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Thalidomide: why it spared mouse pups

You've probably heard about thalidomide, the most famous reminder of why we take such precautions with drug testing before unleashing them on the public.  It was a drug given to pregnant ladies, between about 1956 and 1962, as an anti-emetic.  The only problem was that it was heavily teratogenic to their fetuses: it gave them phocomelia, a condition in which the long bones of the child's limbs are absent and the limb is grossly reduced in size.  Over 10 000 children were born with this, and other, deformities before the drug was fingered and stopped.
 
Although the drug underwent grossly deficient testing, it did endure some testing, on mice. They didn't display phocomelia, however, and so the ill-fated drug was promptly unleashed upon the world.  Last year, scientists discovered why this discrepancy exists. 
 
"... when chicken and human embryos are exposed to thalidomide they produce superoxide, a powerful oxidising agent that causes cell death and birth defects.  Mice are apparently protected from superoxide because they also make glutathione, an antioxidant that mops up the superoxide before it can damage cells.  Human and chicken embryonic cells treated with glutathione had reduced levels of superoxide and less cell death."
 
The good news about this discovery is that thalidomide is actually otherwise quite a useful drug. Amongst other things, it has shown much promise in the treatment of multiple myeloma. Knowing the mechanism by which it produces its deleterious effects therefore opens up the possibility of modifying the drug to avoid them, whilst still retaining its beneficial properties.
 
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