CORVALLIS, Ore. Researchers have discovered how oxidative stress can turn to the dark side a cellular protein that's usually benign, and make it become a powerful, unwanted accomplice in neuronal death.
This finding, reported today in Proceedings of the National Academy of Sciences, could ultimately lead to new therapeutic approaches to many of the world's debilitating or fatal diseases.
The research explains how one form of oxidative stress called tyrosine nitration can lead to cell death. Through the common link of inflammation, this may relate to health problems ranging from heart disease to chronic pain, spinal injury, cancer, aging, and amyotrophic lateral sclerosis, or Lou Gehrig's disease.
As part of the work, the scientists also identified a specific "chaperone" protein damaged by oxidants, which is getting activated in this spiral of cellular decline and death. This insight will provide a new approach to design therapeutic drugs.
The findings were published by scientists from the Linus Pauling Institute at Oregon State University; Maria Clara Franco and Alvaro Estevez, now at the University of Central Florida; and researchers from several other institutions. They culminate a decade of work.
"These are very exciting results and could begin a major shift in medicine," said Joseph Beckman.
Beckman is an LPI principal investigator, distinguished professor of biochemistry, and director of the OSU Environmental Health Sciences Center. He also last year received the Discovery Award from the Medical Research Foundation of Oregon, given to the leading medical scientist in the state.
"Preventing this process of tyrosine nitration may protect against a wide range of degenerative diseases," Beckman said. "The study shows that drugs could effectively target oxidatively-damaged proteins."
Scientists have known for decades about the general concept of oxidative damage to cells, resulting
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Oregon State University