This is pretty interesting; I'll stick it here rather than the CELG thread... pax et bonum, mch
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• US Pharmacopeia
Posted on April 29, 1999 06:34 AM PDT
WESTPORT, Apr 28 (Reuters Health) - Free radical-mediated oxidative damage to embryonic DNA seems to be responsible for thalidomide's teratogenicity, according to a report in the May issue of Nature Medicine.The effect is blocked by pretreatment with a free radical scavenger.
The findings raise the possibility that "...protection against oxidative stress with a free-radical scavenger may separate the therapeutic effects of thalidomide from its teratogenicity," Dr. Barbara Hales, of McGill University, in Montreal, Canada, says in an editorial accompanying the findings.
Dr. Peter G. Wells and colleagues from the University of Toronto, in Ontario, Canada, gave thalidomide by gastric intubation to a group of pregnant rabbits. Half of these females were injected 15 minutes beforehand with a free radical spin trapping agent, alpha-phenyl-N-t-butylnitrone (PBN).
As expected, the offspring of rabbits fed thalidomide alone had a high rate of postpartum death, limb defects, and other complications.However, "...pretreatment...with PBN essentially abolished the teratogenicity...of thalidomide, reduced in utero death...to control levels, and considerably reduced thalidomide-initiated fetal weight loss and postpartum lethality."
Use of antioxidants might be an important preventive therapy "...in high-risk situations in which pregnant women must take [reactive oxygen species]-initiating drugs," according to the researchers.
Nat Med 1999;5:489-490,582-585.
Copyright 1999 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters.Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon.
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