Drug Metabolizing Enzyme Activities and Superoxide Formation in Primary and Immortalized Rat Brain Endothelial Cells

Chat, Mireille; Bayol-Denizot, Claire; Suleman, G; Roux, F.; Minn, Alain

doi:10.1016/s0024-3205(97)01061-8

Cited by 38 publications

(21 citation statements)

References 38 publications

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“…Chat et al (1998) reported a similar level of activity for P450 related enzymes in microsomes prepared from rat primary microvascular cerebrovascular endothelial cells (CVEC) and CVEC that had been immortalized (RBE4). A study that used pieces of tissue excised from the blood brain barrier of rats localized the induced expression of CYP1A to the cerebral veins and arteries, with the only activity in capillary endothelium in the vessels in the choroid plexus (Granberg et al,2003) .…”

Section: Immunochemical Identification Of Cyp1amentioning

confidence: 89%

“…Until now mammalian endothelial cell cultures have been the cells used for studies of the cellular response in the vascular system to exposure to AhR agonists (Farin et al,1994;Stegeman et al,1995;Celander et al,1997;Chat et al,1998;Thum et al,2000;Annas et al,2000b;Savouret et al,2001;Hennig et al,2002a;Borlak et al,2003;Ramadass et al,2003). Although most of the mammalian endothelial cells have been cultured from large vessels differential responses to AHR agonists have been reported, for example, between human umbilical artery vs umbilical vein cells, (Annas et al,2000b).…”

Section: Immunochemical Identification Of Cyp1amentioning

confidence: 99%

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Cytochrome P4501a Induced Differentially in Endothelial Cells Cultured From Different Organs of Anguilla Rostrata

Garrick

Woodin

Stegeman

2005

In Vitro Cell Dev Biol Anim

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Abstract:Endothelial cells are a structural barrier and an active regulator of many bodily processes. CYP1A activity is induced in the endothelium of teleosts and mammals exposed to lipophilic xenobiotics, such as polycyclic aromatic hydrocarbons, and can have significant consequences for endothelial functions. We exposed cultures of characterized endothelial cells from the heart, kidney and rete mirabile of the eel, Anguilla rostrata, to AhR agonists. In heart endothelial cells the maximum response (based on EROD activity) to TCDD, 113 pmol/mg-min, was at 1 nM TCDD and the peak response to βNF, 135 pmol/mg-min, was at 3 µM βNF. The maximum response to

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Section: Immunochemical Identification Of Cyp1amentioning

confidence: 89%

Section: Immunochemical Identification Of Cyp1amentioning

confidence: 99%

Cytochrome P4501a Induced Differentially in Endothelial Cells Cultured From Different Organs of Anguilla Rostrata

Garrick

Woodin

Stegeman

2005

In Vitro Cell Dev Biol Anim

View full text Add to dashboard Cite

show abstract

“…27 gamma-glutamyl transpeptidase (Beuckmann et al, 1995), alkaline phosphatase (Beuckmann et al, 1995), aromatic L-amino acid decarboxylase (Betz et al, 1980;Matter & Balda, 2003b), the phase I metabolising enzymes CYP1A1 (Filbrandt et al, 2004), CYP1B1 (Filbrandt et al, 2004), CYP3A4 (Ghosh et al, 2010;Ghosh et al, 2011), andCyp4x1 (AlAnizy et al, 2006), NADPH-CYP P450 reductase (Chat et al, 1998;Ghersi-Egea et al, 1988;Minn et al, 1991;Ravindranath et al, 1990), epoxide hydrolase (Ghersi-Egea et al, 1988;Minn et al, 1991), and the phase II enzymes, 1-naphthol-UDP-glucuronosyltransferase (Ghersi-Egea et al, 1988) and GSTμ (Shang et al, 2008), and GSTπ (Bauer et al, 2008;Shang et al, 2008). The presence of these enzymes in the brain microvasculature indicates the existence of a metabolic barrier.…”

Section: Blood-brain Barrier Anatomymentioning

confidence: 99%

“…En passage across the barrier and within the brain, drugs can undergo inactivation and elimination comparable to hepatic drug metabolism. In the brain, the following phase I enzymes have been identified: monoamine oxidases, CYP P450, NADPH-CYP P450 reductase, and epoxide hydrolases (Chat et al, 1998;Dutheil et al, 2010;Ghersi-Egea et al, 1998;Ghersi-Egea et al, 1988;Ghersi-Egea et al, 1993;Minn et al, 1991;Ravindranath et al, 1990). Phase II enzymes identified in the brain include UDP-glucuronosyltransferase (UGT), phenol sulfotransferase (PST), and GST (Dutheil et al, 2010;Ghersi-Egea et al, 1998;Ghersi-Egea et al, 1988;Ghersi-Egea et al, 1993;Minn et al, 1991).…”

Section: The Metabolic Blood-brain Barriermentioning

confidence: 99%

The Blood-Brain Barrier in Epilepsy

Bauer¹,

Schlichtiger²,

Pekcec³

et al. 2011

Clinical and Genetic Aspects of Epilepsy

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“…11) ROS produced by CYPs induce oxidative stress which causes various pathological conditions. [11][12][13] Some CYP family proteins, especially the CYP2C subfamily, are expressed in not only brain regions such as the cortex, hippocampus and basal ganglia, 14) but also in vascular endothelial cells, 15) thus suggesting the possibility that ROS derived from CYP result in numerous cerebral vascular disorders.…”

mentioning

confidence: 99%

Effects of Sulfaphenazole after Collagenase-Induced Experimental Intracerebral Hemorrhage in Rats

Hama

Ishihara

Watanabe

et al. 2012

Biological & Pharmaceutical Bulletin

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Treatment of intracerebral hemorrhage is often pointless, although considerable effort has been devoted to developing treatments for ischemic stroke. The purpose of this study was to determine the influence of drugs in improving neurological outcomes with pharmaceutical therapy after intracerebral hemorrhage. The free-radical hypothesis for intracerebral hemorrhage is based on the cytotoxicity triggered by blood components and its degradation products, such as heme and iron as a potent pro-oxidant atom. Sulfaphenazole (SPZ) has a different mechanism such as reactive oxygen species scavenging, in addition to the inhibition of superoxide production by cytochrome P450. The present study investigated the properties of SPZ in collagenase-induced intracerebral hemorrhage rat brain damage. The results show that systemic SPZ treatment after intracerebral hemorrhage reduces striatal dysfunction, the elevation of lipid peroxidation, and brain edema in the rat. These results suggest that SPZ is a potentially effective therapeutic approach for intracerebral hemorrhage as the effect of SPZ was initiated for either 1 h or 3 d post-intracerebral hemorrhage.Key words intracerebral hemorrhage; magnetic resonance imaging; striatum; brain edema; rotation behavior; sulfaphenazole Intracerebral hemorrhage (ICH) results from the rupture of a blood vessel in the brain, and is a major public health problem, because ICH leads to a high rate of death and disability in adults. The 30-d mortality rate is approximately 50%, and most survivors (more than 80%) are left with neurological disabilities.1) Primary ICH accounts for approximately 25% of all strokes in Asian populations including the Japanese, 2) and spontaneous ICH represents one of the most devastating types of stroke.The pathophysiology of ICH is caused by a complex chain of events starting with disruption of the blood-brain barrier (BBB) and infiltration of blood components into the brain parenchyma, resulting in a progressive edema, which starts in the first 24 h and remains elevated over several days.3) The development of therapies relies on the use of animal models. 4)The animal models are commonly produced by manipulation in the striatum, because that is the most common site of ICH (more than 50% of all ICH).1) Rosenberg and coworkers have developed a particularly elegant rat model in which intrastriatal injection of bacterial collagenase (COL) disrupts the basal lamina of cerebral capillaries and causes bleeding into the brain tissue. 5) A highly reproducible brain injury due to ICH and the ability to follow changes in vivo are necessary to properly evaluate treatments.Oxidative stress is thought to be deeply involved in secondary brain injury after ICH.6) The amount of oxidative DNA is increased after ICH in the animal model, and administration of a free radical scavenger, edaravone suppressed DNA oxidation and brain damage after ICH.7) Iron plays a role in a proposed mechanism for the generation of oxidative stress after ICH.8) Iron ions are generated by hemoglobin breakd...

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Drug Metabolizing Enzyme Activities and Superoxide Formation in Primary and Immortalized Rat Brain Endothelial Cells

Cited by 38 publications

References 38 publications

Cytochrome P4501a Induced Differentially in Endothelial Cells Cultured From Different Organs of Anguilla Rostrata

Cytochrome P4501a Induced Differentially in Endothelial Cells Cultured From Different Organs of Anguilla Rostrata

The Blood-Brain Barrier in Epilepsy

Effects of Sulfaphenazole after Collagenase-Induced Experimental Intracerebral Hemorrhage in Rats

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