disease-associated marker can be critical for making a diagnosis, a therapeutic selection and a treatment evaluation," Shi said. "Therefore, determination of acrolein levels gives you more assurance that you have an intense biochemical imbalance and biochemical damage and that you should use an acrolein scavenger as a treatment. We used different levels of hydralazine to see if it causes a dose-dependent reduction of 3-HPMA and found that, in fact, it did. This shows that this method is capable of monitoring the decrease of acrolein through treatment with acrolein-removing medications."
Acrolein damages mitochondria, which provide energy for cells, and in multiple sclerosis compromises the myelin sheath surrounding a nerve cell's axon, preventing nerves from properly conducting electrical impulses. The toxin has a possible role in other diseases, including Alzheimer's disease, cancer and atherosclerosis.
"Due to widespread involvement of acrolein in the body, the benefits of this study have the potential to significantly enhance human health," Shi said. "For example, there is evidence that heightened levels of acrolein could diminish an individual's ability to recover fully from stroke and cancer."
In laboratory animals, hydralazine has been shown to delay onset of multiple sclerosis for several days, which could mean several years in humans. Tests with animals also suggests the drug could help to reduce the most severe symptoms once the disease has progressed.
Acrolein has been found to be elevated by about 60 percent in the spinal cord tissues of mice with a disease similar to multiple sclerosis. The toxin causes harm by reacting with the proteins and lipids that make up cells, including neurons.
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