Scientists have long known that the body rids itself of excess copper and various other minerals by collecting them in the liver and excreting them through the liver's bile. However, a new study led by Johns Hopkins researchers and published June 22 in PLoS ONE suggests that when this route is impaired there's another exit route just for copper: A molecule sequesters only that mineral and routes it from the body through urine.
The researchers, led by Svetlana Lutsenko, Ph.D., a professor of physiology at the Johns Hopkins University School of Medicine, found this additional copper escape hatch by studying an animal model of Wilson's disease, a rare disorder most often diagnosed in children. People with this disease accumulate abnormally large amounts of copper in the liver, eventually leading to liver damage and failure.
Micronutrients such as copper, zinc and iron are indispensible for human development. Copper is required for embryonic development, respiration, and cardiovascular function, among other processes; too little copper can be fatal whereas too much can cause neurological impairment and organ failure.
One diagnostic test for Wilson's disease is to check for high amounts of copper in the urine; copper levels could be especially high in advanced stages of this disorder. For decades doctors and scientists have blamed this high urinary copper on the breakdown of cells in the liver, which purportedly dumped their contents into the bloodstream as they died. These contents were thought to be picked up by the kidneys and eventually excreted in the urine.
However, Lutsenko says, this theory had never been tested. To verify this explanation, she and her colleagues examined mice genetically modified to have Wilson's disease. As in people, these animals' liver function gradually worsens over time due to copper accumulation. Eventually the animals' livers regenerate and liver function improves and with this the resear
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Johns Hopkins Medical Institutions