1
|
Korashy HM and El-Kadi AO: The role of
aryl hydrocarbon receptor in the pathogenesis of cardiovascular
diseases. Drug Metab Rev. 38:411–450. 2006. View Article : Google Scholar : PubMed/NCBI
|
2
|
Kann S, Huang MY, Estes C, Reichard JF,
Sartor MA, Xia Y and Puga A: Arsenite-induced aryl hydrocarbon
receptor nuclear translocation results in additive induction of
phase I genes and synergistic induction of phase II genes. Mol
Pharmacol. 68:336–346. 2005.PubMed/NCBI
|
3
|
Nebert DW, Dalton TP, Okey AB and Gonzalez
FJ: Role of aryl hydrocarbon receptor-mediated induction of the
CYP1 enzymes in environmental toxicity and cancer. J Biol Chem.
279:23847–23850. 2004. View Article : Google Scholar : PubMed/NCBI
|
4
|
Fujii-Kuriyama Y and Mimura J: Molecular
mechanisms of AhR functions in the regulation of cytochrome P450
genes. Biochem Biophys Res Commun. 338:311–317. 2005. View Article : Google Scholar : PubMed/NCBI
|
5
|
Thum T and Borlak J: Testosterone,
cytochrome P450 and cardiac hypertrophy. FASEB J. 16:1537–1549.
2002. View Article : Google Scholar : PubMed/NCBI
|
6
|
Granberg AL, Brunström B and Brandt I:
Cytochrome P450-dependent binding of 7,12-dimethylbenz[a]anthracene
(DMBA) and benzo[a]pyrene (B[a]P) in murine heart, lung and liver
endothelial cells. Arch Toxicol. 74:593–601. 2000. View Article : Google Scholar : PubMed/NCBI
|
7
|
Zordoky BN and El-Kadi AO:
2,3,7,8-Tetrachlorodibenzo-p-dioxin and beta-naphthoflavone induce
cellular hypertrophy in H9c2 cells by an aryl hydrocarbon
receptor-dependant mechanism. Toxicol In Vitro. 24:863–871. 2010.
View Article : Google Scholar : PubMed/NCBI
|
8
|
Senft AP, Dalton TP, Nebert DW, Genter MB,
Puga A, Hutchinson RJ, Kerzee JK, Uno S and Shertzer HG:
Mitochondrial reactive oxygen production is dependent on the
aromatic hydrocarbon receptor. Free Radic Biol Med. 33:1268–1278.
2002. View Article : Google Scholar : PubMed/NCBI
|
9
|
Aboutabl ME and El-Kadi AO: Constitutive
expression and inducibility of CYP1A1 in the H9c2 rat
cardiomyoblast cells. Toxicol In Vitro. 21:1686–1691. 2007.
View Article : Google Scholar : PubMed/NCBI
|
10
|
Dong H, Dalton TP, Miller ML, Chen Y, Uno
S, Shi Z, Shertzer HG, Bansal S, Avadhani NG and Nebert DW:
Knock-in mouse lines expressing either mitochondrial or microsomal
CYP1A1: Differing responses to dietary benzo[a]pyrene as proof of
principle. Mol Pharmacol. 75:555–567. 2009. View Article : Google Scholar : PubMed/NCBI
|
11
|
Schlezinger JJ, White RD and Stegeman JJ:
Oxidative inactivation of cytochrome P-450 1A (CYP1A) stimulated by
3,3′, 4,4′-tetrachlorobiphenyl: Production of reactive oxygen by
vertebrate CYP1As. Mol Pharmacol. 56:588–597. 1999.PubMed/NCBI
|
12
|
Schlezinger JJ and Stegeman JJ: Induction
and suppression of cytochrome P450 1A by
3,3′,4,4′,5-pentachlorobiphenyl and its relationship to oxidative
stress in the marine fish scup (Stenotomus chrysops). Aquat
Toxicol. 52:101–115. 2001. View Article : Google Scholar : PubMed/NCBI
|
13
|
Claypool SM and Koehler CM: The complexity
of cardiolipin in health and disease. Trends Biochem Sci. 37:32–41.
2012. View Article : Google Scholar : PubMed/NCBI
|
14
|
Heid SE, Walker MK and Swanson HI:
Correlation of cardiotoxicity mediated by halogenated aromatic
hydrocarbons to aryl hydrocarbon receptor activation. Toxicol Sci.
61:187–196. 2001. View Article : Google Scholar : PubMed/NCBI
|
15
|
De Abrew KN, Thomas-Virnig CL, Rasmussen
CA, Bolterstein EA, Schlosser SJ and Allen-Hoffmann BL: TCDD
induces dermal accumulation of keratinocyte-derived matrix
metalloproteinase-10 in an organotypic model of human skin. Toxicol
Appl Pharmacol. 276:171–178. 2014. View Article : Google Scholar : PubMed/NCBI
|
16
|
Neri T, Merico V, Fiordaliso F, Salio M,
Rebuzzini P, Sacchi L, Bellazzi R, Redi CA, Zuccotti M and Garagna
S: The differentiation of cardiomyocytes from mouse embryonic stem
cells is altered by dioxin. Toxicol Lett. 202:226–236. 2011.
View Article : Google Scholar : PubMed/NCBI
|
17
|
Zordoky BN and El-Kadi AO: Modulation of
cardiac and hepatic cytochrome P450 enzymes during heart failure.
Curr Drug Metab. 9:122–128. 2008. View Article : Google Scholar : PubMed/NCBI
|
18
|
Gao S, Li H, Cai Y, Ye JT, Liu ZP, Lu J,
Huang XY, Feng XJ, Gao H, Chen SR, et al: Mitochondrial binding of
α-enolase stabilizes mitochondrial membrane: Its role in
doxorubicin-induced cardiomyocyte apoptosis. Arch Biochem Biophys.
542:46–55. 2014. View Article : Google Scholar : PubMed/NCBI
|
19
|
Hunter AL, Bai N, Laher I and Granville
DJ: Cytochrome p450 2C inhibition reduces post-ischemic vascular
dysfunction. Vascul Pharmacol. 43:213–219. 2005. View Article : Google Scholar : PubMed/NCBI
|
20
|
Granville DJ and Gottlieb RA: Having a
heart attack? Avoid the ‘HETE’! Am J Physiol Heart Circ Physiol.
291:H485–H487. 2006. View Article : Google Scholar : PubMed/NCBI
|
21
|
Nithipatikom K, Gross ER, Endsley MP,
Moore JM, Isbell MA, Falck JR, Campbell WB and Gross GJ: Inhibition
of cytochrome P450omega-hydroxylase: A novel endogenous
cardioprotective pathway. Circ Res. 95:e65–e71. 2004. View Article : Google Scholar : PubMed/NCBI
|
22
|
Denison MS, Fisher JM and Whitlock JP Jr:
Protein-DNA interactions at recognition sites for the dioxin-Ah
receptor complex. J Biol Chem. 264:16478–16482. 1989.PubMed/NCBI
|
23
|
Di Lisa F and Bernardi P: Mitochondria and
ischemia-reperfusion injury of the heart: Fixing a hole. Cardiovasc
Res. 70:191–199. 2006. View Article : Google Scholar : PubMed/NCBI
|
24
|
Yue R, Hu H, Yiu KH, Luo T, Zhou Z, Xu L,
Zhang S, Li K and Yu Z: Lycopene protects against
hypoxia/reoxygenation-induced apoptosis by preventing mitochondrial
dysfunction in primary neonatal mouse cardiomyocytes. PLoS One.
7:e507782012. View Article : Google Scholar : PubMed/NCBI
|
25
|
Paradies G, Petrosillo G, Pistolese M, Di
Venosa N, Federici A and Ruggiero FM: Decrease in mitochondrial
complex I activity in ischemic/reperfused rat heart: Involvement of
reactive oxygen species and cardiolipin. Circ Res. 94:53–59. 2004.
View Article : Google Scholar : PubMed/NCBI
|
26
|
Papanicolaou KN, Ngoh GA, Dabkowski ER,
O'Connell KA, Ribeiro RF Jr, Stanley WC and Walsh K: Cardiomyocyte
deletion of mitofusin-1 leads to mitochondrial fragmentation and
improves tolerance to ROS-induced mitochondrial dysfunction and
cell death. Am J Physiol Heart Circ Physiol. 302:H167–H179. 2012.
View Article : Google Scholar : PubMed/NCBI
|