Advanced

Increased smooth muscle cell proliferation by dimethylbenzanthracene is correlated to variations in activity of ornithine decarboxylase but not arylhydrocarbonhydroxylase

Pessah-Rasmussen, H LU ; Stavenow, L.; Xu, C B LU and Berglund, A (1991) In Artery 18(5). p.55-240
Abstract

Polycyclic aromatic hydrocarbons of cigarette smoke have been suggested to be involved in atherogenesis. After being converted to epoxides by monooxidases in the arterial wall the hydrocarbons may exert toxic or mutagenic effects on the smooth muscle cells (SMC). In a previous study we found that dimethylbenzanthracene (DMBA), an inducer of arylhydrocarbonhydroxylase (AHH), increased SMC proliferation and viability. In the present work we intended to study whether these effects were mediated by AHH. Alpha-naphtoflavone (ANF), a non specific AHH inhibitor, decreased SMC proliferation. The effects of ANF were totally counteracted by serum, partially by albumin and not at all by platelet derived growth factor. AHH activity was not... (More)

Polycyclic aromatic hydrocarbons of cigarette smoke have been suggested to be involved in atherogenesis. After being converted to epoxides by monooxidases in the arterial wall the hydrocarbons may exert toxic or mutagenic effects on the smooth muscle cells (SMC). In a previous study we found that dimethylbenzanthracene (DMBA), an inducer of arylhydrocarbonhydroxylase (AHH), increased SMC proliferation and viability. In the present work we intended to study whether these effects were mediated by AHH. Alpha-naphtoflavone (ANF), a non specific AHH inhibitor, decreased SMC proliferation. The effects of ANF were totally counteracted by serum, partially by albumin and not at all by platelet derived growth factor. AHH activity was not detectable nor basally nor after induction in SMC, and this made us conclude that the effects of DMBA and ANF on SMC proliferation were not mediated by AHH. On the other hand the activity of ornithine decarboxylase was influenced by DMBA and ANF in parallel to proliferation, suggesting the involvement of this enzyme in the described DMBA effects on SMC proliferation. This mechanism might be of relevance for the pathogenesis of atherosclerosis especially in relation to cigarette smoking.

(Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
9,10-Dimethyl-1,2-benzanthracene, Animals, Aorta, Thoracic, Aryl Hydrocarbon Hydroxylases, Cattle, Cell Division, Cell Survival, Cells, Cultured, Muscle, Smooth, Vascular, Ornithine Decarboxylase, Rabbits, Journal Article, Research Support, Non-U.S. Gov't
in
Artery
volume
18
issue
5
pages
16 pages
external identifiers
  • scopus:0026058529
ISSN
0098-6127
language
English
LU publication?
yes
id
ef3d614b-ff56-430d-a2aa-df42fe692118
date added to LUP
2017-08-11 15:59:02
date last changed
2017-08-14 16:55:10
@article{ef3d614b-ff56-430d-a2aa-df42fe692118,
  abstract     = {<p>Polycyclic aromatic hydrocarbons of cigarette smoke have been suggested to be involved in atherogenesis. After being converted to epoxides by monooxidases in the arterial wall the hydrocarbons may exert toxic or mutagenic effects on the smooth muscle cells (SMC). In a previous study we found that dimethylbenzanthracene (DMBA), an inducer of arylhydrocarbonhydroxylase (AHH), increased SMC proliferation and viability. In the present work we intended to study whether these effects were mediated by AHH. Alpha-naphtoflavone (ANF), a non specific AHH inhibitor, decreased SMC proliferation. The effects of ANF were totally counteracted by serum, partially by albumin and not at all by platelet derived growth factor. AHH activity was not detectable nor basally nor after induction in SMC, and this made us conclude that the effects of DMBA and ANF on SMC proliferation were not mediated by AHH. On the other hand the activity of ornithine decarboxylase was influenced by DMBA and ANF in parallel to proliferation, suggesting the involvement of this enzyme in the described DMBA effects on SMC proliferation. This mechanism might be of relevance for the pathogenesis of atherosclerosis especially in relation to cigarette smoking.</p>},
  author       = {Pessah-Rasmussen, H and Stavenow, L. and Xu, C B and Berglund, A},
  issn         = {0098-6127},
  keyword      = {9,10-Dimethyl-1,2-benzanthracene,Animals,Aorta, Thoracic,Aryl Hydrocarbon Hydroxylases,Cattle,Cell Division,Cell Survival,Cells, Cultured,Muscle, Smooth, Vascular,Ornithine Decarboxylase,Rabbits,Journal Article,Research Support, Non-U.S. Gov't},
  language     = {eng},
  number       = {5},
  pages        = {55--240},
  series       = {Artery},
  title        = {Increased smooth muscle cell proliferation by dimethylbenzanthracene is correlated to variations in activity of ornithine decarboxylase but not arylhydrocarbonhydroxylase},
  volume       = {18},
  year         = {1991},
}