Volume 87 Issue 20 | p. 40 | Concentrates
Issue Date: May 18, 2009

Thalidomide Defects Possibly Tied To Blood Vessel Loss

An analog of the former morning sickness drug is shown to interfere with vascular growth during limb development in chick embryos
Department: Science & Technology
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A normal chick wing (left) compared with two chicks exposed to CPS49; one wing is missing the "handplate" entirely (center) while the other has significantly shortened digits (right).
Credit: Proc. Natl. Acad. Sci. USA
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A normal chick wing (left) compared with two chicks exposed to CPS49; one wing is missing the "handplate" entirely (center) while the other has significantly shortened digits (right).
Credit: Proc. Natl. Acad. Sci. USA
8720scicon_cps49
 

Thalidomide, once a popular treatment for morning sickness, causes a variety of birth defects, most commonly malformed limbs. A research group led by Neil Vargesson of the University of Aberdeen, in Scotland, has uncovered new details of the mechanism by which thalidomide causes limb deformities (Proc. Natl. Acad. Sci. USA, DOI: 10.1073/pnas.0901505106). The team exposed chick embryos to four thalidomide metabolic by-products or analogs. Three of the compounds showed no effects on embryo development, but the fourth, a fluorinated thalidomide analog called CPS49, destroyed newly formed blood vessels. When the researchers exposed embryos to CPS49 during a period when limb vasculature was rapidly developing, the embryos formed severe wing defects. Other embryonic regions with more mature vessels continued to grow normally, despite a temporary halt to vessel growth. Pregnant women who took thalidomide decades ago likely did so during embryonic limb development, which occurs early on during pregnancy at roughly the same time as the onset of morning sickness. Vargesson and colleagues are continuing to investigate whether the effects on developing vasculature could be tied to thalidomide-induced birth defects in other parts of the body.

 
Chemical & Engineering News
ISSN 0009-2347
Copyright © American Chemical Society

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