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Ostergren, Anna
Alternative names
Publications (4 of 4) Show all publications
Ostergren, A., Fredriksson, A. & Brittebo, E. B. (2006). Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra.. J Neural Transm, 113(3), 313-29
Open this publication in new window or tab >>Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra.
2006 (English)In: J Neural Transm, ISSN 0300-9564, Vol. 113, no 3, p. 313-29Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-75602 (URN)16075188 (PubMedID)
Available from: 2006-02-13 Created: 2006-02-13 Last updated: 2011-01-11
Ostergren, A., Svensson, A.-L., Lindquist, N. G. & Brittebo, E. B. (2005). Dopamine melanin-loaded PC12 cells: a model for studies on pigmented neurons.. Pigment Cell Res, 18(4), 306-14
Open this publication in new window or tab >>Dopamine melanin-loaded PC12 cells: a model for studies on pigmented neurons.
2005 (English)In: Pigment Cell Res, ISSN 0893-5785, Vol. 18, no 4, p. 306-14Article in journal (Refereed) Published
Keywords
Amyloid beta-Protein/toxicity, Animals, Caspases/metabolism, Cell Survival/drug effects, Enzyme Activation, Heat-Shock Proteins/biosynthesis, Melanins/*metabolism/pharmacology, Microscopy; Electron; Transmission, Molecular Chaperones/biosynthesis, Neurons/drug effects/*metabolism/ultrastructure, PC12 Cells, Peptide Fragments/toxicity, Pigmentation, Rats, Research Support; Non-U.S. Gov't
Identifiers
urn:nbn:se:uu:diva-75601 (URN)16029423 (PubMedID)
Available from: 2006-02-13 Created: 2006-02-13 Last updated: 2011-01-11
Granberg, L., Östergren, A., Brandt, I. & Brittebo, E. B. (2003). CYP1A1 and CYP1B1 in blood-brain interfaces: CYP1A1-dependent bioactivation of 7,12-dimethylbenz(a)anthracene in endothelial cells.. Drug Metabolism And Disposition, 31(3), 259-265
Open this publication in new window or tab >>CYP1A1 and CYP1B1 in blood-brain interfaces: CYP1A1-dependent bioactivation of 7,12-dimethylbenz(a)anthracene in endothelial cells.
2003 (English)In: Drug Metabolism And Disposition, ISSN 0090-9556, E-ISSN 1521-009X, Vol. 31, no 3, p. 259-265Article in journal (Refereed) Published
Abstract [en]

Immunohistochemistry and autoradiography were used to identify sites of the cytochrome P450 enzymes (P450) 1A1 and 1B1 expression and activation of 7,12-dimethylbenz(a)anthracene (DMBA), in the brain of rodents pretreated with the aryl hydrocarbon receptor (AhR) agonists beta-naphthoflavone (BNF), 3,3',4,4',5-pentachlorobiphenyl or vehicle. Immunohistochemistry revealed that CYP1A1 was preferentially induced in endothelial cells (EC) in the choroid plexus, in veins in the leptomeninges, and in cerebral veins of AhR agonist-pretreated mice. No induction occurred in cerebral capillary EC. In vehicle-treated mice no localization of CYP1A1 in EC was observed. CYP1B1 was expressed in smooth muscle cells of arteries in the leptomeninges, in cerebral arteries/arterioles and to a low extent in ependymal cells of AhR agonist- and vehicle-treated mice. No CYP1B1 was detected in capillary loops of the choroid plexus or in cerebral capillaries. Following administration of [(3)H]DMBA to BNF-pretreated mice, a marked irreversible binding in EC of the choroid plexus and of veins in the leptomeninges was observed but not in cerebral capillaries. In vehicle-treated mice, there was no [(3)H]DMBA-binding at these sites. Furthermore, a high level of irreversibly bound [(3)H]DMBA occurred in EC at these sites in precision-cut mouse/rat brain slices and in excised blood-brain interfaces incubated with [(3)H]DMBA. Since [(3)H]DMBA binding sites corresponded with the sites of CYP1A1 induction, we conclude that rodents express a constitutively low but highly inducible and functional CYP1A1 in EC of some of the blood-brain interfaces. The role of CYP1A1/1B1 and environmental pollutants in the etiology of cerebrovascular disease needs further consideration.

Keywords
9;10-Dimethyl-1;2-benzanthracene/analysis/*pharmacokinetics, Animals, Aryl Hydrocarbon Hydroxylases/analysis/*metabolism, Biotransformation, Blood-Brain Barrier/*physiology, Brain/metabolism, Cytochrome P-450 CYP1A1/analysis/*metabolism, Endothelium; Vascular/*cytology/*enzymology/metabolism, Female, In Vitro, Mice, Rats, Rats; Sprague-Dawley
National Category
Pharmacology and Toxicology
Research subject
Toxicology
Identifiers
urn:nbn:se:uu:diva-67100 (URN)10.1124/dmd.31.3.259 (DOI)12584151 (PubMedID)
Available from: 2006-03-20 Created: 2006-03-20 Last updated: 2018-01-10Bibliographically approved
Östergren, A., Annas, A., Skog, K., Lindquist, N. G. & Brittebo, E. (2003). Long-term retention of neurotoxic ß-carbolines in brain neuromelanin. Journal of neural transmission, 111(2), 141-157
Open this publication in new window or tab >>Long-term retention of neurotoxic ß-carbolines in brain neuromelanin
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2003 (English)In: Journal of neural transmission, ISSN 0300-9564, E-ISSN 1435-1463, Vol. 111, no 2, p. 141-157Article in journal (Refereed) Published
Abstract [en]

beta-Carbolines show structural resemblance to the neurotoxic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and are metabolized to mitochondrial toxicants. Humans are continuously exposed to low levels of beta-carbolines through cooked food, coffee, alcoholic beverages and tobacco smoke. beta-Carbolines have previously been detected in higher levels in the pigmented substantia nigra than in the cortex of humans. The distribution of 3H-labelled harman and norharman in the brain of pigmented and albino mice and in frogs (a species having neuromelanin) was studied by tape-section and light-microscopic autoradiography. Furthermore, the binding of these beta-carbolines to dopamine-melanin and melanin granules from Sepia officinalis was examined. The results revealed a high affinity binding to melanin and a long-term retention (up to 30 days) in pigmented tissues, including neuromelanin-containing neurons of frogs after a single injection. The role of long-term exposure to food-related beta-carbolines and a retention of these compounds in pigment-containing neurons in the induction of idiopathic Parkinson's disease should be further considered.

Keywords
beta-Carbolines, parkinsonism, neuromelanin, harman, norharman, Parkinson's disease, dopamine–melanin, Sepia officinalis
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:uu:diva-64767 (URN)10.1007/s00702-003-0080-0 (DOI)14767717 (PubMedID)
Available from: 2005-05-26 Created: 2005-05-26 Last updated: 2018-01-10Bibliographically approved
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