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Exonerating uric acid
05-28-2014
by Kelsey Kaustinen  |  Email the author
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SINGAPORE—As is the case with a number of health conditions, the overproduction of one protein or chemical that in normal levels is harmless can often lead to issues. Such is the case with the much-maligned uric acid, the chief cause of the painful condition of gout.
 
As noted by MedlinePlus of the U.S. National Library of Medicine, uric acid is what results when the body breaks down substances known as purines, which are found in some food or drinks. Most uric acid is dissolved in the blood, travels to the kidneys and then is summarily expelled from the body. If uric acid production levels are too high, however, or if the body does not remove enough of it, it can lead to issues such as gout or hyperuricemia.
 
But now a study has emerged that may help uric acid’s reputation, as the chemical has been found to be a major intracellular antioxidant.
 
The study, titled “The uric acid transporter SLC2A9 is a direct target gene of the tumor suppressor p53 contributing to antioxidant defense,” was published online May 26 in Oncogene. Its abstract notes that despite the chemical’s existence as the cause of gout, uric acid “has been linked with human longevity because of its hypothetical antioxidant function.”
 
Koji Itahana, assistant professor of Duke-NUS Graduate Medical School Singapore (Duke-NUS), led the study, which revealed how uric acid enters cells in order to protect them in the event of stress. Uric acid travels through the uric acid transporter SLC2A9, also known as GLUT9, and is then regulated by the p53 protein, which is both one of the most important tumor suppressor proteins and a protein mutated in about half of cancers worldwide.
 
Researchers from Duke-NUS’ Cancer and Stem Cell Biology Program demonstrated first evidence of how the p53-GLUT9 pathway serves to prevent the accumulation of Reactive oxygen species (ROS), molecules that contain highly reactive oxygen. In times of environmental stress, ROS’ can increase significantly, leading to cell damage known as oxidative stress, which in its turn leads to aging, cancer, cardiovascular and neurodegenerative diseases. In the study, “expression of SLC2A9 reduced ROS and protected against DNA damage and cell death, suggesting its antioxidant function.”
 
Itahana’s work also demonstrated that shutting down the p53-GLUT9 pathway may serve as a possible treatment approach for patients with cancer. As noted in the paper’s abstract, “Oxidative stress induced SLC2A9 expression in a p53- dependent manner, and inhibition of SLC2A9 by small interfering RNA or anti-gout drugs such as probenecid significantly increased ROS levels in an uric acid-dependent manner and greatly sensitized cancer cells to chemotherapeutic drugs.”
 
“While the p53-GLUT9 mechanism is a way that helps prevent disease in a healthy body, once the body already has cancer, disrupting that same mechanism may be a way to kill the cancer since cancer has already very high levels of ROS. For instance, if a patient were to take probenecid, a gout drug that inhibits the function of GLUT9, and a chemo drug, ROS levels would become so high that cancer cells may not be able to survive in the body because there is simply no space,” said Itahana.
 
Further proof of the role the pathway might play in cancer was seen in the fact that “decreased SLC2A9 expression was observed in several cancer types and was associated with a poorer prognosis.”
 
This study received support from the Singapore Ministry of Education Academic Research Fund Tier 2 and the Duke-NUS Signature Research Program, with funding from the Ministry of Health.
 
Code: E05281404

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