NEPHROLOGY: Role for the protein Sat1 in kidney stones and liver toxicity
A team of researchers, at the University of Queensland, Australia, has studied the function of the protein Sat1 in mice and determined that it is likely to have an important role in acetaminophen-induced liver toxicity (the most common cause of acute liver failure in the Western world) and urolithiasis (a condition in which stones are present in the urinary system, including the kidneys and bladder).
Kidney and urinary stones and liver toxicity are linked to alterations in oxalate and sulfate homeostasis, respectively. The team, led by Daniel Markovich, generated mice lacking Sat1, a mediator of oxalate and sulfate transport that is localized to the kidney, liver, and intestine. Sat1-deficient mice excreted excess amounts of oxalate in their urine (a common symptom in individuals with calcium oxalate kidney stones) and had calcium oxalate stones in their kidney tubules and bladder. These mice also excreted excess amounts of sulfate in their urine and exhibited enhanced acetaminophen-induced liver toxicity. The authors therefore conclude that Sat1 maintains appropriate levels of oxalate and sulfate and may be critical to the development of calcium oxalate kidney and urinary stones and acetaminophen-induced liver toxicity.
TITLE: Urolithiasis and hepatotoxicity are linked to the anion transporter Sat1 in mice
University of Queensland, St. Lucia, Queensland, Australia.
Phone: 61.7.3365.1400; Fax: 61.7.3365.1766; E-mail: email@example.com.
View this article at: http://www.jci.org/articles/view/31474?key=35d3e1718eeb05731035
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Journal of Clinical Investigation