During the past 15 years, epidemiological,1,2 basic
biological,3- 5 and
experimental studies on atherosclerosis have supported the hypothesis that
antioxidants protect against atherosclerosis6- 8 by
limiting low-density lipoprotein oxidation in the arterial wall. This mechanism
inhibits the pathological accumulation of cholesteryl ester in plaque via
the macrophage scavenger receptor, a process that can cause plaque rupture
and cardiovascular events.9,10 Similarly,
biological mechanisms have been identified in carcinogenesis that may be blocked
by antioxidants.11- 14 In
the past decade, a number of prospective, randomized, placebo-controlled,
3- to 6-year clinical trials have been published, testing the effect of vitamin
E and other antioxidant vitamins or their combinations on clinical manifestations
of cardiovascular disease and cancer.15- 21 These
trials have surprisingly yet consistently shown that commonly used antioxidant
vitamin regimens (vitamins E, C, beta carotene, or a combination) do not significantly
reduce overall cardiovascular events or cancer.
Register and get free email Table of Contents alerts, saved searches, PowerPoint downloads, CME quizzes, and more
Subscribe for full-text access to content from 1998 forward and a host of useful features
Activate your current subscription (AMA members and current subscribers)
Purchase Online Access to this article for 24 hours
The nuclear receptor heterodimer RXR-LXR modulates the expression of
key gene products (apolipoproteins, transporters, or enzymes) affecting lipid
metabolism, via an upstream hormone response element DR4. RXR is activated
by 9-cis retinoic acid and LXR by certain nuclear oxysterols.34 By affecting these sites of gene regulation, antioxidants
could alter lipoprotein metabolism and lipid levels as has been observed.21 For example, isomers of vitamin A (retinoic acid),
the breakdown product of beta carotene, could interfere with binding of the
specific activator 9-cis retinoic acid to RXR; and antioxidants,
including vitamin E, might alter oxysterol levels or their interaction with
the LXR nuclear receptor by as yet unproven mechanisms. RXR indicates retinoid
x receptor; LXR, liver x receptor; DR, direct repeat; Apo, apolipoprotein;
ABC, ATP-binding cassette transmembrane protein; CETP, cholesterol ester transfer
protein; SREBP, sterol regulatory element-binding protein.
Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal
Some tools below are only available to our subscribers or users with an online account.
Download citation file:
Web of Science® Times Cited: 36
Customize your page view by dragging & repositioning the boxes below.
More Listings atJAMACareerCenter.com >
Users' Guides to the Medical Literature
Table 9.2-3 Refuted Evidence From Observational Studiesa
All results at
and access these and other features:
Enter your username and email address. We'll send you a link to reset your password.
Enter your username and email address. We'll send instructions on how to reset your password to the email address we have on record.
Athens and Shibboleth are access management services that provide single sign-on to protected resources. They replace the multiple user names and passwords necessary to access subscription-based content with a single user name and password that can be entered once per session. It operates independently of a user's location or IP address. If your institution uses Athens or Shibboleth authentication, please contact your site administrator to receive your user name and password.