The neurotoxin, called acrolein, is produced within the body after nerve cells are damaged, increasing pain and triggering a cascade of biochemical events thought to worsen the injury's severity.
Researchers have now found that the drug, dimercaprol, removes the toxin by attacking certain chemical features of acrolein, neutralizing it for safe removal by the body. The findings, detailed in a paper published online in the Journal of Neurochemistry, involved research with cell cultures, laboratory animals and other experiments.
"Dimercaprol may be an effective acrolein scavenger and a viable candidate for acrolein detoxification," said Riyi Shi (pronounced Ree Shee), a professor of neuroscience and biomedical engineering in Purdue University's Department of Basic Medical Sciences, College of Veterinary Medicine and Weldon School of Biomedical Engineering.
"An extensive body of evidence exists suggesting the toxic nature of acrolein and its pathological role in a variety of disease processes, prompting the use of acrolein scavengers as a new therapeutic approach for alleviating symptoms and curtailing tissue damage in neuropathic disorders," Shi said. "Previous studies have shown that acrolein levels increase significantly after spinal cord injury. It may be a key factor of secondary injury, which can expand the damage to adjacent tissue."
The drug, also called 2,3-dimercaptopropanol, was developed by British biochemists during World War II as an antidote for lewisite, an obsolete arsenic-based chemical warfare agent. It is now used primarily to treat poisoning by arsenic, mercury, gold, lead, antimony, and other toxic metals. The drug also is used to treat Wilson's disease, a genetic disorder in which the body retains copper.