![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 56, Issue 1, 116-123, July 1999
Division of Cardiology (S.R., G.R.D., J.A., D.G.H.), Department of
Gynecology and Obstetrics (S.P.), and Microchemical Facility (M.S.,
J.P.), Emory University, Atlanta, Georgia
Retrospective epidemiological studies have suggested that antioxidant
therapy may decrease cardiovascular morbidity and mortality rates,
although the mechanisms for this effect remain unclear. In the present
study, we demonstrate that selective antioxidants can enhance
expression of endothelial nitric oxide synthase (eNOS). We found that
the antioxidants nordihydroguaiaretic acid (NDGA), catechol, glutaryl
probucol, and N-acetylcysteine increased eNOS expression
in cultured bovine aortic endothelial cells (BAECs). NDGA seemed to be
the most potent of the phenolic antioxidants, producing a 3-fold
increase in eNOS mRNA. This effect of NDGA was enhanced by nonphenolic
antioxidants such as N-acetylcysteine and ascorbic acid.
Nuclear run-on studies indicated that NDGA increased eNOS
transcription. A similar increase in eNOS protein content was observed
with Western blot analysis after treating BAECs or human aortic
endothelial cells with NDGA. Exposure of BAECs to NDGA enhanced NO
production, as measured by electron paramagnetic resonance spin
trapping and eNOS activity, as measured by
[14C]arginine-to-[14C]citrulline assay.
Methylation of the phenolic hydroxyl groups completely inhibited the
NDGA effect on eNOS mRNA levels. This effect of NDGA was not due to
inhibition of lipoxygenase because cis-5,8,11,14-eicosatetraynoic acid did not alter eNOS
expression. We conclude that antioxidants may not only increase the
bioactivity of nitric oxide but also enhance expression of the eNOS
enzyme. Such an effect may prove useful in conditions such as
hypertension and atherosclerosis, in which nitric oxide production
and/or biological activity is impaired.
This article has been cited by other articles:
|
|
 |
|
  K. Arasaki, K. Tani, T. Yoshimori, D. J. Stephens, and M. Tagaya Nordihydroguaiaretic Acid Affects Multiple Dynein-Dynactin Functions in Interphase and Mitotic Cells Mol. Pharmacol., February 1, 2007; 71(2): 454 - 460. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P Cooke ADMA: its role in vascular disease Vascular Medicine, July 1, 2005; 10(1_suppl): S11 - S17. [Abstract] [PDF]
|
|
|
|
|
|
J. P Cooke ADMA: its role in vascular disease Vascular Medicine, May 1, 2005; 10(2_suppl): S11 - S17. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Toporsian, R. Gros, M. G. Kabir, S. Vera, K. Govindaraju, D. H. Eidelman, M. Husain, and M. Letarte A Role for Endoglin in Coupling eNOS Activity and Regulating Vascular Tone Revealed in Hereditary Hemorrhagic Telangiectasia Circ. Res., April 1, 2005; 96(6): 684 - 692. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. K. Lau, S. B. Leichtweis, P. Hume, R. Mashima, J. Y. Hou, X. Chaufour, B. Wilkinson, N. H. Hunt, D. S. Celermajer, and R. Stocker Probucol Promotes Functional Reendothelialization in Balloon-Injured Rabbit Aortas Circulation, April 22, 2003; 107(15): 2031 - 2036. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Cooke Does ADMA Cause Endothelial Dysfunction? Arterioscler. Thromb. Vasc. Biol., September 1, 2000; 20(9): 2032 - 2037. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. R. Drummond, H. Cai, M. E. Davis, S. Ramasamy, and D. G. Harrison Transcriptional and Posttranscriptional Regulation of Endothelial Nitric Oxide Synthase Expression by Hydrogen Peroxide Circ. Res., February 18, 2000; 86(3): 347 - 354. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Parthasarathy, N. Santanam, S. Ramachandran, and O. Meilhac Oxidants and antioxidants in atherogenesis: an appraisal J. Lipid Res., December 1, 1999; 40(12): 2143 - 2157. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
