A. M. Mitchell, C. R. Wolf, and C. R. Elcombe. "Induction of cytochrome P-450 in cultured rat hepatocytes. The heterogeneous localization of specific isoenzymes using immunocytochemistry." Biochemical Journal 262, no. 1 (1989): 151–58. http://dx.doi.org/10.1042/bj2620151.

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Primary cultures of rat hepatocytes were exposed to phenobarbitone, clofibric acid, beta-naphthoflavone, isosafrole or dexamethasone for 3 days, and the induction of several cytochrome P-450 isoenzymes was demonstrated by increased catalytic activity, by Western blotting and by immunocytochemistry. The profiles of isoenzymes induced in vitro were compared with those induced in liver microsomes of rats dosed with the same agents. Clofibric acid, an agent which has not been thoroughly investigated previously, was shown to induce both in vivo and in vitro several P-450 isoenzymes normally inducib
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Doostzadeh, J., and R. Morfin. "Effects of cytochrome P450 inhibitors and of steroid hormones on the formation of 7-hydroxylated metabolites of pregnenolone in mouse brain microsomes." Journal of Endocrinology 155, no. 2 (1997): 343–50. http://dx.doi.org/10.1677/joe.0.1550343.

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Hydroxylations of pregnenolone (PREG) at the 7 alpha- and 7 beta-positions have been reported in numerous murine tissues and organs and responsible cytochrome P450 (CYP) species await identification. Using thin layer chromatography and gas chromatography-mass spectrometry, we report identification of 7 alpha-hydroxy-PREG and 7 beta-hydroxy-PREG metabolites produced in mouse brain microsome digests and kinetic studies of their production with apparent KM values of 0.5 +/- 0.1 microM and 5.1 +/- 0.6 microM for 7 alpha- and 7 beta-hydroxylation respectively. Investigation of CYP inhibitors and of
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Cantoni, L., M. Rizzardini, M. R. Cabello Porras, R. Carcano, M. Zappone, and M. Carelli. "Interferon beta reduces phenobarbital-and beta-naphthoflavone-mediated induction of cytochrome(s) P-450." Pharmacological Research 31 (January 1995): 364. http://dx.doi.org/10.1016/1043-6618(95)87715-0.

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Wilson, JM, MM Vijayan, CJ Kennedy, GK Iwama, and TW Moon. "beta-Naphthoflavone abolishes interrenal sensitivity to ACTH stimulation in rainbow trout." Journal of Endocrinology 157, no. 1 (1998): 63–70. http://dx.doi.org/10.1677/joe.0.1570063.

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We report for the first time that beta-naphthoflavone (BNF) abolishes ACTH stimulation of cortisol production in rainbow trout (Oncorhynchus mykiss). There was significantly higher hepatic cytochrome P450 content and ethoxyresorufin O-de-ethylase and uridine-5'-diphosphoglucuronic acid transferase activities in BNF-treated fish than in sham-treated controls. BNF did not significantly affect either plasma turnover or tissue distribution of [3H]cortisol-derived radioactivity. Hepatic membrane fluidity and hepatocyte capacity for cortisol uptake were not altered by BNF as compared with the sham-t
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Mohinta, Sonia, Gary Perdew, and Avery August. "Aryl Hydrocarbon Receptor independent production of IL-17A in a murine model of Hypersensitivity Pneumonitis (87.12)." Journal of Immunology 184, no. 1_Supplement (2010): 87.12. http://dx.doi.org/10.4049/jimmunol.184.supp.87.12.

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Abstract AhR (Aryl hydrocarbon Receptor) is a cytosolic transcription factor functioning as a sensor for environmental toxins. Recently, AhR has been suggested to have a cardinal role in Th17 biology. Although AhR is not a direct regulatory factor for Th17 differentiation its activation is required for the functional differentiation of Th17 cells, and production IL-22. To study the role of AhR in T cell differentiation we have used selective ligands of AhR in an in vitro assay and found that AhR agonist beta-naphthoflavone enhances IL-17 production whereas an AhR inhibitor suppresses it, both
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Hayashi, Hitomi, Eriko Taniai, Reiko Morita, et al. "Threshold dose of liver tumor promoting effect of β-naphthoflavone in rats." Journal of Toxicological Sciences 37, no. 3 (2012): 517–26. http://dx.doi.org/10.2131/jts.37.517.

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Small, D. S., and P. J. McNamara. "Acitretin elimination in Sprague-Dawley rats pretreated with phenobarbital or beta-naphthoflavone." Drug Metabolism and Disposition 23, no. 4 (1995): 465–72. https://doi.org/10.1016/s0090-9556(25)06582-1.

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Chatuphonprasert, Waranya, Thewtas Sangkawat, Nobuo Nemoto, and Kanokwan Jarukamjorn. "Suppression of beta-naphthoflavone induced CYP1A expression and lipid-peroxidation by berberine." Fitoterapia 82, no. 6 (2011): 889–95. http://dx.doi.org/10.1016/j.fitote.2011.05.002.

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Hsu, Sheng-Yao, Je-Wen Liou, Tsung-Lin Cheng, et al. "beta-Naphthoflavone protects from peritonitis by reducing TNF-alpha-induced endothelial cell activation." Pharmacological Research 102 (December 2015): 192–99. http://dx.doi.org/10.1016/j.phrs.2015.10.001.

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Smith, A. G., and J. E. Francis. "Chemically-induced formation of an inhibitor of hepatic uroporphyrinogen decarboxylase in inbred mice with iron overload." Biochemical Journal 246, no. 1 (1987): 221–26. http://dx.doi.org/10.1042/bj2460221.

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An inhibitor of hepatic uroporphyrinogen decarboxylase (EC 4.1.1.37) was demonstrated in heat-treated extracts of livers from C57BL/10ScSn mice with iron overload after a single dose (100 mg/kg; 350 mumol/kg) of hexachlorobenzene (HCB). Inhibition was not due to accumulated uroporphyrin since this could be removed by a SEP-PAK C18 cartridge without affecting inhibitor activity. The presence of the inhibitor could be first demonstrated 2 weeks after mice received HCB and before major elevation of hepatic porphyrin levels. Maximum inhibitory potential was reached at about 8 weeks and was still d
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Dissertations / Theses on the topic "Beta-naphthoflavone"

1

Sun, Mingwei. "REGULATION OF CIRCADIAN CLOCKS AND METABOLISM BY SYNTHETIC AHR AGONIST BETA-NAPHTHOFLAVONE IN MICE." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/dissertations/1253.

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The circadian clock system is essential for mammals to adapt to environmental conditions such as light-dark cycles and to manage the optimal timing for cyclical physiological processes, including sleep-wakefulness, fasting-feeding and multiple aspects of metabolism. The circadian timing system is arranged in hierarchical fashion, with the master clock in the suprachiasmatic nucleus (SCN) of the hypothalamus, acting as the pace-maker and maintaining synchrony among clocks found in every organ system throughout the body. The core molecular clock consists of two interconnected transcriptional-tra
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Gambaro, Sabrina Eliana. "Ruolo dei citocromi P450 cerebrali nell’ossidazione della bilirubina: inducibilità ed attività." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10116.

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2012/2013<br>Abstract Hyperbilirubinemia is the most common clinical diagnosis during neona- tal life. The neonatal jaundice may be physiological without any clinical consequence, or can lead to an acute form of bilirubin en- cephalopathy with minimal neurological damage, or to more severe and dangerous condition called kernicterus (permanent neurological sequelae). The Gunn rat is one of the models in which bilirubin encephalopathy was studied. It was shown that jaundiced newborn animals display an hepatic compensatory mechanism for the incapacity to
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Conference papers on the topic "Beta-naphthoflavone"

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Callaway, D., W. Jiang, K. Lingappan, and B. Moorthy. "Decreased Survival and Increased Oxygen-Mediated Lung Injury in Mice Lacking Nrf2: Protection by Beta-Naphthoflavone." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1158.

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You might also be interested in the extended bibliographies on the topic 'Beta-naphthoflavone' for particular source types:
Journal articles
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