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Title: Vanadium-induced inhibition of renal Na+, K+-adenosinetriphosphatase in the chicken after chronic dietary exposure. Author: Phillips TD, Nechay BR, Neldon SL, Kubena LF, Heidelbaugh ND, Shepherd EC, Stein AF, Hayes AW. Journal: J Toxicol Environ Health; 1982 Apr; 9(4):651-61. PubMed ID: 6125598. Abstract: Recent work has shown that V accumulates in the kidney and is a potent inhibitor of Na+, K+-adenosinetriphosphatase (ATPase) in vitro. Thus, as a nutritionally required element, V may regulate cation transport. The effect of chronic intake of the metal on Na+, K+-ATPase in vivo has not been reported. In this study laying strain chickens were fed calcium orthovanadate for 15 mo from d 1 of age at levels of 0, 25, 50, and 100 ppm in the diet. Whole tissue homogenates and 13,000 X g fractions were analyzed for ATPase activities. Concentrations of V producing 50% inhibition of Na+, K+-ATPase activity ranged from 1.0 X 10(-5) M in liver to 1.8 X 10(-6) M in kidney, which was the most sensitive tissue tested in vitro. Mg2+ -ATPase was more resistant to V than Na+, K+-ATPase. Studies in vivo suggested a V-dependent inhibition of renal Na+, K+-ATPase. Correlation of enzyme specific activity and levels of V in kidneys suggested V-ATPase mediated alteration in renal function.[Abstract] [Full Text] [Related] [New Search]